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Prof. Andy Baker
University of Edinburgh

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Research Keywords & Expertise

0 Adenovirus
0 Cardiovascular
0 FMS
0 Gene Therapy
0 Molecular Medicine

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RNA
Cardiovascular
Adenovirus
lncRNA
Gene Therapy
Endothelial cell

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Short Biography

Degrees & Fellowships: 1990 BSc (Joint Hons) School of Pharmacy, University of London, Pharmacology & Toxicology. 1994 PhD University of Wales College of Medicine. 2002 FAHA International Fellow of the American Heart Association. 2007 FESC Fellowship of the European Society of Cardiology. 2010 FRSE Fellowship of the Royal Society of Edinburgh. 2015 FMedSci Fellowship of the Academy of Medical Sciences. Present Post: Oct 2015 BHF Professor of Translational Cardiovascular Sciences, University of Edinburgh. Feb 2016 Gustav Born Chair of Vascular Biology, University of Edinburgh. Jun 2017 Head of Centre for Cardiovascular Science, College of Medicine and Veterinary Medicine, University of Edinburgh. Previous Posts: Aug 2011 - Sep 2015 BHF Chair of Translational Cardiovascular Sciences, University of Glasgow. Nov 2011 - Sep 2015 Deputy Director, Institute of Cardiovascular and Medical Sciences, University of Glasgow. Aug 2010 - Oct 2011 Acting Director Institute of Cardiovascular and Medical Sciences. Feb 2005 - Jul 2011 Professor of Molecular Medicine, University of Glasgow. Aug 2002 - Jan 2005 Personal Readership in Molecular Therapy, University of Glasgow. Aug 1999 - Jul 2002 Senior Lecturer in Molecular Medicine, University of Glasgow.

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Research article
Published: 30 July 2021 in Proceedings of the National Academy of Sciences
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A network of molecular factors drives the development, differentiation, and maintenance of endothelial cells. Friend leukemia integration 1 transcription factor (FLI1) is a bona fide marker of endothelial cells during early development. In zebrafish Tg( f li1:EGFP) y1 , we identified two endothelial cell populations, high-fli1 + and low-fli1 +, by the intensity of green fluorescent protein signal. By comparing RNA-sequencing analysis of non-fli1 expressing cells (fli1 −) with these two (fli1 +) cell populations, we identified several up-regulated genes, not previously recognized as important, during endothelial development. Compared with fli1 − and low-fli1 + cells, high-fli1 + cells showed up-regulated expression of the zinc finger transcription factor PRDI-BF1 and RIZ homology domain containing 16 (prdm16). Prdm16 knockdown (KD) by morpholino in the zebrafish larva was associated with impaired angiogenesis and increased number of low-fli1 + cells at the expense of high-fli1 + cells. In addition, PRDM16 KD in endothelial cells derived from human-induced pluripotent stem cells impaired their differentiation and migration in vitro. Moreover, zebrafish mutants (mut) with loss of function for the oncogene LIM domain only 2 (lmo2) also showed reduced prdm16 gene expression combined with impaired angiogenesis. Prdm16 expression was reduced further in endothelial (CD31+) cells compared with CD31− cells isolated from l mo2-mutants (l mo2-mut) embryos. Chromatin immunoprecipitation–PCR demonstrated that Lmo2 binds to the promoter and directly regulates the transcription of prdm16. This work unveils a mechanism by which prdm16 expression is activated in endothelial cells by Lmo2 and highlights a possible therapeutic pathway by which to modulate endothelial cell growth and repair.

ACS Style

Gianfranco Matrone; Bo Xia; Kaifu Chen; Martin A. Denvir; Andrew H. Baker; John P. Cooke. Fli1+ cells transcriptional analysis reveals an Lmo2–Prdm16 axis in angiogenesis. Proceedings of the National Academy of Sciences 2021, 118, 1 .

AMA Style

Gianfranco Matrone, Bo Xia, Kaifu Chen, Martin A. Denvir, Andrew H. Baker, John P. Cooke. Fli1+ cells transcriptional analysis reveals an Lmo2–Prdm16 axis in angiogenesis. Proceedings of the National Academy of Sciences. 2021; 118 (31):1.

Chicago/Turabian Style

Gianfranco Matrone; Bo Xia; Kaifu Chen; Martin A. Denvir; Andrew H. Baker; John P. Cooke. 2021. "Fli1+ cells transcriptional analysis reveals an Lmo2–Prdm16 axis in angiogenesis." Proceedings of the National Academy of Sciences 118, no. 31: 1.

Journal article
Published: 28 July 2021 in Viruses
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The human adenovirus phylogenetic tree is split across seven species (A–G). Species D adenoviruses offer potential advantages for gene therapy applications, with low rates of pre-existing immunity detected across screened populations. However, many aspects of the basic virology of species D—such as their cellular tropism, receptor usage, and in vivo biodistribution profile—remain unknown. Here, we have characterized human adenovirus type 49 (HAdV-D49)—a relatively understudied species D member. We report that HAdV-D49 does not appear to use a single pathway to gain cell entry, but appears able to interact with various surface molecules for entry. As such, HAdV-D49 can transduce a broad range of cell types in vitro, with variable engagement of blood coagulation FX. Interestingly, when comparing in vivo biodistribution to adenovirus type 5, HAdV-D49 vectors show reduced liver targeting, whilst maintaining transduction of lung and spleen. Overall, this presents HAdV-D49 as a robust viral vector platform for ex vivo manipulation of human cells, and for in vivo applications where the therapeutic goal is to target the lung or gain access to immune cells in the spleen, whilst avoiding liver interactions, such as intravascular vaccine applications.

ACS Style

Emily Bates; John Counsell; Sophie Alizert; Alexander Baker; Natalie Suff; Ashley Boyle; Angela Bradshaw; Simon Waddington; Stuart Nicklin; Andrew Baker; Alan Parker. In Vitro and In Vivo Evaluation of Human Adenovirus Type 49 as a Vector for Therapeutic Applications. Viruses 2021, 13, 1483 .

AMA Style

Emily Bates, John Counsell, Sophie Alizert, Alexander Baker, Natalie Suff, Ashley Boyle, Angela Bradshaw, Simon Waddington, Stuart Nicklin, Andrew Baker, Alan Parker. In Vitro and In Vivo Evaluation of Human Adenovirus Type 49 as a Vector for Therapeutic Applications. Viruses. 2021; 13 (8):1483.

Chicago/Turabian Style

Emily Bates; John Counsell; Sophie Alizert; Alexander Baker; Natalie Suff; Ashley Boyle; Angela Bradshaw; Simon Waddington; Stuart Nicklin; Andrew Baker; Alan Parker. 2021. "In Vitro and In Vivo Evaluation of Human Adenovirus Type 49 as a Vector for Therapeutic Applications." Viruses 13, no. 8: 1483.

Preprint
Published: 22 July 2021
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The human adenovirus phylogenetic tree is split across seven species (A-G). Species D adenoviruses offer potential advantages for gene therapy applications, with low rates of preexisting immunity detected across screened populations. However, many aspects of the basic virology of species D, such as their cellular tropism, receptor usage and in vivo biodistribution profile, remain unknown. Here, we have characterized human adenovirus type 49 (HAdV-D49), a relatively understudied species D member. We report that HAdV-D49 does not appear to use a single pathway to gain cell entry but appears able to interact with various surface molecules for entry. As such, HAdV-D49 can transduce a broad range of cell types in vitro, with variable engagement of blood coagulation FX. Interestingly, when comparing in vivo biodistribution to adenovirus type 5, HAdV-D49 vectors show reduced liver targeting whilst maintaining transduction of lung and spleen. Overall, this presents HAdV-D49 as a robust viral vector platform for ex vivo manipulation of human cells and for in vivo applications where the therapeutic goal is to target the lung or gain access to immune cells in the spleen whilst avoiding liver interactions, such as intravascular vaccine applications.

ACS Style

Emily A. Bates; John R. Counsell; Sophie Alizert; Alexander T. Baker; Natalie Suff; Ashley Boyle; Angela C. Bradshaw; Simon N. Waddington; Stuart A. Nicklin; Andrew H. Baker; Alan L. Parker. In Vitro and In Vivo Evaluation of Human Adenovirus Type 49 as a Vector for Therapeutic Applications. 2021, 1 .

AMA Style

Emily A. Bates, John R. Counsell, Sophie Alizert, Alexander T. Baker, Natalie Suff, Ashley Boyle, Angela C. Bradshaw, Simon N. Waddington, Stuart A. Nicklin, Andrew H. Baker, Alan L. Parker. In Vitro and In Vivo Evaluation of Human Adenovirus Type 49 as a Vector for Therapeutic Applications. . 2021; ():1.

Chicago/Turabian Style

Emily A. Bates; John R. Counsell; Sophie Alizert; Alexander T. Baker; Natalie Suff; Ashley Boyle; Angela C. Bradshaw; Simon N. Waddington; Stuart A. Nicklin; Andrew H. Baker; Alan L. Parker. 2021. "In Vitro and In Vivo Evaluation of Human Adenovirus Type 49 as a Vector for Therapeutic Applications." , no. : 1.

Accepted manuscript
Published: 23 June 2021 in Cardiovascular Research
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While humans lack sufficient capacity to undergo cardiac regeneration following injury, zebrafish can fully recover from a range of cardiac insults. Over the past two decades, our understanding of the complexities of both the independent and co-ordinated injury responses by multiple cardiac tissues during zebrafish heart regeneration has increased exponentially. Although cardiomyocyte regeneration forms the cornerstone of the reparative process in the injured zebrafish heart, recent studies have shown that this is dependent on prior neovascularization and lymphangiogenesis, which in turn require epicardial, endocardial, and inflammatory cell signalling within an extracellular milieu that is optimized for regeneration. Indeed, it is the amalgamation of multiple regenerative systems and gene regulatory patterns that drives the much-heralded success of the adult zebrafish response to cardiac injury. Increasing evidence supports the emerging paradigm that developmental transcriptional programmes are re-activated during adult tissue regeneration, including in the heart, and the zebrafish represents an optimal model organism to explore this concept. In this review, we summarize recent advances from the zebrafish cardiovascular research community with novel insight into the mechanisms associated with endogenous cardiovascular repair and regeneration, which may be of benefit to inform future strategies for patients with cardiovascular disease.

ACS Style

Katherine M Ross Stewart; Sophie L Walker; Andrew H Baker; Paul R Riley; Mairi Brittan. Hooked on heart regeneration: the zebrafish guide to recovery. Cardiovascular Research 2021, 1 .

AMA Style

Katherine M Ross Stewart, Sophie L Walker, Andrew H Baker, Paul R Riley, Mairi Brittan. Hooked on heart regeneration: the zebrafish guide to recovery. Cardiovascular Research. 2021; ():1.

Chicago/Turabian Style

Katherine M Ross Stewart; Sophie L Walker; Andrew H Baker; Paul R Riley; Mairi Brittan. 2021. "Hooked on heart regeneration: the zebrafish guide to recovery." Cardiovascular Research , no. : 1.

Research article
Published: 30 April 2021 in Circulation Research
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Rationale: In the microenvironment of atherosclerotic lesions, vascular smooth muscle cells (vSMCs) switch to a dedifferentiated state but the underlying molecular mechanisms driving this switch are not fully understood. Long noncoding RNAs (lncRNAs) are dysregulated during vascular pathology, but relatively little is known about their involvement in controlling vSMCs function. Cardiac mesoderm enhancer-associated noncoding RNA (CARMN) is a lncRNA located immediately upstream of the microRNAs-143 and -145 (miR-143 and miR-145 ), both involved in vSMCs function. Objective: We investigated the role of the lncRNA CARMN, independent from miR-143 and miR-145, as a potential regulator of vSMC phenotypes in vitro and the consequences of its loss during the development of atherosclerosis in vivo. We hypothesized that loss of CARMN is a primary event controlling the functional switch towards proatherogenic vSMC phenotype and accelerates the development of the plaques in vivo. Method and Results: Expression of CARMN lncRNA was silenced using locked nucleic acids antisense oligonucleotides (GapmeRs) in human coronary arterial smooth muscle cells, revealing that GapmeR-mediated loss of CARMN negatively affects miR-143 and miR-145 microRNA expression. RNA sequencing of CARMN-depleted human coronary arterial smooth muscle cells revealed large transcriptomic changes, associated with vSMC proliferation, migration, inflammation, lipid metabolism, and dedifferentiation. The use of miR-143 and miR-145 mimics revealed that CARMN regulates human coronary arterial smooth muscle cell proliferation in a microRNA-independent manner. In humans and mice, CARMN and associated microRNAs were downregulated in advanced versus early atherosclerotic lesions. Using a CRISPR (clustered regularly interspaced short palindromic repeats)-Cas9 (CRISPR-associated protein 9) knockout approach, we explored the implications of CARMN depletion during atherosclerosis in vivo. Consistent with in vitro results, the knockout of CARMN impaired the expression of miR-143 and miR-145 under homeostatic conditions. Importantly, when atherosclerosis was induced in these mice, CARMN knockout increased the volume, size, proinflammatory Lgals3 (galectin 3)-expressing cells content, and altered plaque composition, yielding an advanced phenotype. Conclusions: We identified the early loss of CARMN lncRNA as critical event which primes vSMCs towards a proatherogenic phenotype in vitro and accelerates the development of atherosclerosis in vivo.

ACS Style

Francesca Vacante; Julie Rodor; Mukesh K. Lalwani; Amira D. Mahmoud; Matthew Bennett; Azzurra L. De Pace; Eileen Miller; Kim Van Kuijk; Jenny de Bruijn; Marion Gijbels; Thomas C. Williams; Michael B. Clark; Jessica P. Scanlon; Amanda C. Doran; Rusty Montgomery; David E. Newby; Mauro Giacca; Dónal O’Carroll; Patrick W.F. Hadoke; Laura Denby; Judith C. Sluimer; Andrew H. Baker. CARMN Loss Regulates Smooth Muscle Cells and Accelerates Atherosclerosis in Mice. Circulation Research 2021, 128, 1258 -1275.

AMA Style

Francesca Vacante, Julie Rodor, Mukesh K. Lalwani, Amira D. Mahmoud, Matthew Bennett, Azzurra L. De Pace, Eileen Miller, Kim Van Kuijk, Jenny de Bruijn, Marion Gijbels, Thomas C. Williams, Michael B. Clark, Jessica P. Scanlon, Amanda C. Doran, Rusty Montgomery, David E. Newby, Mauro Giacca, Dónal O’Carroll, Patrick W.F. Hadoke, Laura Denby, Judith C. Sluimer, Andrew H. Baker. CARMN Loss Regulates Smooth Muscle Cells and Accelerates Atherosclerosis in Mice. Circulation Research. 2021; 128 (9):1258-1275.

Chicago/Turabian Style

Francesca Vacante; Julie Rodor; Mukesh K. Lalwani; Amira D. Mahmoud; Matthew Bennett; Azzurra L. De Pace; Eileen Miller; Kim Van Kuijk; Jenny de Bruijn; Marion Gijbels; Thomas C. Williams; Michael B. Clark; Jessica P. Scanlon; Amanda C. Doran; Rusty Montgomery; David E. Newby; Mauro Giacca; Dónal O’Carroll; Patrick W.F. Hadoke; Laura Denby; Judith C. Sluimer; Andrew H. Baker. 2021. "CARMN Loss Regulates Smooth Muscle Cells and Accelerates Atherosclerosis in Mice." Circulation Research 128, no. 9: 1258-1275.

Research article
Published: 16 April 2021 in Circulation Research
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Rationale: Endothelial-to-mesenchymal transition (EndMT) is a dynamic biological process involved in pathological vascular remodeling. However, the molecular mechanisms that govern this transition remain largely unknown, including the contribution of long noncoding RNAs (lncRNAs). Objectives: To investigate the role of lncRNAs in EndMT and their relevance to vascular remodeling. Methods and Results: To study EndMT in vitro, primary endothelial cells were treated with transforming growth factor-β2 and interleukin-1β. Single-cell and bulk RNA-seq (RNA-sequencing) were performed to investigate the transcriptional architecture of EndMT and identify regulated lncRNAs. The functional contribution of seven lncRNAs during EndMT was investigated based on a DsiRNA (dicer-substrate short interfering RNAs) screening assay. The loss of lncRNA MIR503HG was identified as a common signature across multiple human endothelial cell types undergoing EndMT in vitro. MIR503HG depletion induced a spontaneous EndMT phenotype, while its overexpression repressed hallmark EndMT changes, regulating 29% of its transcriptome signature. Importantly, the phenotypic changes induced by MIR503HG were independent of miR-424 and miR-503, which overlap the lncRNA locus. The pathological relevance of MIR503HG downregulation was confirmed in vivo using sugen/hypoxia–induced pulmonary hypertension in mice, as well as in human clinical samples, in lung sections and blood outgrowth endothelial cells from pulmonary arterial hypertension patients. Overexpression of human MIR503HG in sugen/hypoxia mice led to reduced mesenchymal marker expression, suggesting MIR503HG therapeutic potential. We also revealed that MIR503HG interacts with the PTBP1 (polypyrimidine tract binding protein 1) and regulates its protein level. PTBP1 regulation of EndMT markers suggests that the role of MIR503HG in EndMT might be mediated in part by PTBP1. Conclusions: This study reports a novel lncRNA transcriptional profile associated with EndMT and reveals the crucial role of the loss of MIR503HG in EndMT and its relevance to pulmonary hypertension.

ACS Style

João P. Monteiro; Julie Rodor; Axelle Caudrillier; Jessica P. Scanlon; Ana-Mishel Spiroski; Tatiana Dudnakova; Beatrice Pflüger-Müller; Alena Shmakova; Alex von Kriegsheim; Lin Deng; Richard S. Taylor; John R. Wilson-Kanamori; Shiau-Haln Chen; Kevin Stewart; Adrian Thomson; Tijana Mitić; John D. McClure; Jean Iynikkel; Patrick W.F. Hadoke; Laura Denby; Angela C. Bradshaw; Paola Caruso; Nicholas W. Morrell; Jason C. Kovacic; Igor Ulitsky; Neil C. Henderson; Andrea Caporali; Matthias S. Leisegang; Ralf P. Brandes; Andrew H. Baker. MIR503HG Loss Promotes Endothelial-to-Mesenchymal Transition in Vascular Disease. Circulation Research 2021, 128, 1173 -1190.

AMA Style

João P. Monteiro, Julie Rodor, Axelle Caudrillier, Jessica P. Scanlon, Ana-Mishel Spiroski, Tatiana Dudnakova, Beatrice Pflüger-Müller, Alena Shmakova, Alex von Kriegsheim, Lin Deng, Richard S. Taylor, John R. Wilson-Kanamori, Shiau-Haln Chen, Kevin Stewart, Adrian Thomson, Tijana Mitić, John D. McClure, Jean Iynikkel, Patrick W.F. Hadoke, Laura Denby, Angela C. Bradshaw, Paola Caruso, Nicholas W. Morrell, Jason C. Kovacic, Igor Ulitsky, Neil C. Henderson, Andrea Caporali, Matthias S. Leisegang, Ralf P. Brandes, Andrew H. Baker. MIR503HG Loss Promotes Endothelial-to-Mesenchymal Transition in Vascular Disease. Circulation Research. 2021; 128 (8):1173-1190.

Chicago/Turabian Style

João P. Monteiro; Julie Rodor; Axelle Caudrillier; Jessica P. Scanlon; Ana-Mishel Spiroski; Tatiana Dudnakova; Beatrice Pflüger-Müller; Alena Shmakova; Alex von Kriegsheim; Lin Deng; Richard S. Taylor; John R. Wilson-Kanamori; Shiau-Haln Chen; Kevin Stewart; Adrian Thomson; Tijana Mitić; John D. McClure; Jean Iynikkel; Patrick W.F. Hadoke; Laura Denby; Angela C. Bradshaw; Paola Caruso; Nicholas W. Morrell; Jason C. Kovacic; Igor Ulitsky; Neil C. Henderson; Andrea Caporali; Matthias S. Leisegang; Ralf P. Brandes; Andrew H. Baker. 2021. "MIR503HG Loss Promotes Endothelial-to-Mesenchymal Transition in Vascular Disease." Circulation Research 128, no. 8: 1173-1190.

Journal article
Published: 16 March 2021 in Cardiovascular Research
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ACS Style

Monika M Gladka; Andrew H Baker. Jumping on base editing to repair the diseased cardiovascular system in vivo. Cardiovascular Research 2021, 117, e46 -e48.

AMA Style

Monika M Gladka, Andrew H Baker. Jumping on base editing to repair the diseased cardiovascular system in vivo. Cardiovascular Research. 2021; 117 (4):e46-e48.

Chicago/Turabian Style

Monika M Gladka; Andrew H Baker. 2021. "Jumping on base editing to repair the diseased cardiovascular system in vivo." Cardiovascular Research 117, no. 4: e46-e48.

Preprint content
Published: 14 March 2021
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Pre-existing immune responses towards adenoviral vector limit the use of a vector based on particular serotypes and its clinical applicability for gene therapy and/or vaccination. Therefore, there is a significant interest to vectorize novel adenoviral types that have low seroprevalence in the human population. Here, we describe the discovery and vectorization of a chimeric human adenovirus, which we call HAdV-20-42-42. Full genome sequencing revealed that this virus is closely related to human serotype 42, except for the penton-base which is derived from serotype 20. The HAdV-20-42-42 vector could be propagated stably to high titers on existing E1-complementing packaging cell lines. Receptor binding studies revealed that the vector utilized both CAR and CD46 as receptors for cell entry. Furthermore, the HAdV-20-42-42 vector was potent in transducing human and murine cardiovascular cells and tissues, irrespective of the presence of blood coagulation factor X. In addition, the vector did not sequester in the liver upon intravenous administration in rodents. Finally, we demonstrate that potent T-cell responses against vector-delivered antigens could be induced upon vaccination. In summary, from the data obtained we conclude that HAdV-20-42-42 provides a valuable addition to the portfolio of adenoviral vectors available to develop safe and efficacious products in the fields of gene therapy and vaccination. IMPORTANCE Adenoviral vectors are currently under investigation for a broad range of therapeutic indications in diverse fields, such as oncology and gene therapy, as well as for vaccination both for human and veterinary use. A wealth of data shows that pre-existing immune responses may limit the use of a vector. Particularly in the current climate of global pandemic, there is a need to expand the toolbox with novel adenoviral vectors for vaccine development. Our data demonstrates that we have successfully vectorized a novel adenovirus serotype with low seroprevalence. The cell transduction data and antigen-specific immune responses induced in vivo demonstrate that this vector is highly promising for the development of gene therapy and vaccine products.

ACS Style

Mónika Z. Ballmann; Svjetlana Raus; Ruben Engelhart; Győző L. Kaján; Chantal van der Zalm; Tibor Papp; Lijo John; Selina Khan; Jerome Custers; Wilfried A.M. Bakker; Hilde M. van der Schaar; Niklas Arnberg; Angelique A.C. Lemckert; Menzo Havenga; Andrew H. Baker. Human AdV-20-42-42, a promising novel adenoviral vector for gene therapy and vaccine product development. 2021, 1 .

AMA Style

Mónika Z. Ballmann, Svjetlana Raus, Ruben Engelhart, Győző L. Kaján, Chantal van der Zalm, Tibor Papp, Lijo John, Selina Khan, Jerome Custers, Wilfried A.M. Bakker, Hilde M. van der Schaar, Niklas Arnberg, Angelique A.C. Lemckert, Menzo Havenga, Andrew H. Baker. Human AdV-20-42-42, a promising novel adenoviral vector for gene therapy and vaccine product development. . 2021; ():1.

Chicago/Turabian Style

Mónika Z. Ballmann; Svjetlana Raus; Ruben Engelhart; Győző L. Kaján; Chantal van der Zalm; Tibor Papp; Lijo John; Selina Khan; Jerome Custers; Wilfried A.M. Bakker; Hilde M. van der Schaar; Niklas Arnberg; Angelique A.C. Lemckert; Menzo Havenga; Andrew H. Baker. 2021. "Human AdV-20-42-42, a promising novel adenoviral vector for gene therapy and vaccine product development." , no. : 1.

Letter
Published: 23 February 2021 in Circulation
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ACS Style

Ian R. McCracken; Gaye Saginc; Liqun He; AliK Huseynov; Alison Daniels; Sarah Fletcher; Claire Peghaire; Viktoria Kalna; Maarja Andaloussi-Mäe; Lars Muhl; Nicky M. Craig; Samantha J. Griffiths; Jürgen G. Haas; Christine Tait-Burkard; Urban Lendahl; Graeme M. Birdsey; Christer Betsholtz; Michela Noseda; Andrew H. Baker; Anna M. Randi. Lack of Evidence of Angiotensin-Converting Enzyme 2 Expression and Replicative Infection by SARS-CoV-2 in Human Endothelial Cells. Circulation 2021, 143, 865 -868.

AMA Style

Ian R. McCracken, Gaye Saginc, Liqun He, AliK Huseynov, Alison Daniels, Sarah Fletcher, Claire Peghaire, Viktoria Kalna, Maarja Andaloussi-Mäe, Lars Muhl, Nicky M. Craig, Samantha J. Griffiths, Jürgen G. Haas, Christine Tait-Burkard, Urban Lendahl, Graeme M. Birdsey, Christer Betsholtz, Michela Noseda, Andrew H. Baker, Anna M. Randi. Lack of Evidence of Angiotensin-Converting Enzyme 2 Expression and Replicative Infection by SARS-CoV-2 in Human Endothelial Cells. Circulation. 2021; 143 (8):865-868.

Chicago/Turabian Style

Ian R. McCracken; Gaye Saginc; Liqun He; AliK Huseynov; Alison Daniels; Sarah Fletcher; Claire Peghaire; Viktoria Kalna; Maarja Andaloussi-Mäe; Lars Muhl; Nicky M. Craig; Samantha J. Griffiths; Jürgen G. Haas; Christine Tait-Burkard; Urban Lendahl; Graeme M. Birdsey; Christer Betsholtz; Michela Noseda; Andrew H. Baker; Anna M. Randi. 2021. "Lack of Evidence of Angiotensin-Converting Enzyme 2 Expression and Replicative Infection by SARS-CoV-2 in Human Endothelial Cells." Circulation 143, no. 8: 865-868.

Journal article
Published: 02 February 2021 in International Journal of Molecular Sciences
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Vascular smooth muscle cells (VSMCs) provide vital contractile force within blood vessel walls, yet can also propagate cardiovascular pathologies through proliferative and pro-inflammatory activities. Such phenotypes are driven, in part, by the diverse effects of long non-coding RNAs (lncRNAs) on gene expression. However, lncRNA characterisation in VSMCs in pathological states is hampered by incomplete lncRNA representation in reference annotation. We aimed to improve lncRNA representation in such contexts by assembling non-reference transcripts in RNA sequencing datasets describing VSMCs stimulated in vitro with cytokines, growth factors, or mechanical stress, as well as those isolated from atherosclerotic plaques. All transcripts were then subjected to a rigorous lncRNA prediction pipeline. We substantially improved coverage of lncRNAs responding to pro-mitogenic stimuli, with non-reference lncRNAs contributing 21–32% for each dataset. We also demonstrate non-reference lncRNAs were biased towards enriched expression within VSMCs, and transcription from enhancer sites, suggesting particular relevance to VSMC processes, and the regulation of neighbouring protein-coding genes. Both VSMC-enriched and enhancer-transcribed lncRNAs were large components of lncRNAs responding to pathological stimuli, yet without novel transcript discovery 33–46% of these lncRNAs would remain hidden. Our comprehensive VSMC lncRNA repertoire allows proper prioritisation of candidates for characterisation and exemplifies a strategy to broaden our knowledge of lncRNA across a range of disease states.

ACS Style

Matthew Bennett; Igor Ulitsky; Iraide Alloza; Koen Vandenbroeck; Vladislav Miscianinov; Amira Mahmoud; Margaret Ballantyne; Julie Rodor; Andrew Baker. Novel Transcript Discovery Expands the Repertoire of Pathologically-Associated, Long Non-Coding RNAs in Vascular Smooth Muscle Cells. International Journal of Molecular Sciences 2021, 22, 1484 .

AMA Style

Matthew Bennett, Igor Ulitsky, Iraide Alloza, Koen Vandenbroeck, Vladislav Miscianinov, Amira Mahmoud, Margaret Ballantyne, Julie Rodor, Andrew Baker. Novel Transcript Discovery Expands the Repertoire of Pathologically-Associated, Long Non-Coding RNAs in Vascular Smooth Muscle Cells. International Journal of Molecular Sciences. 2021; 22 (3):1484.

Chicago/Turabian Style

Matthew Bennett; Igor Ulitsky; Iraide Alloza; Koen Vandenbroeck; Vladislav Miscianinov; Amira Mahmoud; Margaret Ballantyne; Julie Rodor; Andrew Baker. 2021. "Novel Transcript Discovery Expands the Repertoire of Pathologically-Associated, Long Non-Coding RNAs in Vascular Smooth Muscle Cells." International Journal of Molecular Sciences 22, no. 3: 1484.

Communication
Published: 19 January 2021 in International Journal of Molecular Sciences
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Long non-coding RNAs (lncRNAs) have structural and functional roles in development and disease. We have previously shown that the LINC00961/SPAAR (small regulatory polypeptide of amino acid response) locus regulates endothelial cell function, and that both the lncRNA and micropeptide counter-regulate angiogenesis. To assess human cardiac cell SPAAR expression, we mined a publicly available scRNSeq dataset and confirmed LINC00961 locus expression and hypoxic response in a murine endothelial cell line. We investigated post-natal growth and development, basal cardiac function, the cardiac functional response, and tissue-specific response to myocardial infarction. To investigate the influence of the LINC00961/SPAAR locus on longitudinal growth, cardiac function, and response to myocardial infarction, we used a novel CRISPR/Cas9 locus knockout mouse line. Data mining suggested that SPAAR is predominantly expressed in human cardiac endothelial cells and fibroblasts, while murine LINC00961 expression is hypoxia-responsive in mouse endothelial cells. LINC00961–/– mice displayed a sex-specific delay in longitudinal growth and development, smaller left ventricular systolic and diastolic areas and volumes, and greater risk area following myocardial infarction compared with wildtype littermates. These data suggest the LINC00961/SPAAR locus contributes to cardiac endothelial cell and fibroblast function and hypoxic response, growth and development, and basal cardiovascular function in adulthood.

ACS Style

Ana-Mishel Spiroski; Rachel Sanders; Marco Meloni; Ian R. McCracken; Adrian Thomson; Mairi Brittan; Gillian A. Gray; Andrew H. Baker. The Influence of the LINC00961/SPAAR Locus Loss on Murine Development, Myocardial Dynamics, and Cardiac Response to Myocardial Infarction. International Journal of Molecular Sciences 2021, 22, 969 .

AMA Style

Ana-Mishel Spiroski, Rachel Sanders, Marco Meloni, Ian R. McCracken, Adrian Thomson, Mairi Brittan, Gillian A. Gray, Andrew H. Baker. The Influence of the LINC00961/SPAAR Locus Loss on Murine Development, Myocardial Dynamics, and Cardiac Response to Myocardial Infarction. International Journal of Molecular Sciences. 2021; 22 (2):969.

Chicago/Turabian Style

Ana-Mishel Spiroski; Rachel Sanders; Marco Meloni; Ian R. McCracken; Adrian Thomson; Mairi Brittan; Gillian A. Gray; Andrew H. Baker. 2021. "The Influence of the LINC00961/SPAAR Locus Loss on Murine Development, Myocardial Dynamics, and Cardiac Response to Myocardial Infarction." International Journal of Molecular Sciences 22, no. 2: 969.

Review
Published: 13 January 2021 in Molecular Therapy
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ACS Style

Andrew H. Baker; Mairi Brittan. Lost in Translation: Progress and Challenges in Advanced Therapies to Treat CVDs. Molecular Therapy 2021, 29, 426 -427.

AMA Style

Andrew H. Baker, Mairi Brittan. Lost in Translation: Progress and Challenges in Advanced Therapies to Treat CVDs. Molecular Therapy. 2021; 29 (2):426-427.

Chicago/Turabian Style

Andrew H. Baker; Mairi Brittan. 2021. "Lost in Translation: Progress and Challenges in Advanced Therapies to Treat CVDs." Molecular Therapy 29, no. 2: 426-427.

Journal article
Published: 18 December 2020 in European Heart Journal
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ACS Style

Andrew H. Baker; Mauro Giacca. Antagonism of miRNA in heart failure: first evidence in human. European Heart Journal 2020, 42, 189 -191.

AMA Style

Andrew H. Baker, Mauro Giacca. Antagonism of miRNA in heart failure: first evidence in human. European Heart Journal. 2020; 42 (2):189-191.

Chicago/Turabian Style

Andrew H. Baker; Mauro Giacca. 2020. "Antagonism of miRNA in heart failure: first evidence in human." European Heart Journal 42, no. 2: 189-191.

Preprint
Published: 05 October 2020
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Long non-coding RNAs (lncRNAs) have structural and functional roles in development and disease. We have previously shown that the LINC00961/SPAAR locus regulates endothelial cell function, and that both the lncRNA and micropeptide counter-regulate angiogenesis. To assess human cardiac cell SPAAR expression we mined a publicly available scRNSeq dataset and confirmed LINC00961 locus expression and hypoxic response in a murine endothelial cell line. We investigated post-natal growth and development, basal cardiac function, the cardiac functional response and tissue-specific response to myocardial infarction. To investigate the contribution of the LINC00961/SPAAR locus to determination of longitudinal growth, cardiac function, and response to myocardial infarction, we used a novel CRISPR/Cas9 locus knockout mouse line. Data mining suggested that SPAAR is predominantly expressed in human cardiac endothelial cells and fibroblasts, while murine LINC00961 expression is hypoxia-responsive in mouse endothelial cells. LINC00961-/- mice displayed a sex-specific delay in longitudinal growth and development, smaller left ventricular systolic and diastolic areas and volumes, and greater risk area following myocardial infarction compared with wildtype littermates. These data suggest a role for the LINC00961/SPAAR locus in cardiac endothelial cell and fibroblast cell function and hypoxic-response, and in growth and development, and basal cardiovascular function in adulthood.

ACS Style

Ana-Mishel Spiroski; Rachel Sanders; Marco Meloni; Ian McCracken; Adrian Thomson; Mairi Brittan; Gillian Gray; Andrew H. Baker. The Influence of the LINC00961/SPAAR Locus Loss on Murine Development, Myocardial Dynamics, and Cardiac Response to Myocardial Infarction. 2020, 1 .

AMA Style

Ana-Mishel Spiroski, Rachel Sanders, Marco Meloni, Ian McCracken, Adrian Thomson, Mairi Brittan, Gillian Gray, Andrew H. Baker. The Influence of the LINC00961/SPAAR Locus Loss on Murine Development, Myocardial Dynamics, and Cardiac Response to Myocardial Infarction. . 2020; ():1.

Chicago/Turabian Style

Ana-Mishel Spiroski; Rachel Sanders; Marco Meloni; Ian McCracken; Adrian Thomson; Mairi Brittan; Gillian Gray; Andrew H. Baker. 2020. "The Influence of the LINC00961/SPAAR Locus Loss on Murine Development, Myocardial Dynamics, and Cardiac Response to Myocardial Infarction." , no. : 1.

Physiology
Published: 25 September 2020 in Frontiers in Physiology
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Cardiovascular disease (CVD) is the leading cause of mortality worldwide claiming almost 17. 9 million deaths annually. A primary cause is atherosclerosis within the coronary arteries, which restricts blood flow to the heart muscle resulting in myocardial infarction (MI) and cardiac cell death. Despite substantial progress in the management of coronary heart disease (CHD), there is still a significant number of patients developing chronic heart failure post-MI. Recent research has been focused on promoting neovascularisation post-MI with the ultimate goal being to reduce the extent of injury and improve function in the failing myocardium. Cardiac cell transplantation studies in pre-clinical models have shown improvement in cardiac function; nonetheless, poor retention of the cells has indicated a paracrine mechanism for the observed improvement. Cell communication in a paracrine manner is controlled by various mechanisms, including extracellular vesicles (EVs). EVs have emerged as novel regulators of intercellular communication, by transferring molecules able to influence molecular pathways in the recipient cell. Several studies have demonstrated the ability of EVs to stimulate angiogenesis by transferring microRNA (miRNA, miR) molecules to endothelial cells (ECs). In this review, we describe the process of neovascularisation and current developments in modulating neovascularisation in the heart using miRNAs and EV-bound miRNAs. Furthermore, we critically evaluate methods used in cell culture, EV isolation and administration.

ACS Style

Despoina Kesidou; Paula A. Da Costa Martins; Leon J. De Windt; Mairi Brittan; Abdelaziz Beqqali; Andrew Howard Baker. Extracellular Vesicle miRNAs in the Promotion of Cardiac Neovascularisation. Frontiers in Physiology 2020, 11, 1 .

AMA Style

Despoina Kesidou, Paula A. Da Costa Martins, Leon J. De Windt, Mairi Brittan, Abdelaziz Beqqali, Andrew Howard Baker. Extracellular Vesicle miRNAs in the Promotion of Cardiac Neovascularisation. Frontiers in Physiology. 2020; 11 ():1.

Chicago/Turabian Style

Despoina Kesidou; Paula A. Da Costa Martins; Leon J. De Windt; Mairi Brittan; Abdelaziz Beqqali; Andrew Howard Baker. 2020. "Extracellular Vesicle miRNAs in the Promotion of Cardiac Neovascularisation." Frontiers in Physiology 11, no. : 1.

Journal article
Published: 25 June 2020 in Cardiovascular Research
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Emmanouil G Solomonidis; Andrew H Baker; Mairi Brittan. Tissue-selective endothelial arousal revealed by vascular endothelial growth factor gene transfer. Cardiovascular Research 2020, 117, 18 -20.

AMA Style

Emmanouil G Solomonidis, Andrew H Baker, Mairi Brittan. Tissue-selective endothelial arousal revealed by vascular endothelial growth factor gene transfer. Cardiovascular Research. 2020; 117 (1):18-20.

Chicago/Turabian Style

Emmanouil G Solomonidis; Andrew H Baker; Mairi Brittan. 2020. "Tissue-selective endothelial arousal revealed by vascular endothelial growth factor gene transfer." Cardiovascular Research 117, no. 1: 18-20.

Research article
Published: 10 April 2020 in Circulation Research
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Rationale: Despite increasing understanding of the prognostic importance of vascular stiffening linked to perivascular fibrosis in hypertension, the molecular and cellular regulation of this process is poorly understood. Objectives: To study the functional role of microRNA-214 (miR-214) in the induction of perivascular fibrosis and endothelial dysfunction driving vascular stiffening. Methods and Results: Out of 381 miRs screened in the perivascular tissues in response to Ang II (angiotensin II)-mediated hypertension, miR-214 showed the highest induction (8-fold, P =0.0001). MiR-214 induction was pronounced in perivascular and circulating T cells, but not in perivascular adipose tissue adipocytes. Global deletion of miR-214 − /− prevented Ang II-induced periaortic fibrosis, Col1a1 , Col3a1, Col5a1 , and Tgfb1 expression, hydroxyproline accumulation, and vascular stiffening, without difference in blood pressure. Mechanistic studies revealed that miR-214 −/− mice were protected against endothelial dysfunction, oxidative stress, and increased Nox2, all of which were induced by Ang II in WT mice. Ang II-induced recruitment of T cells into perivascular adipose tissue was abolished in miR-214 −/− mice. Adoptive transfer of miR-214 −/− T cells into RAG1 −/− mice resulted in reduced perivascular fibrosis compared with the effect of WT T cells. Ang II induced hypertension caused significant change in the expression of 1380 T cell genes in WT, but only 51 in miR-214 −/− . T cell activation, proliferation and chemotaxis pathways were differentially affected. MiR-214 −/− prevented Ang II-induction of profibrotic T cell cytokines ( IL-17 , TNF-α, IL-9 , and IFN-γ ) and chemokine receptors (CCR1, CCR2, CCR4, CCR5, CCR6, and CXCR3). This manifested in reduced in vitro and in vivo T cell chemotaxis resulting in attenuation of profibrotic perivascular inflammation. Translationally, we show that miR-214 is increased in plasma of patients with hypertension and is directly correlated to pulse wave velocity as a measure of vascular stiffness. Conclusions: T-cell–derived miR-214 controls pathological perivascular fibrosis in hypertension mediated by T cell recruitment and local profibrotic cytokine release.

ACS Style

Ryszard Nosalski; Mateusz Siedlinski; Laura Denby; Eilidh McGinnigle; Michal Nowak; Aurelie Nguyen Dinh Cat; Laura Medina-Ruiz; Marco Cantini; Dominik Skiba; Grzegorz Wilk; Grzegorz Osmenda; Julie Rodor; Manuel Salmeron-Sanchez; Gerard Graham; Pasquale Maffia; Delyth Graham; Andrew Baker; Tomasz J. Guzik. T-Cell–Derived miRNA-214 Mediates Perivascular Fibrosis in Hypertension. Circulation Research 2020, 126, 988 -1003.

AMA Style

Ryszard Nosalski, Mateusz Siedlinski, Laura Denby, Eilidh McGinnigle, Michal Nowak, Aurelie Nguyen Dinh Cat, Laura Medina-Ruiz, Marco Cantini, Dominik Skiba, Grzegorz Wilk, Grzegorz Osmenda, Julie Rodor, Manuel Salmeron-Sanchez, Gerard Graham, Pasquale Maffia, Delyth Graham, Andrew Baker, Tomasz J. Guzik. T-Cell–Derived miRNA-214 Mediates Perivascular Fibrosis in Hypertension. Circulation Research. 2020; 126 (8):988-1003.

Chicago/Turabian Style

Ryszard Nosalski; Mateusz Siedlinski; Laura Denby; Eilidh McGinnigle; Michal Nowak; Aurelie Nguyen Dinh Cat; Laura Medina-Ruiz; Marco Cantini; Dominik Skiba; Grzegorz Wilk; Grzegorz Osmenda; Julie Rodor; Manuel Salmeron-Sanchez; Gerard Graham; Pasquale Maffia; Delyth Graham; Andrew Baker; Tomasz J. Guzik. 2020. "T-Cell–Derived miRNA-214 Mediates Perivascular Fibrosis in Hypertension." Circulation Research 126, no. 8: 988-1003.

Research article
Published: 01 March 2020 in Arteriosclerosis, Thrombosis, and Vascular Biology
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Objective: Long noncoding RNAs (lncRNAs) are an emergent class of molecules with diverse functional roles, widely expressed in human physiology and disease. Although some lncRNAs have been identified in cardiovascular disease, their potential as novel targets in the prevention of atherosclerosis is unknown. We set out to discover important lncRNAs in unstable plaque and gain insight into their functional relevance. Approach and Results: Analysis of RNA sequencing previously performed on stable and unstable atherosclerotic plaque identified a panel of 47 differentially regulated lncRNAs. We focused on LINC01272, a lncRNA upregulated in unstable plaque previously detected in inflammatory bowel disease, which we termed PELATON (plaque enriched lncRNA in atherosclerotic and inflammatory bowel macrophage regulation). Here, we demonstrate that PELATON is highly monocyte- and macrophage-specific across vascular cell types, and almost entirely nuclear by cellular fractionation (90%–98%). In situ hybridization confirmed enrichment of PELATON in areas of plaque inflammation, colocalizing with macrophages around the shoulders and necrotic core of human plaque sections. Consistent with its nuclear localization, and despite containing a predicted open reading frame, PELATON did not demonstrate any protein-coding potential in vitro. Functionally, knockdown of PELATON significantly reduced phagocytosis, lipid uptake and reactive oxygen species production in high-content analysis, with a significant reduction in phagocytosis independently validated. Furthermore, CD36, a key mediator of phagocytic oxLDL (oxidized low-density lipoprotein) uptake was significantly reduced with PELATON knockdown. Conclusions: PELATON is a nuclear expressed, monocyte- and macrophage-specific lncRNA, upregulated in unstable atherosclerotic plaque. Knockdown of PELATON affects cellular functions associated with plaque progression.

ACS Style

John Hung; Jessica P. Scanlon; Amira D. Mahmoud; Julie Rodor; Margaret Ballantyne; Margaux A.C. Fontaine; Lieve Temmerman; Jakub Kaczynski; Katie L. Connor; Raghu Bhushan; Erik A.L. Biessen; David E. Newby; Judith Sluimer; Andrew H. Baker. Novel Plaque Enriched Long Noncoding RNA in Atherosclerotic Macrophage Regulation (PELATON). Arteriosclerosis, Thrombosis, and Vascular Biology 2020, 40, 697 -713.

AMA Style

John Hung, Jessica P. Scanlon, Amira D. Mahmoud, Julie Rodor, Margaret Ballantyne, Margaux A.C. Fontaine, Lieve Temmerman, Jakub Kaczynski, Katie L. Connor, Raghu Bhushan, Erik A.L. Biessen, David E. Newby, Judith Sluimer, Andrew H. Baker. Novel Plaque Enriched Long Noncoding RNA in Atherosclerotic Macrophage Regulation (PELATON). Arteriosclerosis, Thrombosis, and Vascular Biology. 2020; 40 (3):697-713.

Chicago/Turabian Style

John Hung; Jessica P. Scanlon; Amira D. Mahmoud; Julie Rodor; Margaret Ballantyne; Margaux A.C. Fontaine; Lieve Temmerman; Jakub Kaczynski; Katie L. Connor; Raghu Bhushan; Erik A.L. Biessen; David E. Newby; Judith Sluimer; Andrew H. Baker. 2020. "Novel Plaque Enriched Long Noncoding RNA in Atherosclerotic Macrophage Regulation (PELATON)." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 3: 697-713.

Comment
Published: 14 February 2020 in Molecular Therapy
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Andrew H. Baker; Roland W. Herzog. Did Dendritic Cell Activation, Induced by Adenovirus-Antibody Complexes, Play a Role in the Death of Jesse Gelsinger? Molecular Therapy 2020, 28, 704 -706.

AMA Style

Andrew H. Baker, Roland W. Herzog. Did Dendritic Cell Activation, Induced by Adenovirus-Antibody Complexes, Play a Role in the Death of Jesse Gelsinger? Molecular Therapy. 2020; 28 (3):704-706.

Chicago/Turabian Style

Andrew H. Baker; Roland W. Herzog. 2020. "Did Dendritic Cell Activation, Induced by Adenovirus-Antibody Complexes, Play a Role in the Death of Jesse Gelsinger?" Molecular Therapy 28, no. 3: 704-706.

Journal article
Published: 06 February 2020 in Scientific Reports
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Gadolinium chelates are widely used in cardiovascular magnetic resonance imaging (MRI) as passive intravascular and extracellular space markers. Manganese, a biologically active paramagnetic calcium analogue, provides novel intracellular myocardial tissue characterisation. We previously showed manganese-enhanced MRI (MEMRI) more accurately quantifies myocardial infarction than gadolinium delayed-enhancement MRI (DEMRI). Here, we evaluated the potential of MEMRI to assess myocardial viability compared to gold-standard 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET) viability. Coronary artery ligation surgery was performed in male Sprague-Dawley rats (n = 13) followed by dual MEMRI and 18F-FDG PET imaging at 10–12 weeks. MEMRI was achieved with unchelated (EVP1001-1) or chelated (mangafodipir) manganese. T1 mapping MRI was followed by 18F-FDG micro-PET, with tissue taken for histological correlation. MEMRI and PET demonstrated good agreement with histology but native T1 underestimated infarct size. Quantification of viability by MEMRI, PET and MTC were similar, irrespective of manganese agent. MEMRI showed superior agreement with PET than native T1. MEMRI showed excellent agreement with PET and MTC viability. Myocardial MEMRI T1 correlated with 18F-FDG standard uptake values and influx constant but not native T1. Our findings indicate that MEMRI identifies and quantifies myocardial viability and has major potential for clinical application in myocardial disease and regenerative therapies.

ACS Style

Nick Spath; Adriana Tavares; Gillian A. Gray; Andrew Baker; Ross J. Lennen; Carlos J. Alcaide-Corral; Marc R. Dweck; David E. Newby; Phillip C. Yang; Maurits Jansen; Scott I. Semple. Manganese-enhanced T1 mapping to quantify myocardial viability: validation with 18F-fluorodeoxyglucose positron emission tomography. Scientific Reports 2020, 10, 2018 -10.

AMA Style

Nick Spath, Adriana Tavares, Gillian A. Gray, Andrew Baker, Ross J. Lennen, Carlos J. Alcaide-Corral, Marc R. Dweck, David E. Newby, Phillip C. Yang, Maurits Jansen, Scott I. Semple. Manganese-enhanced T1 mapping to quantify myocardial viability: validation with 18F-fluorodeoxyglucose positron emission tomography. Scientific Reports. 2020; 10 (1):2018-10.

Chicago/Turabian Style

Nick Spath; Adriana Tavares; Gillian A. Gray; Andrew Baker; Ross J. Lennen; Carlos J. Alcaide-Corral; Marc R. Dweck; David E. Newby; Phillip C. Yang; Maurits Jansen; Scott I. Semple. 2020. "Manganese-enhanced T1 mapping to quantify myocardial viability: validation with 18F-fluorodeoxyglucose positron emission tomography." Scientific Reports 10, no. 1: 2018-10.