María del Socorro Pina-Canseco

Dr. María del Socorro Pina-Canseco

Centro de Investigación Facultad de Medicina UNAM-UABJO, Universidad Autónoma Benito Juárez de Oaxaca
orcid

Research Focus & Metrics

Academic Career Length

20Years (2007-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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25 February 2021 in Biosensors
Verified
Journal Article
Open access
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Jose Luis Cano PerezJose Luis Cano Perez
Jose Luis Cano Perez
JGJaime Gutiérrez Gutiérrez
Jaime Gutiérrez Gutiérrez
Christian Perezcampos-MayoralChristian Perezcampos-Mayoral
Christian Perezcampos-Mayoral
Eduardo Perez-CamposEduardo Perez-Campos
Eduardo Perez-Campos
María del Socorro Pina-CansecoMaría del Socorro Pina-Canseco
María del Socorro Pina-Canseco
RRRoberto Rojas-Laguna
Roberto Rojas-Laguna
Diabetes mellitus is a chronic metabolic disorder, being globally one of the most deadly diseases. This disease requires continually monitoring of the body’s glucose levels. There are different types of sensors for measuring glucose, most of them invasive to the patient. Fiber optic sensors have been proven to have advantages compared to conventional sensors and they have great potential for various applications, especially in the biomedical area. Compared to other sensors, they are smaller, easy to handle, mostly non-invasive, thus leading to a lower risk of infection, high precision, well correlated and inexpensive. The objective of this review article is to compare different types of fiber optic sensors made with different experimental techniques applied to biomedicine, especially for glucose sensing. Observations are made on the way of elaboration, as well as the advantages and disadvantages that each one could have in real applications.

1 November 2014 in European Journal of Medicinal Chemistry
Verified
Journal Article
Closed access
AMAdriana Moreno-Rodríguez
Adriana Moreno-Rodríguez
PSPaz María Salazar-Schettino
Paz María Salazar-Schettino
JBJuan Luis Bautista
Juan Luis Bautista
FHFrancisco Hernández-Luis
Francisco Hernández-Luis
HTHugo Torrens
Hugo Torrens
Eduardo Perez-CamposEduardo Perez-Campos
Eduardo Perez-Campos

Verified
Journal Article
Open access
PDF file
María Eugenia Sanchez-LeonMaría Eugenia Sanchez-Leon
María Eugenia Sanchez-Leon
KLKaren Julissa Loaeza-Reyes
Karen Julissa Loaeza-Reyes
CMCarlos Alberto Matias-Cervantes
Carlos Alberto Matias-Cervantes
GAGabriel Mayoral Andrade
Gabriel Mayoral Andrade
Eduardo Perez-CamposEduardo Perez-Campos
Eduardo Perez-Campos
María del Socorro Pina-CansecoMaría del Socorro Pina-Canseco
María del Socorro Pina-Canseco
LOX-1, ORL-1, or lectin-like oxidized low-density lipoprotein receptor 1 is a transmembrane glycoprotein that binds and internalizes ox-LDL in foam cells. LOX-1 is the main receptor for oxidized low-density lipoproteins (ox-LDL). The LDL comes from food intake and circulates through the bloodstream. LOX-1 belongs to scavenger receptors (SR), which are associated with various cardiovascular diseases. The most important and severe of these is the formation of atherosclerotic plaques in the intimal layer of the endothelium. These plaques can evolve into complicated thrombi with the participation of fibroblasts, activated platelets, apoptotic muscle cells, and macrophages transformed into foam cells. This process causes changes in vascular endothelial homeostasis, leading to partial or total obstruction in the lumen of blood vessels. This obstruction can result in oxygen deprivation to the heart. Recently, LOX-1 has been involved in other pathologies, such as obesity and diabetes mellitus. However, the development of atherosclerosis has been the most relevant due to its relationship with cerebrovascular accidents and heart attacks. In this review, we will summarize findings related to the physiologic and pathophysiological processes of LOX-1 to support the detection, diagnosis, and prevention of those diseases.

1 June 2012 in Biochemistry and Cell Biology
Verified
Journal Article
Closed access
CMChristophe Mariller
Christophe Mariller
SHStephan Hardivillé
Stephan Hardivillé
EHEsthelle Hoedt
Esthelle Hoedt
IHIsabelle Huvent
Isabelle Huvent
María del Socorro Pina-CansecoMaría del Socorro Pina-Canseco
María del Socorro Pina-Canseco
APAnnick Pierce
Annick Pierce
Delta-lactoferrin (ΔLf) is a transcription factor of which the expression is downregulated in cancer. It is a healthy tissue marker and a high expression level of its transcripts was correlated with a good prognosis in breast cancer. ΔLf results from alternative promoter usage of the hLf gene leading to the production of 2 isoforms with alternative N-termini: lactoferrin, which is secreted, and ΔLf, its nucleocytoplasmic counterpart. ΔLf possesses antiproliferative properties and induces cell cycle arrest. It is an efficient transcription factor interacting in vivo via a ΔLf response element found in the Skp1, Bax, DcpS, and SelH promoters. Since ΔLf possesses different target genes, modifications in its activity or concentration may have crucial effects on cell homeostasis. Posttranslational modifications modulate ΔLf transcription factor activity. Our earlier investigations showed that O-GlcNAcylation negatively regulates ΔLf transcriptional activity, whilst inhibiting its ubiquitination and increasing its half-life. On the other hand, phosphorylation potentiates ΔLf transcriptional activity. Recently, we showed that ΔLf is also modified by SUMOylation. Therefore, cooperation and (or) competition among SUMOylation, ubiquitination, phosphorylation, and O-GlcNAcylation may contribute to the establishment of a fine regulation of ΔLf transcriptional activity depending on the type of target gene and cellular homeostasis.

20 August 2021 in Biomedicines
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Journal Article
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Juan Manuel Velázquez-EnríquezJuan Manuel Velázquez-Enríquez
Juan Manuel Velázquez-Enríquez
JSJovito Santos
Jovito Santos
ARAlma Ramírez-Hernández
Alma Ramírez-Hernández
EREdilburga Reyes-Jiménez
Edilburga Reyes-Jiménez
ALArmando López-Martínez
Armando López-Martínez
RBRafael Baltiérrez-Hoyos
Rafael Baltiérrez-Hoyos
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, irreversible, and highly fatal disease. It is characterized by the increased activation of both fibroblast and myofibroblast that results in excessive extracellular matrix (ECM) deposition. Extracellular vesicles (EVs) have been described as key mediators of intercellular communication in various pathologies. However, the role of EVs in the development of IPF remains poorly understood. This study aimed to characterize the differentially expressed proteins contained within EVs cargo derived from the fibroblast cell lines LL97A (IPF-1) and LL29 (IPF-2) isolated from lungs bearing IPF as compared to those derived from the fibroblast cell lines CCD8Lu (NL-1) and CCD19Lu (NL-2) isolated from healthy donors. Isolated EVs were subjected to label-free quantitative proteomic analysis by LC-MS/MS, and as a result, 331 proteins were identified. Differentially expressed proteins were obtained after the pairwise comparison, including all experimental groups. A total of 86 differentially expressed proteins were identified in either one or more comparison groups. Of note, proteins involved in fibrogenic processes, such as tenascin-c (TNC), insulin-like-growth-factor-binding protein 7 (IGFBP7), fibrillin-1 (FBN1), alpha-2 collagen chain (I) (COL1A2), alpha-1 collagen chain (I) (COL1A1), and lysyl oxidase homolog 1 (LOXL1), were identified in EVs cargo isolated from IPF cell lines. Additionally, KEGG pathway enrichment analysis revealed that differentially expressed proteins participate in focal adhesion, PI3K-Akt, and ECM–receptor interaction signaling pathways. In conclusion, our findings reveal that proteins contained within EVs cargo might play key roles during IPF pathogenesis.

11 April 2017 in Current Vascular Pharmacology
Verified
Journal Article
Closed access
NCNancy Cortez-Espinosa
Nancy Cortez-Espinosa
Laura Pérez-Campos MayoralLaura Pérez-Campos Mayoral
Laura Pérez-Campos Mayoral
Eduardo Perez-CamposEduardo Perez-Campos
Eduardo Perez-Campos
Hector Alejandro Cabrera-FuentesHector Alejandro Cabrera-Fuentes
Hector Alejandro Cabrera-Fuentes
Eduardo Perez-CamposEduardo Perez-Campos
Eduardo Perez-Campos
PCPedro Hernandez Cruz
Pedro Hernandez Cruz
The association between type 2 diabetes mellitus (T2DM) and systemic inflammation may increase platelet reactivity and the accelerated development of vascular disease. Platelets are able to modulate the function of immune cells via the direct release of growth factors and pro-inflammatory chemokines through the production of microvesicles. The microvesicles trigger a transcellular delivery system of bioactive molecules to other cells acting as vectors in the exchange of biological information. Here, we consider the influence of platelets and platelet-derived microvesicles on cells of the immune system and the implications in the pathogenesis of T2DM.