Prof. Dr. Alessandro Castorina
School of Life Sciences, Faculty of Science, University of Technology Sydney, PO Box 123, Broadway, Sydney, New South Wales 2007, Australia
'%3e%3cpath%20d='M22.1642%2019.0924C21.7317%2018.068%2021.1041%2017.1375%2020.3163%2016.3527C19.5309%2015.5656%2018.6006%2014.9381%2017.5766%2014.5048C17.5674%2014.5002%2017.5582%2014.4979%2017.5491%2014.4933C18.9774%2013.4616%2019.9059%2011.7811%2019.9059%209.88504C19.9059%206.74408%2017.3611%204.19922%2014.2201%204.19922C11.0792%204.19922%208.53429%206.74408%208.53429%209.88504C8.53429%2011.7811%209.46282%2013.4616%2010.8912%2014.4956C10.882%2014.5002%2010.8728%2014.5025%2010.8636%2014.5071C9.83652%2014.9404%208.91487%2015.5617%208.1239%2016.355C7.33685%2017.1404%206.70933%2018.0707%206.276%2019.0947C5.85031%2020.0972%205.62072%2021.172%205.59967%2022.2609C5.59905%2022.2853%205.60335%2022.3097%205.61229%2022.3325C5.62123%2022.3553%205.63465%2022.376%205.65174%2022.3935C5.66883%2022.4111%205.68926%2022.425%205.71182%2022.4345C5.73437%2022.444%205.7586%2022.4489%205.78308%2022.4489H7.15868C7.25956%2022.4489%207.3398%2022.3686%207.3421%2022.2701C7.38795%2020.5001%208.09868%2018.8425%209.35506%2017.5861C10.655%2016.2862%2012.3814%2015.5709%2014.2201%2015.5709C16.0588%2015.5709%2017.7852%2016.2862%2019.0852%2017.5861C20.3415%2018.8425%2021.0523%2020.5001%2021.0981%2022.2701C21.1004%2022.3709%2021.1807%2022.4489%2021.2815%2022.4489H22.6571C22.6816%2022.4489%2022.7058%2022.444%2022.7284%2022.4345C22.751%2022.425%2022.7714%2022.4111%2022.7885%2022.3935C22.8056%2022.376%2022.819%2022.3553%2022.8279%2022.3325C22.8369%2022.3097%2022.8412%2022.2853%2022.8406%2022.2609C22.8176%2021.165%2022.5907%2020.0989%2022.1642%2019.0924ZM14.2201%2013.8284C13.1678%2013.8284%2012.1773%2013.418%2011.4322%2012.6729C10.6871%2011.9278%2010.2767%2010.9374%2010.2767%209.88504C10.2767%208.83271%2010.6871%207.84227%2011.4322%207.09715C12.1773%206.35204%2013.1678%205.94165%2014.2201%205.94165C15.2724%205.94165%2016.2629%206.35204%2017.008%207.09715C17.7531%207.84227%2018.1635%208.83271%2018.1635%209.88504C18.1635%2010.9374%2017.7531%2011.9278%2017.008%2012.6729C16.2629%2013.418%2015.2724%2013.8284%2014.2201%2013.8284Z'%20fill='%238590A2'/%3e%3c/g%3e%3c/svg%3e)
Co-authors
Following
Followers
Research Focus & Metrics
Explore full metrics on Scilit
Academic Career Length
19Years (2008-Present)
(Calculated once Scilit publication data is synced: current year − year of first publication + 1)
Representative Publications
View All Publications
Journal Article
PCPaola Castrogiovanni
Paola Castrogiovanni
Michelino Di Rosa
Silvia RavalliAlessandro CastorinaCGClaudia Guglielmino
Claudia Guglielmino
Giuseppe Musumeci +4
The purpose of this study was to investigate the influence of moderate physical activity (MPA) on the expression of osteoarthritis (OA)-related (IL-1β, IL-6, TNF-α, MMP-13) and anti-inflammatory and chondroprotective (IL-4, IL-10, lubricin) biomarkers in the synovium of an OA-induced rat model. A total of 32 rats were divided into four groups: Control rats (Group 1); rats performing MPA (Group 2); anterior cruciate ligament transection (ACLT)-rats with OA (Group 3); and, ACLT-rats performing MPA (Group 4). Analyses were performed using Hematoxylin & Eosin (H&E) staining, histomorphometry and immunohistochemistry. In Group 3, OA biomarkers were significantly increased, whereas, IL-4, IL-10, and lubricin were significantly lower than in the other experimental groups. We hypothesize that MPA might partake in rescuing type B synoviocyte dysfunction at the early stages of OA, delaying the progression of the disease.
19 June 2020 in Neural Regeneration Research
Journal Article
SBSarah Thomas Broome
Sarah Thomas Broome
KLKrystal Louangaphay
Krystal Louangaphay
KKKevin A. Keay
Kevin A. Keay
GLGian Marco Leggio
Gian Marco Leggio
Giuseppe MusumeciAlessandro CastorinaThe dopaminergic system controls several vital central nervous system functions, including the control of movement, reward behaviors and cognition. Alterations of dopaminergic signaling are involved in the pathogenesis of neurodegenerative and psychiatric disorders, in particular Parkinson’s disease, which are associated with a subtle and chronic inflammatory response. A substantial body of evidence has demonstrated the non-neuronal expression of dopamine, its receptors and of the machinery that governs synthesis, secretion and storage of dopamine across several immune cell types. This review aims to summarize current knowledge on the role and expression of dopamine in immune cells. One of the goals is to decipher the complex mechanisms through which these cell types respond to dopamine, in order to address the impact this has on neurodegenerative and psychiatric pathologies such as Parkinson’s disease. A further aim is to illustrate the gaps in our understanding of the physiological roles of dopamine to encourage more targeted research focused on understanding the consequences of aberrant dopamine production on immune regulation. These highlights may prompt scientists in the field to consider alternative functions of this important neurotransmitter when targeting neuroinflammatory/neurodegenerative pathologies.
1 January 2019 in Heliyon
Journal Article
MSMarta Anna Szychlinska
Marta Anna Szychlinska
Michelino Di RosaAlessandro Castorina
Ali MobasheriGiuseppe MusumeciOsteoarthritis (OA) is a degenerative disease of the articular cartilage, resulting in pain and total joint disability. Recent studies focused on the role of the metabolic syndrome in inducing or worsening joint damage suggest that chronic low-grade systemic inflammation may represent a possible linking factor. This finding supports the concept of a new phenotype of OA, a metabolic OA. The gut microbiome is fundamental for human physiology and immune system development, among the other important functions. Manipulation of the gut microbiome is considered an important topic for the individual health in different medical fields such as medical biology, nutrition, sports, preventive and rehabilitative medicine. Since intestinal microbiota dysbiosis is strongly associated with the pathogenesis of several metabolic and inflammatory diseases, it is conceivable that also the pathogenesis of OA might be related to it. However, the mechanisms and the contribution of intestinal microbiota metabolites in OA pathogenesis are still not clear. The aim of this narrative review is to review recent literature concerning the possible contribution of dysbiosis to OA onset and to discuss the importance of gut microbiome homeostasis maintenance for optimal general health preservation.
29 October 2021 in Heliyon
Journal Article
Grazia Maugeri
Velia D'AgataBTBruno Trovato
Bruno Trovato
Federico RoggioAlessandro CastorinaGiuseppe Musumeci +2
Peripheral nerve injury is a complex condition with a variety of signs and symptoms depending on the severity and nerves involved. Peripheral nerve damage may lead to sensory and motor functions deficits and even lifelong disability, causing important socioeconomic costs worldwide. Despite the increase in knowledge of the mechanisms of injury and regeneration, a full functional recovery is still unsatisfying in the majority of patients. It is well known that exercise promotes physical and psychological well-being, by ameliorating general health. In the last years, there has been a growing interest in evaluating the effects of exercise on the peripheral nervous system. Experimental works with rodent models showed the potential utility of exercise following peripheral nerve injuries, as evinced by increasing axon regeneration, muscle reinnervation, better recovery of strength, muscle mass and higher expression of neurotrophic factors. Moreover, clinical evidence showed positive trends in favour of physical therapy following peripheral nerve damage based on the improvement of range of motion (ROM), muscle power grade and pain. After a brief overview of peripheral nerve anatomy and the different types of nerve injury, the present review aims to summarize the impact of exercise on peripheral nerve regeneration. Some clinical evidence regarding the effect of exercise after peripheral nerve injury will also be discussed.
Journal Article
SGSalvatore Giunta
Salvatore GiuntaAlessandro CastorinaRMRubina Marzagalli
Rubina Marzagalli
Marta Anna SzychlinskaKPKarin Pichler
Karin PichlerGiuseppe Musumeci +1
Osteoarthritis (OA); the most common form of degenerative joint disease, is associated with variations in pro-inflammatory growth factor levels, inflammation and hypocellularity resulting from chondrocyte apoptosis. Pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide endowed with a range of trophic effects in several cell types; including chondrocytes. However; its role in OA has not been studied. To address this issue, we investigated whether PACAP expression is affected in OA cartilage obtained from experimentally-induced OA rat models, and then studied the effects of PACAP in isolated chondrocytes exposed to IL-1β in vitro to mimic the inflammatory milieu of OA cartilage. OA induction was established by histomorphometric and histochemical analyses. Changes in PACAP distribution in cartilage, or its concentration in synovial fluid (SF), were assessed by immunohistochemistry and ELISA. Results showed that PACAP abundance in cartilage tissue and SF was high in healthy controls. OA induction decreased PACAP levels both in affected cartilage and SF. In vitro, PACAP prevented IL-1β-induced chondrocyte apoptosis, as determined by MTT assay; Hoechst staining and western blots of apoptotic-related proteins. These changes were also accompanied by decreased i-NOS and COX-2 levels, suggesting an anti-inflammatory effect. Altogether, these findings support a potential role for PACAP as a chondroprotective agent for the treatment of OA.
7 May 2015 in Cell and tissue research
Journal Article
Giuseppe MusumeciGMGaetano Magro
Gaetano MagroVCVenera Cardile
Venera CardileMCMarinella Coco
Marinella Coco
RMRubina Marzagalli
Rubina Marzagalli
Alessandro Castorina +6
About Me
Alessandro Castorina is an Associate Professor at the University of Technology Sydney (UTS). He completed his PhD in Neuropharmacology at the University of Catania in 2009. Immediately after, he received a post-doctoral fellowship to study the role of the neuropeptides pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP) in models of neurodegenerative diseases. In 2011, he was appointed as Lecturer at the University of Catania, where he established his research group on neuropeptide research. In 2015, he joined the Laboratory of Neural Structure and Function (University of Sydney) as a Senior Research Fellow to investigate how brain PACAP/VIP regulates social behavior in preclinical models of chronic nerve pain. In 2016, he was appointed as Senior Lecturer at UTS, where he established the Laboratory of Cellular and Molecular Neuroscience (LCMN) to focus on the role of PACAP/VIP in neuroinflammatory diseases of the CNS, including Parkinson’s disease, multiple sclerosis (MS), and others. In 2020, he became the Director of the Surgical and Anatomical Science Facility (2020–2021), and in 2021, he was promoted to Associate Professor. His laboratory uses models in vitro and in vivo to study the biological activities of the neuropeptides PACAP and VIP in the CNS to unveil new therapeutic opportunities to reverse the course of several neurodegenerative diseases, particularly MS and other demyelinating disorders.