ArticleOxidative medicine and cellular longevity2018
Pro-BDNF Contributes to Hypoxia/Reoxygenation Injury in Myocardial Microvascular Endothelial Cells: Roles of Receptors p75
Article in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Psycho-cardiovascular interaction network in cardiovascular health and disease: signaling pathways and molecular mechanisms.Precision clinical medicine · 2026Review
- BDNF mediates the heart-brain axis: implications for cardiovascular diseases and mental disorders.European archives of psychiatry and clinical neuroscience · 2026Review
- Vagus Nerve Stimulation Mitigates Sepsis-Induced Lung Injury via Pulmonary proBDNF Suppression.Journal of inflammation research · 2026Article
- The biology of exosomes and exosomal non-coding RNAs in cardiovascular diseases.Frontiers in pharmacology · 2025Review
- Role of Brain-Derived Neurotrophic Factor in Anxiety or Depression After Percutaneous Coronary Intervention.Molecular neurobiology · 2024Review
- BDNF-loaded PDADMAC-heparin multilayers: a novel approach for neuroblastoma cell study.Scientific reports · 2023Article
- Sortilins in the blood-brain barrier: impact on barrier integrity.Neural regeneration research · 2023Article
- Role of GADD45A in myocardial ischemia/reperfusion through mediation of the JNK/p38 MAPK and STAT3/VEGF pathways.International journal of molecular medicine · 2022Article
- Moderate Aerobic Exercise Regulates Follicular Dysfunction by Initiating Brain-Derived Neurotrophic Factor (BDNF)-Mediated Anti-Apoptotic Signaling Pathways in Polycystic Ovary Syndrome.Journal of clinical medicine · 2022Article
- Clinical Correlates Identify ProBDNF and Thrombo-Inflammatory Markers as Key Predictors of Circulating p75Frontiers in aging neuroscience · 2022Article
- Association of Apoptosis-Mediated CD4Frontiers in cardiovascular medicine · 2021Article
- CircHIPK3 Plays Vital Roles in Cardiovascular Disease.Frontiers in cardiovascular medicine · 2021Review
- Recombinant Extracellular Domain (p75ECD) of the Neurotrophin Receptor p75 Attenuates Myocardial Ischemia-Reperfusion Injury by Inhibiting the p-JNK/Caspase-3 Signaling Pathway in Rat Microvascular Pericytes.Journal of the American Heart Association · 2020Article
- Tetrahydroxystilbene Glucoside Ameliorates Infrasound-Induced Central Nervous System (CNS) Injury by Improving Antioxidant and Anti-Inflammatory Capacity.Oxidative medicine and cellular longevity · 2020Article
- Exosomal circHIPK3 Released from Hypoxia-Pretreated Cardiomyocytes Regulates Oxidative Damage in Cardiac Microvascular Endothelial Cells via the miR-29a/IGF-1 Pathway.Oxidative medicine and cellular longevity · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to identify the role of the precursor of the brain-derived neurotrophic factor (pro-BDNF) in myocardial hypoxia/reoxygenation injury (H/R) and to address the underlying mechanisms. For this purpose, myocardial microvascular endothelial cells (MMECs) exposed to a high concentration of glucose (30 mM) for 48 h were subjected to 4 h of hypoxia followed by 2 h of reoxygenation. Terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) staining and flow-cytometric analysis were performed to detect apoptosis. Cell scratch and capillary-like-structure formation assays were employed to evaluate cell function. The levels of apoptosis-related proteins were evaluated by Western blotting and immunofluorescence assays. Our results showed that H/R resulted in MMEC injury, as indicated by significant increases in TUNEL-positive cell numbers and a reduction in MMEC migration and in capillary-like-structure formation coupled with increased pro-BDNF protein expression. In addition, overexpression of pro-BDNF in MMECs via a viral vector led to increased pro-BDNF expression, and this upregulation induced apoptosis. Mechanistic experiments revealed that H/R did not influence BDNF, JNK, and caspase 3 expression, but upregulated pro-BDNF, p75
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Registered trials
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