ArticleCell death & disease2014
Agonist antibodies activating the Met receptor protect cardiomyoblasts from cobalt chloride-induced apoptosis and autophagy.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 69 citations in OpenAlex.
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- Potential mechanisms underlying the effect of hepatocyte growth factor on liver injury in short bowel syndrome model rats.Pediatric surgery international · 2023Article
- Circulating Hepatocyte Growth Factor Reflects Activation of Vascular Repair in Response to Stress.JACC. Basic to translational science · 2022Article
- Dimerization of kringle 1 domain from hepatocyte growth factor/scatter factor provides a potent MET receptor agonist.Life science alliance · 2022Article
- Immune-associated pivotal biomarkers identification and competing endogenous RNA network construction in post-operative atrial fibrillation by comprehensive bioinformatics and machine learning strategies.Frontiers in immunology · 2022Article
- Autophagic Upregulation Is Cytoprotective in Ischemia/Reperfusion-Injured Retina and Retinal Progenitor Cells.International journal of molecular sciences · 2021Article
- Exercise-induced peptide TAG-23 protects cardiomyocytes from reperfusion injury through regulating PKG-cCbl interaction.Basic research in cardiology · 2021Article
- HGF and MET: From Brain Development to Neurological Disorders.Frontiers in cell and developmental biology · 2021Review
- Engineering, Characterization, and Biological Evaluation of an Antibody Targeting the HGF Receptor.Frontiers in immunology · 2021Article
- Targeting autophagy to overcome drug resistance: further developments.Journal of hematology & oncology · 2020Review
- Cyclic Peptide-Based Biologics Regulating HGF-MET.International journal of molecular sciences · 2020Review
- The Long-Lasting Protective Effect of HGF in Cardiomyoblasts Exposed to Doxorubicin Requires a Positive Feed-Forward Loop Mediated by Erk1,2-Timp1-Stat3.International journal of molecular sciences · 2020Article
- Activation of the MET receptor attenuates doxorubicin-induced cardiotoxicity in vivo and in vitro.British journal of pharmacology · 2020Article
- Autophagy-dependent and -independent modulation of oxidative and organellar stress in the diabetic heart by glucose-lowering drugs.Cardiovascular diabetology · 2020Review
- Advances in understanding mechanisms of long-term sperm storage-the soft-shelled turtle model.Histology and histopathology · 2020Article
- Targeting the HGF/MET Axis in Cancer Therapy: Challenges in Resistance and Opportunities for Improvement.Frontiers in cell and developmental biology · 2020Review
- Telmisartan cardioprotects from the ischaemic/hypoxic damage through a miR-1-dependent pathway.Journal of cellular and molecular medicine · 2019Article
- Combination of HGF and IGF-1 promotes connexin 43 expression and improves ventricular arrhythmia after myocardial infarction through activating the MAPK/ERK and MAPK/p38 signaling pathways in a rat model.Cardiovascular diagnosis and therapy · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Met, the tyrosine kinase receptor for hepatocyte growth factor (HGF), mainly activates prosurvival pathways, including protection from apoptosis. In this work, we investigated the cardioprotective mechanisms of Met activation by agonist monoclonal antibodies (mAbs). Cobalt chloride (CoCl2), a chemical mimetic of hypoxia, was used to induce cardiac damage in H9c2 cardiomyoblasts, which resulted in reduction of cell viability by (i) caspase-dependent apoptosis and (ii) - surprisingly - autophagy. Blocking either apoptosis with the caspase inhibitor benzyloxycarbonyl-VAD-fluoromethylketone or autophagosome formation with 3-methyladenine prevented loss of cell viability, which suggests that both processes contribute to cardiomyoblast injury. Concomitant treatment with Met-activating antibodies or HGF prevented apoptosis and autophagy. Pro-autophagic Redd1, Bnip3 and phospho-AMPK proteins, which are known to promote autophagy through inactivation of the mTOR pathway, were induced by CoCl2. Mechanistically, Met agonist antibodies or HGF prevented the inhibition of mTOR and reduced the flux of autophagosome formation. Accordingly, their anti-autophagic function was completely blunted by Temsirolimus, a specific mTOR inhibitor. Targeted Met activation was successful also in the setting of low oxygen conditions, in which Met agonist antibodies or HGF demonstrated anti-apoptotic and anti-autophagic effects. Activation of the Met pathway is thus a promising novel therapeutic tool for ischaemic injury.
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