ArticleIn vitro cellular & developmental biology. Animal2016
Downregulation of RACK1 is associated with cardiomyocyte apoptosis after myocardial ischemia/reperfusion injury in adult rats.
Article in In vitro cellular & developmental biology. Animal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- OTUD1 deficiency attenuates myocardial ischemia/reperfusion induced cardiomyocyte apoptosis by regulating RACK1 phosphorylation.Acta pharmacologica Sinica · 2025Article
- Roflumilast reduces myocardial ischemia reperfusion injury in vivo and in vitro by activating the AMPK signaling pathway.Experimental and therapeutic medicine · 2023Article
- CPNE3 interaction with RACK1 protects against myocardial ischemia/reperfusion injury.Experimental and therapeutic medicine · 2022Article
- PSMB4 inhibits cardiomyocyte apoptosis via activating NF-κB signaling pathway during myocardial ischemia/reperfusion injury.Journal of molecular histology · 2021Article
- Receptor for activated C kinase 1 in rats with ischemia-reperfusion injury: intravenous versus inhalation anaesthetic agents.International journal of medical sciences · 2018Article
- Mitochondrial phosphatase PGAM5 regulates Keap1-mediated Bcl-xL degradation and controls cardiomyocyte apoptosis driven by myocardial ischemia/reperfusion injury.In vitro cellular & developmental biology. Animal · 2017Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The receptor for activated C kinase 1 (RACK1) is a multifaceted scaffolding protein that mediates the shuttling of activated protein kinase C (PKC) to cellular membranes. In addition, RACK1 could decrease cell apoptosis in a variety of disease models. However, the function of RACK1 in cardiomyocyte apoptosis after myocardial ischemia/reperfusion (I/R) is unknown. In this study, male Sprague-Dawley rats were anesthetized and subjected to myocardial I/R insult consisting of 30 min left anterior descending coronary artery (LAD) occlusion followed by reperfusion for 1, 2, 4, 6, 8, 12, and 24 h. The expression of RACK1 was decreased after myocardial I/R and was associated with cardiomyocyte apoptosis. To further verify the relationship between RACK1 and cardiomyocyte apoptosis, H9c2 cardiomyocytes were cultured under hypoxia for 6 h, then maintained in the regular incubator to reoxygenation. After H9c2 cells were transfected with Flag-RACK1 to overexpress RACK1, RACK1 expression was upregulated in hypoxia/reoxygenation (H/R) 4 h group accompanied with the decrease of cleaved caspase-3 and the increase of Bcl-2 expression. Terminal transferase-mediated biotin dUTP nick end labeling (TUNEL) assay showed that RACK1 overexpression inhibited H9c2 cell apoptosis induced by H/R treatment. Our data suggested that RACK1 might suppress cardiomyocyte apoptosis after I/R, providing a novel molecular target for the therapy of ischemia heart disease.
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