{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang L"],"funding":["NHLBI NIH HHS"],"pagination":["39338-48"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3501087"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["287(47)"],"pubmed_abstract":["Histone deacetylases (HDACs) play a critical role in the regulation of gene transcription, cardiac development, and diseases. The aim of this study was to test whether inhibition of HDACs induces myocardial repair and cardiac function restoration through c-kit signaling in mouse myocardial infarction models. Myocardial infarction in wild type Kit(+/+) and Kit(W)/Kit(W-v) mice was created following thoracotomy by applying permanent ligation to the left anterior descending artery. The HDAC inhibitor, trichostatin A (TSA, 0.1 mg/kg), was intraperitoneally injected daily for a consecutive 8 weeks after myocardial infarction. 5-Bromo-2-deoxyuridine (BrdU, 50 mg/kg) was intraperitoneally delivered every other day to pulse-chase label in vivo endogenous cardiac replication. Eight weeks later, inh"],"journal":["The Journal of biological chemistry"],"pubmed_title":["Inhibition of histone deacetylase-induced myocardial repair is mediated by c-kit in infarcted hearts."],"pmcid":["PMC3501087"],"funding_grant_id":["R01 HL089405"],"pubmed_authors":["Chin YE","Zhao TC","Dubielecka PM","Zhang L","Wang Y","Chen B","Zhao Y","Wei L","Qin GJ"],"additional_accession":[]},"is_claimable":false,"name":"Inhibition of histone deacetylase-induced myocardial repair is mediated by c-kit in infarcted hearts.","description":"Histone deacetylases (HDACs) play a critical role in the regulation of gene transcription, cardiac development, and diseases. The aim of this study was to test whether inhibition of HDACs induces myocardial repair and cardiac function restoration through c-kit signaling in mouse myocardial infarction models. Myocardial infarction in wild type Kit(+/+) and Kit(W)/Kit(W-v) mice was created following thoracotomy by applying permanent ligation to the left anterior descending artery. The HDAC inhibitor, trichostatin A (TSA, 0.1 mg/kg), was intraperitoneally injected daily for a consecutive 8 weeks after myocardial infarction. 5-Bromo-2-deoxyuridine (BrdU, 50 mg/kg) was intraperitoneally delivered every other day to pulse-chase label in vivo endogenous cardiac replication. Eight weeks later, inh","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012 Nov","modification":"2025-04-04T19:07:32.517Z","creation":"2019-03-27T01:00:41Z"},"accession":"S-EPMC3501087","cross_references":{"pubmed":["23024362"],"doi":["10.1074/jbc.M112.379115","10.1074/jbc.m112.379115"]}}