BRD7 Mediates Hyperglycaemia-Induced Myocardial Apoptosis via Endoplasmic Reticulum Stress Signalling Pathway

作者: Xiao-meng Wang , Ying-cui Wang , Xiang-juan Liu , Qi Wang , Chun-mei Zhang

DOI: 10.1111/JCMM.13041

关键词: Diabetic cardiomyopathySmall hairpin RNAApoptosisEndoplasmic reticulumKinaseCell cycleBiologyInternal medicineCell biologyEndocrinologyUnfolded protein responseTranscription Factor CHOP

摘要: Bromodomain-containing protein 7 (BRD7) is a tumour suppressor that known to regulate many pathological processes including cell growth, apoptosis and cycle. Endoplasmic reticulum (ER) stress-induced plays key role in diabetic cardiomyopathy (DCM). However, the molecular mechanism of hyperglycaemia-induced myocardial still unclear. We intended determine BRD7 high glucose (HG)-induced cardiomyocytes. In vivo, we established type 1 rat model by injecting high-dose streptozotocin (STZ), lentivirus-mediated short hairpin RNA (shRNA) was used inhibit expression. Rats with DCM exhibited severe remodelling, fibrosis, left ventricular dysfunction apoptosis. The expression up-regulated heart rats, inhibition had beneficial effects against diabetes-induced damage. vitro, H9c2 cardiomyoblasts investigate HG-induced Treating HG elevated level via activation extracellular signal-regulated kinase 1/2 (ERK1/2) increased ER detecting spliced/active X-box binding (XBP-1s) C/EBP homologous (CHOP). Furthermore, down-regulation attenuated CHOP inhibiting nuclear translocation XBP-1s without affecting total XBP-1s. conclusion, appeared protect cardiomyocyte stress signalling pathway.

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