Overexpression of small ubiquitin ‑like modifier 2 ameliorates high glucose‑induced reductions in cardiomyocyte proliferation via the transforming growth factor‑β/Smad pathway.

Overexpression of small ubiquitin‑like modifier 2 ameliorates high glucose‑induced reductions in cardiomyocyte proliferation via the transforming growth factor‑β/Smad pathway. Mol Med Rep. 2018 Oct 01;: Authors: Zhao C, Shen Q Abstract Hyperglycemia may induce diabetic cardiomyopathy (DC). In the current study, the mechanism underlying the alleviation of high glucose (HG)‑induced impairments in the proliferation of H9c2 embryo cardiomyocyte proliferation by small ubiquitin‑like modifier 2 (SUMO2) overexpression was investigated. H9c2 cell morphology was identified as classical long shuttle type by optical microscopy. The viability of HG‑injured H9c2 cells was evaluated by a Cell Counting Kit‑8 assay and the results indicated that viability was inhibited in a dose‑dependent (5.6, 10, 20 and 30 mmol/l) and time‑dependent (6, 12 and 24 h) manner. H9c2 cells treated with 20 mmol/l HG for 24 h were selected for subsequent experiments due to the extent of injury caused at a low density. Flow cytometry was conducted to confirm cell cycle arrest between G1/S phases and apoptosis promotion in HG‑injured H9c2 cells, and the subsequent alleviating effect of SUMO2 overexpression on these HG‑induced effects. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blot analysis were performed to detect mRNA and protein expression levels of cell cycle‑and apoptosis‑associated factors. ...
Source: Molecular Medicine Reports - Category: Molecular Biology Tags: Mol Med Rep Source Type: research