English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

In the present study, the role of microRNA-663b (miR-663b) in cardiomyocyte injury was examined. Reverse transcription-quantitative PCR (RT-qPCR) was performed to detect miR-663b expression in hypoxia-induced H9c2 cells. The results revealed that miR-663b expression was significantly upregulated in hypoxia-induced H9c2 cells compared with control cells. TargetScan analysis and dual-luciferase reporter assays demonstrated that miR-663b directly targeted the B-cell lymphoma 2 like 1 (BCL2L1) gene. RT-qPCR and western blotting data indicated that BCL2L1 expression was significantly downregulated in hypoxia-induced H9c2 cells compared with control cells. Under hypoxic conditions, H9c2 cells were transfected with miR-663b inhibitor, inhibitor control, miR-663b inhibitor + control small interfering (si)RNA or miR-663b inhibitor + BCL2L1-siRNA for 48 h. ELISA against creatine kinase-muscle/brain (CK-MB) and cardiac troponin 1 (cTnI) demonstrated that the miR-663b inhibitor reduced CK-MD and cTnI release and increased mitochondrial viability when compared with hypoxia-treated cells. Additionally, the miR-663b inhibitor significantly increased H9c2 cell viability and decreased cell apoptosis under hypoxic conditions. The results of ELISA further revealed that the miR-663b inhibitor decreased the release of various inflammatory factors, including tumour necrosis factor α, interleukin (IL) 1β and IL-6 in H9c2 cells under hypoxic conditions. These changes were reversed following BCL2L1 knockdown. In conclusion, miR-663b inhibition protected cardiomyocytes against hypoxia-induced injury by targeting BCL2L1 and may potentially be a novel target for the treatment of patients with myocardial infarction.

Downregulation of miRNA‑663b protects against hypoxia‑induced injury in cardiomyocytes by targeting BCL2L1