Overexpression of miR-150-5p Alleviates Apoptosis in Sepsis-Induced Myocardial Depression.
Xiao Geng ZhuTie Ning ZhangRi WenChun-Feng LiuPublished in: BioMed research international (2020)
Sepsis-induced myocardial depression has high mortality and is very common in intensive care units. Previous studies have found that microRNAs play an important role in regulating sepsis-induced myocardial depression. miR-150-5p is involved in many biological processes; however, the mechanism underlying its role in sepsis-induced myocardial depression is still unclear. In this study, we generated rat models of septic shock induced by lipopolysaccharide. Whole genomic RNA sequencing was performed on 12 left ventricles collected after LPS treatment to identify miRNAs. Most of the target genes of the differently expressed microRNAs were involved in apoptosis, according to Gene Ontology. We also observed apoptosis in the heart tissue and in H9C2 cardiomyocytes stimulated with lipopolysaccharide, indicating that cell apoptosis may be an important mechanism in sepsis-induced myocardial depression. Furthermore, the expression of miR-150-5p was reduced, and overexpression of miR-150-5p with mimics resulted in a decrease in apoptosis, decreased expression of cleaved caspase3 and Bax, and increased expression of Bcl-2. Additionally, after H9C2 cells were transfected with miR-150-5p mimics or an inhibitor, the expression of Akt2 decreased or increased, respectively. These findings suggest that miR-150-5p can alleviate apoptosis and may be a novel therapeutic target for sepsis-induced myocardial depression.
Keyphrases
- septic shock
- high glucose
- intensive care unit
- oxidative stress
- cell cycle arrest
- diabetic rats
- acute kidney injury
- depressive symptoms
- cell death
- poor prognosis
- endoplasmic reticulum stress
- left ventricular
- induced apoptosis
- cell proliferation
- inflammatory response
- drug induced
- heart failure
- endothelial cells
- type diabetes
- gene expression
- cardiovascular disease
- copy number
- signaling pathway
- immune response
- risk factors
- pi k akt
- extracorporeal membrane oxygenation