Inhibition of microRNA-665 Alleviates Septic Acute Kidney Injury by Targeting Bcl-2.

Sepsis can easily cause acute kidney injury (AKI) and seriously endanger human health. This article aims to investigate and study the role of microRNA-665 (miR-665) in septic AKI and the underlying molecular mechanism. Lipopolysaccharide (LPS) was used to construct cell and animal models of septic AKI. The expression of miR-665 in cells and kidney tissues was detected by quantitative reverse-transcription polymerase chain reaction (RT-PCR). The contents of inflammatory factors (TNF-α, IL-1ß, and IL-6) in the cell supernatant were detected using commercial kits. Renal tissue damage was observed by hematoxylin-eosin (HE) staining. Kidney function was assessed by serum Cr, serum BUN, and urine NAG levels. The apoptosis of HK-2 cells was analyzed by flow cytometry and TUNEL staining. Luciferase activity assay was performed for the verification of the target of miR-665. The expression of miR-665 was increased in the cell model and animal model of septic AKI constructed by LPS. By transfecting miR-665 inhibitor in HK-2 cells and injecting miR-665 antagomir (antagomiR-665) through the tail vein of rats, the expression of miR-665 in HK-2 cells and rat kidneys was remarkably reduced. Silencing miR-665 dramatically inhibited the expression of inflammatory factors (TNF-α, IL-1ß, and IL-6) in LPS-induced HK-2 cells and reduced LPS-induced apoptosis in HK-2 cells. At the same time, the levels of serum Cr, serum BUN, and urine NAG decreased markedly, and the damage of the kidney was also alleviated. Finally, luciferase reporter experiments demonstrated that miR-665 directly targets Bcl-2. We revealed that miR-665 expression was increased in septic AKI, and silencing miR-665 could inhibit LPS-induced inflammation and apoptosis of the kidney by targeting Bcl-2, thereby improving renal function.

Identification of protein complexes associated with myocardial infarction using a bioinformatics approach.

Myocardial infarction (MI) is a leading cause of mortality and disability worldwide. Determination of the molecular mechanisms underlying the disease is crucial for identifying possible therapeutic targets and designing effective treatments. On the basis that MI may be caused by dysfunctional protein complexes rather than single genes, the present study aimed to use a bioinformatics approach to identifying complexes that may serve important roles in the development of MI. By investigating the proteins involved in these identified complexes, numerous proteins have been reported that are related to MI, whereas other proteins interacted with MI­related proteins, which implied that these protein complexes may indeed be related to the development of MI. The protein complexes detected in the present study may aid in our understanding of the molecular mechanisms that underlie MI pathogenesis.