A signature of microRNA-155 in the pathogenesis of diabetic complications

Abstract

The current study was designed to explore the potential involvement of miR-155 in the pathogenesis of diabetes complications. Male rats were divided into control and diabetic groups (n = 6). Type 2 diabetes was induced by a single-dose injection of nicotinamide (110 mg/kg; intraperitoneal (i.p.)), 15 min before injection of streptozotocin (STZ; 50 mg/kg; i.p.) in 12-h fasted rats. Two months after induction of diabetes, the rats were sacrificed for subsequent measurements. The nuclear factor kappa B (NF-κB) activity was higher in diabetic peripheral blood mononuclear cells (PBMCs), aorta, heart, kidney, liver, and sciatic nerve, than the control counterparts. Also, apoptosis rate was increased in these tissues, except the aorta. NF-κB messenger RNA (mRNA) expression level was higher in the kidney, heart, PBMCs, and sciatic nerve of diabetic rats than their control counterparts. Except the liver, the miR-155 expression level was significantly decreased in diabetic kidney, heart, aorta, PBMCs, and sciatic nerve versus the controls. Moreover, the expression of miR-155 was negatively correlated with NF-κB activity and apoptosis rate. These results suggest that changes in the expression of miR-155 may participate in the pathogenesis of diabetes-related complications, but causal relationship between miR-155 dysregulation and diabetic complications is unknown.

MicroRNA expression profile in plasma from type 1 diabetic patients: Case-control study and bioinformatic analysis

“…Moreover, miR-155-5p positively regulates host antiviral immune response by promoting type I IFN signaling through targeting SOCS1, a negative regulator of the type I IFN pathway [47]. Consequently, miR-155-5p dysregulation has been associated with different cancers, cardiovascular diseases, viral infections, rheumatoid arthritis, and chronic diabetic complications [45,46,48].…”

MiR-3202 – Promoted H5V Cell Apoptosis by Directly Targeting Fas Apoptotic Inhibitory Molecule 2 (FAIM2) in High Glucose Condition

“…At the same time, mRNA expression and function are susceptible to environmental factors, especially hyperglycemic conditions, which usually further result in disease complications. In addition, platelet and plasma miR-144 and miR-223 have been shown to be significantly altered in type 2 diabetes mellitus (T2DM) patients [5]; changes in the expression of miR-155 may play a role in the pathogenesis of diabetes-related complications [6]. Studies have shown that miR-3202 is downregulated in patients with early-onset post-stroke depression [7], that its expression is upregulated by radon in the lung BEAS-2B cell line [8], and that it is upregulated as secreted miRNAs isolated from LNCaP prostate cancer cells compared with normal human prostate epithelial cells (PrECs) [9].…”

Inhibition of miR-155 Protects Against LPS-induced Cardiac Dysfunction and Apoptosis in Mice

“…16,17,18,19,20,21,22,23,24 The dysregulation of miR-155 has recently been reported to play important roles in multiple cardiovascular diseases like atherosclerosis, hypertrophic cardiac remodeling, acute myocardial infarction, myocardial ischemia-reperfusion injury, and diabetic cardiomyopathy. 25,26,27,28,29,30 Additionally, miR-155 is a well-known immunomodulatory miRNA that can be induced by lipopolysaccharide (LPS) and control inflammatory processes in multiple cells and organs. 31,32,33,34 However, the role of miR-155 in sepsis-induced myocardial dysfunction remains largely unknown.…”