Abstract
Objectives: The objective of the study was to investigate the expression pattern of microRNA-29b (miRNA-29b) in patients with diabetic nephropathy (DN) compared to Type 2 diabetes mellitus (T2DM) and healthy subjects.
 Methods: Blood samples were obtained from 30 patients with DN, 30 patients with T2DM and 30 healthy subjects as controls. Serum reactive oxygen species (ROS) and interleukine-10 (IL-10) level were measured by enzyme-linked immunosorbent assay, and quantitative polymerase chain reaction was employed to screen the expression of serum miRNA-29b and anti-apoptotic B-cell lymphoma 2 (Bcl-2).
 Results: The results showed a significant increase in ROS levels (p<0.05) in DN group compared with T2DM and control groups. IL-10 levels were significantly increased compared to other groups (p<0.05). The gene expression of miRNA-29b was significantly increased with downregulation of Bcl-2 (p<0.05) in DN compared to T2DM and control groups (p<0.05).
 Conclusions: The study suggested that miRNA-29b expression is involved in the pathogenesis of DN. Hyperglycemia induced oxidative stress-mediated apoptosis, and an increase in expression of pro-inflammatory miRNA-29b exerts anti-protective effect by upregulating target genes related to inflammation and apoptosis, taken together, the results identify the regulatory role of miRNA-29b in DN.
Highlights
Diabetic nephropathy (DN) is the most common and prevalent macrovascular complication of both Type 1 diabetes mellitus (T1DM) and Type 2 diabetes mellitus (T2DM) [1,2], which is characterized by the presence of trace albuminuria followed by a diminished glomerular filtration rate [3]The mechanism involved in the pathogenesis of DN still unclear
In DN, oxidative stress caused an increase in apoptotic Bax protein expression, with downregulation of B-cell lymphoma 2 (Bcl-2) expression [7], which led to unbalance in the interaction between pro-apoptotic and anti-apoptotic Bcl-2 family members [8] and loss of normal kidney cells by excessive apoptosis and progression of renal fibrosis [9]
DN analysis compared with the T2DM patients and the control, the hemoglobin A1c (HbA1c) levels were significantly higher in DN (p
Summary
Diabetic nephropathy (DN) is the most common and prevalent macrovascular complication of both Type 1 diabetes mellitus (T1DM) and Type 2 diabetes mellitus (T2DM) [1,2], which is characterized by the presence of trace albuminuria followed by a diminished glomerular filtration rate [3]The mechanism involved in the pathogenesis of DN still unclear. There is growing evidence support that is DN mainly a chronic inflammatory process, and increasing numbers of inflammatory mediators have been shown to play key roles in its development [4]. In DN, oxidative stress caused an increase in apoptotic Bax protein expression, with downregulation of Bcl-2 expression [7], which led to unbalance in the interaction between pro-apoptotic and anti-apoptotic Bcl-2 family members [8] and loss of normal kidney cells by excessive apoptosis and progression of renal fibrosis [9]. It has been demonstrated that miRNAs contributed to a variety of physiological and pathological process including angiogenesis, inflammation, and oxidative stress in T1DM and T2DM [10,11,12]
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