Abstract
Diabetic nephropathy (DN) is an important microvascular complication of diabetes and is the main cause of end-stage renal disease. Type 2 mannose receptor C (MRC2) is a member of the mannose receptor protein family, which has been confirmed to have the ability to promote the cell migration signaling pathway and invasion. By complementary DNA chip screening and analysis, we found that the expression of MRC2 was upregulated in the kidneys of mice with diabetic nephropathy. However, the role of MRC2 in diabetic nephropathy is still unclear. This work studied the effect of MRC2 on diabetic nephropathy. After verifying the results of the chip by quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting, we used small interfering RNAs (siRNAs) to knock down the expression of MRC2 in mouse mesangial cells (MMCs) and analyzed the level of cell proliferation and apoptosis using western blotting, Cell Counting Kit-8, and flow cytometry. The results showed that the MRC2 knockdown inhibited MMC proliferation and induced cell apoptosis. These results suggest that MRC2 may be a molecular marker and a therapeutic target for diabetic nephropathy.
Highlights
Diabetic nephropathy (DN) is an important microvascular complication of diabetes and is the main cause of end-stage renal disease
Our group previously studied the Type 2 mannose receptor C (MRC2) expression in a DN mouse model using sequencing [11], The results showed that the expression of MRC2 in DN mice was significantly higher than that in normal mice
To study the difference in MRC2 expression in patients with and without DN, we carried out quantitative real-time polymerase chain reaction (qRT-PCR) assays on peripheral blood samples
Summary
Diabetic nephropathy (DN) is an important microvascular complication of diabetes and is the main cause of end-stage renal disease. 30% of patients with type 1 diabetes and 20% of patients with type 2 diabetes develop DN, with end-stage renal disease accounting for approximately 50% of the leading causes of death from chronic kidney disease [2]. Its pathogenesis is complex and is closely related to many factors, such as oxidative stress, cell proliferation, inflammatory reaction, glucose and lipid metabolism disorders, and genetic susceptibility [3, 4]. DN treatment mainly controls hypoglycemia, blood pressure, and lipid regulation, but its therapeutic effects are limited; exploring the molecular mechanism of glomerular mesangial cell proliferation is important to understand DN and its development, which will facilitate the search for potential therapeutic targets
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