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.

中文翻译：

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MRC2促进糖尿病肾病增殖并抑制细胞凋亡

糖尿病肾病（DN）是糖尿病的重要微血管并发症，是导致终末期肾病的主要原因。2型甘露糖受体C（MRC2）是甘露糖受体蛋白家族的成员，已被证实具有促进细胞迁移信号通路和侵袭的能力。通过互补DNA芯片筛选和分析，我们发现糖尿病肾病小鼠肾脏中MRC2的表达上调。然而，MRC2在糖尿病肾病中的作用尚不清楚。这项工作研究了 MRC2 对糖尿病肾病的影响。在通过定量实时聚合酶链反应 (qRT-PCR) 和蛋白质印迹验证芯片的结果后，我们使用小干扰 RNA (siRNA) 来抑制小鼠系膜细胞 (MMC) 中 MRC2 的表达，并使用蛋白质印迹、细胞计数试剂盒 8 和流式细胞术分析细胞增殖和凋亡的水平。结果表明，MRC2敲低抑制MMC增殖并诱导细胞凋亡。这些结果表明 MRC2 可能是糖尿病肾病的分子标志物和治疗靶点。