Chemerin/Chemr23 Association With Endothelial-Mesenchymal Transition In Diabetic Nephropathy

This study was aimed to analyze the association of chemerin/chemR23 with endothelial-mesenchymal transition (EndMT) in the kidney of rats during the progression of diabetic nephropathy (DN). Eighty male Sprague-Dawley rats were randomly distributed to age-matched control and diabetic nephropathy model groups. Diabetes was induced by intraperitoneal injection of streptozotocin (STZ). Morphological changes in the renal tissues were observed after periodic acid-Schiff staining. Chemerin and chemR23 expression was determined by immunohistochemistry. Co-expression of alpha-smooth muscle actin (alpha-SMA) and CD31 was determined by immunofluorescence double-labeling. Expression of all these markers was analyzed by Western blotting. Expression of chemerin, chemR23, and transforming growth factor-beta 1 (TGF-beta 1) genes at mRNA level was determined by qRT-PCR. Mild glomerular hypertrophy was observed at 4 weeks and mild glomerular basement membrane thickening and mesangial matrix proliferation at 12 weeks. Immunohistochemistry showed much higher levels of chemerin and chemR23 in diabetic rats compared with the control group. Expression of chemerin, chemR23, and a-SMA proteins increased with disease progression, while CD31 protein expression decreased. Expression of chemerin, chemR23, and TGF-beta 1 mRNAs also increased. alpha-SMA and CD31 co-expression increased with disease progression from 4 weeks. Spearman correlation analysis showed that chemerin mRNA levels correlated positively with Chem R23, TGF-beta 1, alpha-SMA expression, and CD31 and a-SMA double-positive cell numbers, but negatively with CD31 protein expression. In conclusion, chemerin expression correlates with EndMT in DN model rats.