[Effect of integrin-linked kinase on renal tubular epithelial cell transdifferentiation in diabetic rats].
OBJECTIVE
To determine the effect of integrin-linked kinase(ILK) in renal tubular epithelial cells and its relation to tubular epithelial-myofibroblast transdifferentiation.


METHODS
Wistar rats were randomly divided into 3 groups, Group normal control (n=10), Group diabetic without therapy(n=10) and Group diabetic with Losartan 20mg/(kg . d)(n=10). Five rats were killed in each group at the 8th and 16th week. The left kidneys were kept for HE and Masson staining to observe the pathological variations in the renal interstitium. ILK, alpha-SMA and Vimentin in renal tubular epithelial cells were detected by immunohistochemistry analysis.


RESULTS
Compared with the control group, ILK, alpha-SMA and Vimentin in renal tubular epithelial cells in Group diabetes gradually increased in immunohistochemistry (P<0.01); ILK was consistent with the pathological variation of renal interstitium and was positively correlated to alpha-SMA(rs=0.621, P<0.05). In comparison with the Group diabetes, the expression of ILK, alpha-SMA and Vimentin in renal tubular epithelial cells was apparently declined (P<0.01) in Group diabetes with Losartan.


CONCLUSIONS
Tubular epithelial myofibroblast transdifferentiation and the over-expression of ILK, between which there may be significant connections, are important events in the progression of diabetic nephropathy. Losartan, a blocker of angiotension II type I receptor, which may down-regulate the expression of ILK in diabetic renal tubular epithelial cells, can restrain the procession of epithelial-myofibroblast transdifferentiation.
Ning
Jian-Ping
JP
Department of Nephrology, Xiangya Hospital, Central South University, Changsha 41000, China. ningjp632@yahoo.com.cn
Yang
Shen
S
Ning
Chen
C
Zeng
Ying-Hui
YH
Liu
Lun-Zhi
LZ
Liu
Jun
J
D000199:Actins / Q000096:biosynthesis; D000818:Animals; D054338:Cell Transdifferentiation; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy / Q000503:physiopathology*; D003928:Diabetic Nephropathies / Q000188:drug therapy / Q000503:physiopathology; D004847:Epithelial Cells / Q000187:drug effects / Q000201:enzymology* / Q000473:pathology; D005347:Fibroblasts / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D007150:Immunohistochemistry; D007684:Kidney Tubules / Q000473:pathology; D019808:Losartan / Q000494:pharmacology / Q000627:therapeutic use; D008297:Male; D017346:Protein Serine-Threonine Kinases / Q000096:biosynthesis*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D014746:Vimentin / Q000096:biosynthesis; D000099200:Scaffold Protein ILK
D000199:Actins; D019808:Losartan; D017346:Protein Serine-Threonine Kinases; D014746:Vimentin; D000099200:Scaffold Protein ILK