Expression of the Integrin-Linked Kinase in a Rat Kidney Model of Chronic Allograft Nephropathy |
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Authors: | Conghui Han Hequn Zou Qingqin Li Yuxin Wang Yanling Shi Tianyu Lv Ling Chen Wenying Zhou |
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Institution: | (1) Department of Urology, The Affiliated Xuzhou Hospital of Southeast University, Xuzhou, 221000, Jiangsu Province, China;(2) Department of Nephrology, The No.3 Affiliated Hospital of Southern Medical University, Guangzhou, 518000, China;(3) Department of Nephrology, The 2nd Hospital of Xiamen, 361021 Xiamen, China;(4) Deptartment of Nephrology, The No.1 Affiliated Hospital of Wenzhou Medical College, Wenzhou, 325000, China;(5) Department of Nephrology, The No.5 Affiliated Hospital of Sun Yet-Sen University, Zhuhai, 519000, China; |
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Abstract: | The purpose of this study was to investigate the expression and significance of integrin-linked kinase (ILK) in the pathogenesis
of chronic allograft nephropathy (CAN) in rats. For this, kidneys of Fisher (F344) rats were orthotopically transplanted into
Lewis (LEW) rats. The animals were evaluated at 4, 8, 12, 16, and 24 weeks post-transplantation for renal function and histopathology.
ILK protein expression was determined by Western-blot and immunohistological assays, and mRNA by RT-PCR. Our data show that
24-h urinary protein excretion in CAN rats increased significantly at week 16 as compared with F344/LEW controls. Allografts
showed markedly increased mononuclear cells infiltration and presented with severe interstitial fibrosis and tubular atrophy
at 16 and 24 weeks. ILK expression (protein/mRNA) was upregulated in rat kidneys with CAN, and the increase became more significant
over time after transplantation. ILK expression correlated significantly with 24-h urinary protein excretion, serum creatinine
levels, tubulointerstitial mononuclear cells infiltration, smooth muscle cells (SMCs) migration in vascular wall, and interstitial
fibrosis. Therefore, it was concluded that ILK overexpression was the key event that involved mononuclear cells infiltration
and vascular SMCs migration at early stage, and interstitial fibrosis and allograft nephroangiosclerosis at later stage of
CAN pathogenesis in rats. |
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