Expression and Significance of ILK and Correlation Factor in the Animal Model of Renal Interstitial Fibrosis
|Keywords||Integrin-linked kinase Renal tubular epithelial cells - myofibroblast transdifferentiation Renal interstitial fibrosis Transforming growth factor - beta1 alpha - smooth muscle actin|
Objective: renal interstitial fibrosis (RIF) is caused by a variety of extracellular matrix (ECM) in the renal interstitial excessive deposition of interstitial fibroblast proliferation and the formation, a variety of kidney disease progress to end-stage common pathway and pathology. Expression of alpha-SMA of myofibroblasts (MyoF) synthesis ECM cells has been shown that approximately 36% of the RIF process MyoF by tubular epithelial cells transformed from, this process is called tubules epithelial cells (EMT). TGF-beta1 is recognized fibrogenic factor, through a variety of signal transduction pathways to induce the occurrence and development of the EMT. ILK effector molecules of the signal transduction pathway, mediated by TGF-beta1-induced renal tubular EMT key steps, eventually leading to the occurrence of renal interstitial fibrosis. In this study, histopathological observation, immunohistochemistry and RT-PCR method to understand the expression of ILK, α-SMA and TGF-beta1 in renal interstitial fibrosis in animal models, explore the formation of renal interstitial fibrosis relationship. Methods: 1. Establishment of animal model of renal interstitial fibrosis: Select 72 SD rats were randomly divided into three groups: normal group, unilateral ureteral ligation surgery group, sham operation group, operation group, the establishment of renal interstitial fibrosis model UUO model the surgery group rats after general anesthesia in nearly left kidney uttermost free and ligation of the left ureter; sham-operated rats only underwent open surgery free left ureter; normal group received no treatment . Rats in each group were sacrificed after 1, 3, 7, 14 days, whichever is the left kidney, left kidney gross morphology was observed under light microscope renal pathological changes and interstitial fibrosis. 2 immunohistochemistry chemical detection of renal ILK quality and TGF-beta1, alpha-SMA expression, further analysis between the groups ILK and TGF-β1, α-SMA expression level of renal interstitial injury extent The relationship between ILK and TGF-β1, α-SMA correlation between each other. 3 semi-quantitative reverse transcription method determination the ILKmRNA expression in the UUO model, and analyze its relationship with the degree of renal interstitial damage. Results: 1. Unilateral ureteral ligation build the success of renal interstitial fibrosis in animal models, no rats died. (2) changes in renal tissue morphology: with the control group, sham operation group than UUO group rats were significantly enlarged kidneys, renal cortical thinning, hydronephrosis, and aggravated with the extension of the time limit. 3 Immunohistochemical analysis showed that: almost no positive expression of ILK in normal kidney tissue, UUO model, ILK mainly expressed in renal interstitial renal interstitial disease severity, a significant increase in positive area, each group between expression was significant difference (P lt; 0.001), and renal quality lesions extent was significant with positive correlation (r 0.842, P lt; 0.001); TGF-beta1 in normal renal quality in just a trace of expression, With the gradual increase in the expression of renal interstitial lesion severity, TGF-beta1 expression between the groups was significant difference (P lt; 0.001), and the degree of renal interstitial disease was a significant positive correlation (r = 0.892, P lt; 0.001); alpha-SMA in normal kidney tissue, only expressed in the vascular smooth muscle layer, trace expression in renal tubular epithelial cells, with emphasis enhanced expression of renal interstitial lesions among the groups alpha-SMA expression significant difference (P lt; 0.001), and renal matter lesions between the degree of positive correlation (r = 0.854, P lt; 0.001). Conclusion: 1.ILK as TGF-beta1 downstream signaling factors involved in EMT, EMT may be caused by an important means of renal interstitial fibrosis. 2.TGF-β1 may play an important role in the occurrence of RIF, EMT may be an important way of TGF-beta1 induced renal interstitial fibrosis. 3.α-SMA as MyoF marker proteins involved in EMT, play an important role in renal interstitial fibrosis. In the severity of renal tubular interstitial ILK and TGF-beta1, alpha-SMA expression positively correlated, suggesting that ILK may play an important role in TGF-beta1 mediated induction of EMT process.