| Objective:To explore the role and mechanism research of human renal microvascular endothelial-mesenchymal transition (EndMT) in transplant renal interstitial fibrosis formation.Methods:Based on renal allograft tissue samples from 25 cases of Chronic renal allograft dysfunction (CAD) patients and 25 normal renal tissue samples, observing the renal function and renal tubular atrophy and renal glomerular collapse and the degree of interstitial fibrosis by blood biochemical, periodic acid-schiff staining (PAS) and mason trichromatic staining. Using immunohistochemical and indirect immunofluorescence double staining to detect the two groups in renal tissue samples of vascular endothelial cell marker CD34 and myofibroblast marker α-Smooth muscle actin (α-SMA), and the expression and distribution of transforming growth factor-β1(TGF-β1).Human umbilical vein endothelial cell (HUVEC) as the object of study stimulated by TGF-β1 (5 ng/ml) respectively 0-72 h in vitro. Western blotting are used to observe the expression of CD34 and α-SMA.Results:Compared with normal group, patients in CAD group serum creatinine levels increased significantly, and PAS and Masson staining show that the apparent in CAD patients transplanted kidney renal tubular atrophy, glomerular collapse and interstitial fibrosis. Indirect immunofluorescence staining and immunohistochemical results show that CD34 positive expression reduce and α-SMA and TGF-β1 positive expression higher significantly in CAD group compared with normal group. Indirect immunofluorescence double staining shows parts of CD34 and α-SMA staining double positive in the CAD group glomerular and interstitial microvascular endothelial cells. With the increase time of TGF-β1 affect,CD34 expression gradually reduce and a-SMA expression gradually increased.Conclusion:Human renal microvascular EndMT may be mediated by TGF-β1 and plays an important role in transplant renal interstitial fibrosis formation. |
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