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Its mechanism of hepatocyte growth factor (HGF) systemic scleroderma skin fibroblasts of type I collagen

Author: ZhanYi
Tutor: XiaoZuo
School: Central South University
Course: Dermatology
Keywords: Systemic scleroderma Hepatocyte growth factor Cyclooxygenase-2 Fibroblast
CLC: R593.25
Type: Master's thesis
Year: 2008
Downloads: 67
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Abstract


Objective: To study the hepatocyte growth factor in patients with systemic scleroderma skin fibroblast cell type I collagen expression and to explore its possible mechanism provide the basis for the clinical find effective treatment for systemic scleroderma . Method: 1. Patients with systemic scleroderma and normal skin biopsy specimens each of the five cases of primary cultured fibroblasts , keratin and vimentin staining of fibroblasts identification. 2.MTT method to detect HGF proliferative activity of dermal fibroblasts . Method detection 3.RT-PCR SSc patients and normal skin fibroblasts of type I collagen , COX -1 and COX - 2 of the mRNA expression levels . 4.RT-PCR was used to detect the different time points HGF SSc patients with skin type I collagen in fibroblasts , COX - 2 of the mRNA expression levels . 5 . Selective COX-2 inhibitor NS398 with HGF joint intervention , RT-PCR method to detect changes in mRNA expression of collagen type I in the different time points SSc skin fibroblasts . Results: 1 . Cultured cells with fibroblast morphology , cytokeratin negative , positive staining for vimentin . 2.20ng/ml HGF within 48 hours of skin fibroblast proliferation activity had no significant effect . 3.SSc patients skin into fibroblasts and normal skin fibroblasts compared to COX - 2 mRNA of decreased expression of type I collagen mRNA expression increased , while no significant differences in mRNA expression of COX-1 . 4.HGF can be induced SSc skin fibroblasts COX-2 mRNA expression ( P <0.05 ) , and the expression level of HGF effect was time-dependent increase . HGF inhibit SSc skin into the mRNA expression of type I collagen in fibroblasts ( P <0.05 ) , the expression level of HGF effect was time-dependent decline . 5 a selective COX -2 inhibitor NS398 can be significantly weakened inhibition of HGF SSc skin into the expression of type I collagen in fibroblasts ( P <0.05 ) . Conclusion : HGF induced SSc fibroblasts in the skin of patients with COX-2 expression , and inhibits the synthesis of type I collagen . Selective COX-2 inhibitor NS398 significantly weakened HGF fibroblasts of SSc patients with skin collagen synthesis inhibition , suggesting that HGF has anti -fibrosis , the mechanism may be dependent on the expression of COX-2 .

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CLC: > Medicine, health > Internal Medicine > Systemic disease > Autoimmune diseases > Autoimmune diseases, connective tissue disease > Scleroderma
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