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On angiotensin on hypertrophic scar fibroblasts fibronectin synthesis in.doc

On angiotensin on hypertrophic scar fibroblasts fibronectin synthesis in.doc

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On angiotensin on hypertrophic scar fibroblasts fibronectin synthesis in

 PAGE \* MERGEFORMAT 12 On angiotensin on hypertrophic scar fibroblasts fibronectin synthesis in Author: Chen Yanqing Shi-Rong Li CAO Chuan-Li Dan Xia Shan Fung Chi [Paper Keywords] Angiotensin Ⅱ ; reverse transcription polymerase chain reaction; hypertrophic scar; Fibroblast; fibronectin [Abstract] Objective: To investigate the angiotensin Ⅱ (Ang Ⅱ ) and its type Ⅰ , Ⅱ receptor blocker, and calcineurin-kinase (CaN) of the blocker cyclosporin A (CsA) on hypertrophic scars source of fibroblast fibronectin mRNA and protein expression in the role. Methods: In vitro isolated and cultured hypertrophic scar fibroblasts, respectively, a certain concentration of Ang Ⅱ (10-9-10-5l / L), and Ang Ⅱ 10-6mmol / L with a different antagonist losartan, PD123319, ring Cytochalasin A (the concentration of both 10-5mmol / L) by adding cell culture medium to stimulate the 48h, respectively, by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot used to detect Westernblot hypertrophic scar fibroblasts fibronectin (FN ) mRNA and protein expression. Results: In vitro cultured successfully hypertrophic scar fibroblasts. After Ang Ⅱ stimulated 48h after, FN mRNA and protein expression was significantly increased, higher concentration is proportional to the degree of AngII; join losaartan and cyclosporin A after, FN original mRNA and protein expression of Ang Ⅱ group than alone declined to join the PD123319 later, FNmRNA and protein expression of Ang Ⅱ alone group compared with no significant change. Conclusion: Ang Ⅱ may call a hypertrophic scar fibroblasts FN synthesis, may scar the development process play an important role, the role primarily through the Ang Ⅱ type Ⅰ receptor-mediated completed and the role of the CaN signaling pathway may be related to about. Hypertrophic scar fibroblasts is based on the excessive proliferation and excessive deposition of extracellular matrix of connective tissue disease as the main feature. Its pathogenesis has

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