Effect of Angiotensin II Receptors on Collagen Synthesis of Fibroblasts Derived from Human Hypertrophic Scars
摘要
BACKGROUND: It has been reported that Angiotensin Ⅱ (Ang Ⅱ) is related to occurrence and development of dermatofibrosis; however, less is explored about the expression and effect of AT1 and AT2 receptors in the fibroblasts of human hypertrophic scar. OBJECTIVE: To observe the expression of Ang Ⅱ type 1 (AT1) and type 2 (AT2) receptors in human hypertrophic scars, and explore their effects on collagen synthesis of fibroblasts. DESIGN, TIME AND SETTING: Randomized control experiment was performed at the Experimental Center, Guangzhou General Hospital of Guangzhou Military Area Command of Chinese PLA between August 2006 and November 2007. PARTICIPANTS: Samples of hypertrophic scars were taken from 18 patients (10 males and 8 females, 19-47 years old). Seven specimens of normal skin served as control. All of the specimens collected were divided into two parts, one part for immunohistochemical staining after fixated by 4% paraformaldehyde, the other part for culturing fibroblasts. METHODS: The expression of both AT1 and AT2 receptors in fibroblasts of hypertrophic scars was detected with immunohistochemical staining and radioligand receptor binding assay. Collagen synthesis was examined in cultured fibroblasts of hypertrophic scars by measuring [3H]-proline incorporation into collagenous proteins. MAIN OUTCOME MEASURES: The expression of both AT1 and AT2 receptors in human hypertrophic scars;the [3H]-proline incorporation value in cultured fibroblasts. RESULTS: Positive staining signals of both AT1 and AT2 receptors were found in fibroblasts of hypertrophic scars. Similar results were also observed in cultured fibroblasts of hypertrophic scars,expression level of AT1 and AT2 receptors were (10.69±2.15) fmol/10^6 cells and (4.9±1.05) fmol/10^6 cells, respectively. In cultured fibroblasts, Ang Ⅱ stimulation significantly increased collagen synthesis, which was inhibited by valsartan, an AT1 receptor blocker, but augmented by PD123319, an AT2 receptor antagonist. CON