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    尾加压素Ⅱ诱导乳鼠心肌成纤维细胞增殖及胶原合成的信号转导机制研究

    Intracellular Signaling Mechanism of the Proliferation and Collagen Synthesis of Cardiac Myofibroblasts Induced by UrotensinⅡ

      摘要
    • 摘要: 目的 探讨尾加压素Ⅱ(urotensin Ⅱ，UⅡ)对乳鼠心肌成纤维细胞(cardiac myofibroblasts，CFs)增殖及胶原合成的影响。方法 体外培养CFs作为实验模型，不同浓度UⅡ处理细胞后，通过ELISA法检测各组培养细胞上清中TGF-β1的含量变化，分别利用CKK-8细胞增殖法及Western blot分析UⅡ受体拮抗剂(SB-611812)及PKA特异性阻断剂(KT5720)对UⅡ诱导的CFs增殖及胶原蛋白col-Ⅰ、col-Ⅲ表达的影响。结果 UⅡ 10-10，10-9，10-8 mol·L-1处理细胞后，CFs培养上清中TGF-β1的含量及各组CFs的吸光度值与对照组相比明显增加(P<0.05)，而在10-7 mol·L-1 UⅡ处理细胞后，上述参数与对照组比较无显著差异。1 mol·L-1 SB-611812+10-8 mol·L-1 UⅡ组和1 mol·L-1 KT5720+10-8 mol·L-1 UⅡ组的TGF-β1的含量及CFs的吸光度值均显著高于对照组(P<0.05)，但显著低于10-8 mol·L-1 UⅡ组(P<0.05)，且两组col-Ⅰ、col-Ⅲ型胶原蛋白表达均低于10-8 mol·L-1 UⅡ组。结论 UⅡ上调TGF-β1水平促进了CFs的增殖，诱导细胞表达胶原蛋白col-Ⅰ、col-Ⅲ，这一过程可能涉及cAMP-PKA信号转导通路。

       

      Abstract: OBJECTIVE To investigate the effects of urotensin Ⅱ(UⅡ) on the proliferation and collagen synthesis of cardiac myofibroblasts (CFs) of new-born SD rats. METHODS CFs isolated from new-born SD rats were cultured as cell model in vitro. The level of TGF-β1 in CFs supernatant was detected by ELISA assay, and the proliferation and collagen synthesis of CFs treated with UⅡ, SB-611812 and KT5720 were respectively observed by CKK-8 assay and Western blot. RESULTS After CFs treated by 10-10, 10-9, 10-8 mol·L-1 UⅡ, the level of TGF-β1 in CFs supernatant and the OD values were significantly higher than that in control group(P<0.05), but the indices in the 10-7 mol·L-1 UⅡ group were not significantly different from those of control group. The level of TGF-β1 and the OD values in 1 mol·L-1 SB-611812+10-8 mol·L-1 UⅡgroup or 1 mol·L-1 KT5720+10-8?mol·L-1 UⅡ group increased significantly compared with control group(P<0.05), but decreased compared with the 10-8?mol·L-1 UⅡ group (P<0.05). The expression of col-Ⅰand col-Ⅲ in 1 mol·L-1 SB-611812+10-8 mol·L-1 UⅡ group and 1 mol·L-1 KT5720+10-8 mol·L-1 UⅡ group decreased significantly compared with the 10-8 mol·L-1 UⅡ group. CONCLUSION UⅡcan stimulate the proliferation of CFs by up-regulating the level of TGF-β1 and induce expression of col-Ⅰand col-Ⅲ, the process maybe involve the cAMP-PKA pathway.

       

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