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首页> 外文期刊>American Journal of Physiology >IGF-I and TGF-beta1 have distinct effects on phenotype and proliferation of intestinal fibroblasts.
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IGF-I and TGF-beta1 have distinct effects on phenotype and proliferation of intestinal fibroblasts.

机译：IGF-I和TGF-beta1对肠道成纤维细胞的表型和增殖有明显的影响。

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Insulin-like growth factor I (IGF-I) and transforming growth factor-beta1 (TGF-beta1) are upregulated in myofibroblasts at sites of fibrosis in experimental enterocolitis and in Crohn's disease (CD). We compared the sites of expression of IGF-I and TGF-beta1 in a rat peptidoglycan-polysaccharide (PG-PS) model of chronic granulomatous enterocolitis and fibrosis. We used the human colonic CCD-18Co fibroblast/myofibroblast cell line to test the hypothesis that TGF-beta1 and IGF-I interact to regulate proliferation, collagen synthesis, and activated phenotype typified by expression of alpha-smooth muscle actin and organization into stress fibers. IGF-I potently stimulated while TGF-beta1 inhibited basal DNA synthesis. TGF-beta1 and IGF-I each had similar but not additive effects to induce type I collagen. TGF-beta1 but not IGF-I potently stimulated expression of alpha-smooth muscle actin and stress fiber formation. IGF-I in combination with TGF-beta1 attenuated stress fiber formation without reducing alpha-smooth muscle actin expression. Stress fibers were not a prerequisite for increased collagen synthesis. TGF-beta1 upregulated IGF-I mRNA, which led us to examine the effects of IGF-I in cells previously activated by TGF-beta1 pretreatment. IGF-I potently stimulated proliferation of TGF-beta1-activated myofibroblasts without reversing activated fibrogenic phenotype. We conclude that TGF-beta1 and IGF-I both stimulate type I collagen synthesis but have differential effects on activated phenotype and proliferation. We propose that during intestinal inflammation, regulation of activated phenotype and proliferation may require sequential actions of TGF-beta1 and IGF-I, but they may act in concert to increase collagen deposition.
机译：在实验性小肠结肠炎和克罗恩病（CD）的纤维化部位，成肌纤维细胞中胰岛素样生长因子I（IGF-I）和转化生长因子β1（TGF-beta1）上调。我们比较了慢性肉芽肿性小肠结肠炎和纤维化的大鼠肽聚糖多糖（PG-PS）模型中IGF-I和TGF-β1表达的位点。我们使用人类结肠CCD-18Co成纤维细胞/成肌纤维细胞细胞系来检验TGF-β1和IGF-I相互作用调节增殖，胶原蛋白合成和活化表型的假说，以α-平滑肌肌动蛋白的表达为代表并组织成应激纤维。 IGF-I有效刺激，而TGF-beta1抑制基础DNA合成。 TGF-beta1和IGF-I各自具有相似但无累加的诱导I型胶原蛋白的作用。 TGF-beta1而非IGF-I可以有效地刺激α平滑肌肌动蛋白的表达和应力纤维的形成。 IGF-I与TGF-β1的结合可减轻应力纤维的形成，而不会降低α-平滑肌肌动蛋白的表达。应激纤维不是增加胶原蛋白合成的先决条件。 TGF-beta1上调了IGF-I mRNA，这使我们检查了IGF-I在先前由TGF-beta1预处理激活的细胞中的作用。 IGF-1可以有效刺激TGF-β1激活的成纤维细胞的增殖，而不会逆转激活的纤维原性表型。我们得出的结论是，TGF-beta1和IGF-I都刺激I型胶原蛋白的合成，但对激活的表型和增殖具有不同的影响。我们建议在肠道炎症过程中，激活表型和增殖的调节可能需要TGF-beta1和IGF-I的顺序作用，但它们可能协同作用以增加胶原蛋白的沉积。

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