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首页> 外文期刊>Journal of Cellular Physiology >Diverse signaling pathways regulate fibroblast differentiation and transformation through Rho kinase activation.
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Diverse signaling pathways regulate fibroblast differentiation and transformation through Rho kinase activation.

机译：不同的信号通路调节成纤维细胞通过ρ分化和转换激酶激活。

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This study examined the role of agonist-induced Rho kinase (ROCK) involvement in the morphological outcome of pulmonary-derived fibroblasts. Normal human lung fibroblasts (NHLF) spontaneously differentiate into network-like structures in a two-dimensional growth factor reduced Matrigel matrix-based assay. Sphingosine 1-phosphate (SPP), a bioactive phospholipid that regulates angiogenesis, inhibited fibroblast morphogenesis in a dose-dependent manner, virtually eliminating the presence of multi-cellular structures at 500 nM. Pretreatment with the Rho kinase-specific inhibitor, H1152, eradicated the high dose SPP-induced inhibition. Similarly, NHLFs transfected with Rho kinase siRNA prevented SPP-induced inhibition of the fibroblast morphogenesis. Alternatively, transforming growth factor-beta1 (TGF-beta1), a cytokine recognized as a key mediator of wound healing, terminally differentiates NHLF into myofibroblasts as evidenced by the expression of the smooth muscle cell isoform of alpha-actin (alpha-SMA). H1152 suppressed TGF-beta1-induced alpha-SMA expression in a dose-dependent manner. Similarly, treatment with Rho kinase siRNA reduced alpha-SMA expression by greater than 50%. SPP treatment had no effect on TGF-beta1-induced transformation into myofibroblasts, and TGF-beta1 treatment did not alter fibroblast morphogenesis. This study suggests a dual regulatory role for Rho kinase in cellular regulation of fibroblasts in which SPP-induced Rho kinase activation via a G-protein coupled receptor suppresses fibroblast morphogenesis while TGF-beta1-induced Rho kinase activation through a serine/threonine kinase receptor culminates in transformation into myofibroblasts.
机译：本研究调查了agonist-induced的角色ρ激酶(岩石)参与pulmonary-derived形态学的结果成纤维细胞。自发分化成网络结构在一个二维生长因子减少人工基底膜依赖于分析。1-phosphate (SPP),生物活性磷脂调节血管生成,抑制纤维母细胞形态发生在剂量依赖性的方式,几乎消除的存在多细胞结构在500海里。ρkinase-specific抑制剂、H1152根除高剂量SPP-induced抑制。同样,NHLFs转染ρ激酶核阻止SPP-induced抑制的成纤维细胞形态发生。转变增长factor-beta1 (TGF-beta1)细胞因子被认为是一个关键调解人的伤口治疗,晚期区分NHLFmyofibroblasts的表达就证明了这一点alpha-actin的平滑肌细胞对碘氧基苯甲醚(alpha-SMA)。alpha-SMA表达剂量依赖性的方式。同样,治疗ρ激酶核alpha-SMA表达减少了超过50%。对TGF-beta1-induced SPP治疗没有效果转换成myofibroblasts和TGF-beta1治疗没有改变纤维母细胞形态发生。这项研究表明双重监管的作用ρ激酶在细胞调节成纤维细胞SPP-inducedρ激酶激活通过g蛋白耦合受体抑制纤维母细胞形态发生而TGF-beta1-inducedρ激酶通过一个丝氨酸/苏氨酸激酶激活受体在转型为高潮myofibroblasts。

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