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首页> 外文期刊>Journal of Cell Science >Hypoxia suppresses myofibroblast differentiation by changing RhoA activity
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Hypoxia suppresses myofibroblast differentiation by changing RhoA activity

机译：缺氧通过改变RhoA活性来抑制肌纤维细胞分化

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摘要

Fibroblasts show a high range of phenotypic plasticity, including transdifferentiation into myofibroblasts. Myofibroblasts are responsible for generation of the contraction forces that are important for wound healing and scar formation. Overactive myofibroblasts, by contrast, are involved in abnormal scarring. Cell stretching and extracellular signals such as transforming growth factor beta can induce the myofibroblastic program, whereas microenvironmental conditions such as reduced tissue oxygenation have an inhibitory effect. We investigated the effects of hypoxia on myofibroblastic properties and linked this to RhoA activity. Hypoxia reversed the myofibroblastic phenotype of primary fibroblasts. This was accompanied by decreased alpha SMA (ACTA2) expression, alterations in cell contractility, actin reorganization and RhoA activity. We identified a hypoxia-inducible induction of ARHGAP29, which is critically involved in myocardin-related transcription factor-A (MRTF-A) signaling, the differentiation state of myofibroblasts and modulates RhoA activity. This novel link between hypoxia and MRTF-A signaling is likely to be important for ischemia-induced tissue remodeling and the fibrotic response.
机译：成纤维细胞显示出高度的表型可塑性，包括转化为肌纤维细胞。肌纤维细胞负责产生对于伤口愈合和瘢痕形成重要的收缩力。相比之下，过度活性的肌纤维细胞涉及异常的疤痕。细胞拉伸和细胞外信号，例如转化生长因子β可以诱导肌纤维增生程序，而诸如减少组织氧合的微环境条件具有抑制作用。我们调查了缺氧对肌纤维细胞性质的影响，并将其与RHOA活性联系起来。缺氧逆转了原发性成纤维细胞的肌纤维细胞表型。这伴随着αSMA（Acta2）表达，细胞收缩性的改变，肌动蛋白重组和RhOA活性。我们鉴定了Arhgap29的缺氧诱导诱导，其批判性地参与心肌素相关的转录因子-A（MRTF-A）信号传导，肌纤维细胞分化状态并调节RHOA活性。缺氧和MRTF-A信号之间的这种新颖的链接可能对缺血诱导的组织重塑和纤维化反应很重要。

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  • 来源
    《Journal of Cell Science》 |2019年第5期|共13页
  • 作者

    Leinhos Lisa; Peters Johannes; Krull Sabine; Helbig Lena; Vogler Melanie; Levay Magdolna; van Belle Gijsbert J.; Ridley Anne J.; Lutz Susanne; Katschinski Doerthe M.; Zieseniss Anke;

  • 作者单位

    Georg August Univ Gottingen Univ Med Ctr Inst Cardiovasc Physiol D-37073 Gottingen Germany;

    Georg August Univ Gottingen Univ Med Ctr Inst Cardiovasc Physiol D-37073 Gottingen Germany;

    Georg August Univ Gottingen Univ Med Ctr Inst Cardiovasc Physiol D-37073 Gottingen Germany;

    Georg August Univ Gottingen Univ Med Ctr Inst Cardiovasc Physiol D-37073 Gottingen Germany;

    Georg August Univ Gottingen Univ Med Ctr Inst Cardiovasc Physiol D-37073 Gottingen Germany;

    Heidelberg Univ Med Fac Mannheim European Ctr Angiosci Expt Pharmacol D-68167 Mannheim Germany;

    Georg August Univ Gottingen Univ Med Ctr Inst Cardiovasc Physiol D-37073 Gottingen Germany;

    Kings Coll London Randall Ctr Cell &

    Mol Biophys London SE1 1UL England;

    Georg August Univ Gottingen Univ Med Ctr Inst Pharmacol &

    Toxicol D-37075 Gottingen Germany;

    Georg August Univ Gottingen Univ Med Ctr Inst Cardiovasc Physiol D-37073 Gottingen Germany;

    Georg August Univ Gottingen Univ Med Ctr Inst Cardiovasc Physiol D-37073 Gottingen Germany;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

    Hypoxia; RhoA; MRTF-A; Myofibroblast; Hypoxia-inducible-factor; ARHGAP29;

    机译：缺氧;rhoA;mrtf-a;myofibroblast;缺氧诱导因子;arhgap29;

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