TRPV4 integrates matrix mechanosensing with Ca2+ signaling to regulate extracellular matrix remodeling,The FEBS Journal

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TRPV4 integrates matrix mechanosensing with Ca2+ signaling to regulate extracellular matrix remodeling
The FEBS Journal ( IF 5.5 ) Pub Date : 2020-12-09 , DOI: 10.1111/febs.15665
Chenfan Ji ₁ , Christopher A McCulloch ₂

Affiliation

In healthy connective tissues, mechanosensors trigger the generation of Ca²⁺ signals, which enable cells to maintain the structure of the fibrillar collagen matrix through actomyosin contractile forces. Transient receptor potential vanilloid type 4 (TRPV4) is a mechanosensitive Ca²⁺-permeable channel that, when expressed in cell-matrix adhesions of the plasma membrane, regulates extracellular matrix (ECM) remodeling. In high prevalence disorders such as fibrosis and tumor metastasis, dysregulated matrix remodeling is associated with disruptions of Ca²⁺ homeostasis and TRPV4 function. Here, we consider that ECM polymers transmit cell-activating mechanical signals to TRPV4 in cell adhesions. When activated, TRPV4 regulates fibrillar collagen remodeling, thereby altering the mechanical properties of the ECM. In this review, we integrate functionally connected processes of matrix remodeling to highlight how TRPV4 in cell adhesions and matrix mechanics are reciprocally regulated through Ca²⁺ signaling.

中文翻译：

TRPV4 将基质机械传感与 Ca2+ 信号整合以调节细胞外基质重塑

在健康的结缔组织中，机械传感器触发 Ca ²⁺信号的产生，这使细胞能够通过肌动球蛋白收缩力维持纤维状胶原基质的结构。瞬时受体电位香草素类型 4 (TRPV4) 是一种机械敏感性 Ca ²⁺可渗透通道，当在质膜的细胞-基质粘附中表达时，可调节细胞外基质 (ECM) 重塑。在纤维化和肿瘤转移等高发疾病中，失调的基质重塑与 Ca ^{2+ 的}破坏有关稳态和 TRPV4 功能。在这里，我们认为 ECM 聚合物在细胞粘附中将细胞激活机械信号传递给 TRPV4。当被激活时，TRPV4 调节纤维状胶原重塑，从而改变 ECM 的机械特性。在这篇综述中，我们整合了基质重塑的功能连接过程，以强调 TRPV4 在细胞粘附和基质力学中是如何通过 Ca ²⁺信号相互调节的。

更新日期：2020-12-09

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