Journal
FEBS JOURNAL
Volume 288, Issue 20, Pages 5867-5887Publisher
WILEY
DOI: 10.1111/febs.15665
Keywords
cell contractility; collagen; fibrosis; matrix signaling; remodeling; TRPV4
Categories
Funding
- CIHR [MOP-503020]
- Canada Research Chair in Matrix Dynamics
- CIHR Canada Graduate Scholarship
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In healthy tissues, mechanosensors trigger the generation of Ca2+ signals for maintaining cell structure, while in diseases, dysregulated matrix remodeling is associated with disruptions of Ca2+ homeostasis and TRPV4 function. This review highlights the reciprocal regulation between TRPV4 in cell adhesions and matrix mechanics through Ca2+ signaling.
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.
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