ArticlePloS one2022
The TSP-1 domain of the matricellular protein CCN5 is essential for its nuclear localization and anti-fibrotic function.
Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- The matricellular protein CCN5 (WISP2) inhibits cellular senescence in cardiac myoblasts and fibroblasts.Scientific reports · 2026Article
- CCN Proteins as Matricellular Regulators of Bone in Aging and Disease.Current osteoporosis reports · 2025Review
- Oxidative DNA damage promotes vascular ageing associated with changes in extracellular matrix-regulating proteins.Cardiovascular research · 2025Article
- The matricellular protein CCN5 prevents anti-VEGF drug-induced epithelial-mesenchymal transition of retinal pigment epithelium.Scientific reports · 2024Article
- Structural insights into regulation of CCN protein activities and functions.Journal of cell communication and signaling · 2023Review
- CCN proteins: opportunities for clinical studies-a personal perspective.Journal of cell communication and signaling · 2023Review
- The matricellular protein Drosophila Cellular Communication Network Factor is required for synaptic transmission and female fertility.Genetics · 2023Article
- The role of CCNs in controlling cellular communication in the tumor microenvironment.Journal of cell communication and signaling · 2023Review
- The carboxyl-terminal TSP1-homology domain is the biologically active effector peptide of matricellular protein CCN5 that counteracts profibrotic CCN2.The Journal of biological chemistry · 2023Article
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Authors and funding
6 authors.
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Abstract
The matricellular protein CCN5 exerts anti-fibrotic activity in hearts partly by inducing reverse trans-differentiation of myofibroblasts (MyoFBs) to fibroblasts (FBs). CCN5 consists of three structural domains: an insulin-like growth factor binding protein (IGFBP), a von Willebrand factor type C (VWC), and a thrombospondin type 1 (TSP-1). In this study, we set out to elucidate the roles of these domains in the context of the reverse trans-differentiation of MyoFBs to FBs. First, human cardiac FBs were trans-differentiated to MyoFBs by treatment with TGF-β; this was then reversed by treatment with recombinant human CCN5 protein or various recombinant proteins comprising individual or paired CCN5 domains. Subcellular localization of these recombinant proteins was analyzed by immunocytochemistry, cellular fractionation, and western blotting. Anti-fibrotic activity was also evaluated by examining expression of MyoFB-specific markers, α-SMA and fibronectin. Our data show that CCN5 is taken up by FBs and MyoFBs mainly via clathrin-mediated endocytosis, which is essential for the function of CCN5 during the reverse trans-differentiation of MyoFBs. Furthermore, we showed that the TSP-1 domain is essential and sufficient for endocytosis and nuclear localization of CCN5. However, the TSP-1 domain alone is not sufficient for the anti-fibrotic function of CCN5; either the IGFBP or VWC domain is needed in addition to the TSP-1 domain.
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