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Signalling by Transforming Growth Factor Beta Isoforms in Wound Healing and Tissue Regeneration.

ABSTRACT: Transforming growth factor beta (TGF?) signalling is essential for wound healing, including both non-specific scar formation and tissue-specific regeneration. Specific TGF? isoforms and downstream mediators of canonical and non-canonical signalling play different roles in each of these processes. Here we review the role of TGF? signalling during tissue repair, with a particular focus on the prototypic isoforms TGF?1, TGF?2, and TGF?3. We begin by introducing TGF? signalling and then discuss the role of these growth factors and their key downstream signalling mediators in determining the balance between scar formation and tissue regeneration. Next we discuss examples of the pleiotropic roles of TGF? ligands during cutaneous wound healing and blastema-mediated regeneration, and how inhibition of the canonical signalling pathway (using small molecule inhibitors) blocks regeneration. Finally, we review various TGF?-targeting therapeutic strategies that hold promise for enhancing tissue repair.

SUBMITTER: Gilbert RWD

PROVIDER: S-EPMC5831781 | biostudies-literature | 2016 Jun

REPOSITORIES: biostudies-literature

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Signalling by Transforming Growth Factor Beta Isoforms in Wound Healing and Tissue Regeneration.

Gilbert Richard W D RWD Vickaryous Matthew K MK Viloria-Petit Alicia M AM

Journal of developmental biology 20160622 2

Transforming growth factor beta (TGFβ) signalling is essential for wound healing, including both non-specific scar formation and tissue-specific regeneration. Specific TGFβ isoforms and downstream mediators of canonical and non-canonical signalling play different roles in each of these processes. Here we review the role of TGFβ signalling during tissue repair, with a particular focus on the prototypic isoforms TGFβ1, TGFβ2, and TGFβ3. We begin by introducing TGFβ signalling and then discuss the ...[more]

PMID: 29615587

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Project description:Fibromodulin (FMOD) is a small leucine-rich proteoglycan required for scarless fetal cutaneous wound repair. Interestingly, increased FMOD levels have been correlated with decreased transforming growth factor (TGF)-β1 expression in multiple fetal and adult rodent models. Our previous studies demonstrated that FMOD-deficiency in adult animals results in delayed wound closure and increased scar size accompanied by loose package collagen fiber networks with increased fibril diameter. In addition, we found that FMOD modulates in vitro expression and activities of TGF-β ligands in an isoform-specific manner. In this study, temporospatial expression profiles of TGF-β ligands and receptors in FMOD-null and wild-type (WT) mice were compared by immunohistochemical staining and quantitative reverse transcriptase-polymerase chain reaction using a full-thickness, primary intention wound closure model. During the inflammatory stage, elevated inflammatory infiltration accompanied by increased type I TGF-β receptor levels in individual inflammatory cells was observed in FMOD-null wounds. This increased inflammation was correlated with accelerated epithelial migration during the proliferative stage. On the other hand, significantly more robust expression of TGF-β3 and TGF-β receptors in FMOD-null wounds during the proliferative stage was associated with delayed dermal cell migration and proliferation, which led to postponed granulation tissue formation and wound closure and increased scar size. Compared with WT controls, expression of TGF-β ligands and receptors by FMOD-null dermal cells was markedly reduced during the remodeling stage, which may have contributed to the declined collagen synthesis capability and unordinary collagen architecture. Taken together, this study demonstrates that a single missing gene, FMOD, leads to conspicuous alternations in TGF-β ligand and receptor expression at all stages of wound repair in various cell types. Therefore, FMOD critically coordinates temporospatial distribution of TGF-β ligands and receptors in vivo, suggesting that FMOD modulates TGF-β bioactivity in a complex way beyond simple physical binding to promote proper wound healing.

Dataset Information

Signalling by Transforming Growth Factor Beta Isoforms in Wound Healing and Tissue Regeneration.

Publications

Signalling by Transforming Growth Factor Beta Isoforms in Wound Healing and Tissue Regeneration.

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