Thrombospondin-4 is a soluble dermal inflammatory signal that activates the fibroblast migration for skin regeneration and wound healing
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ABSTRACT:
PROVIDER: PRJNA745989 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15108237.fastq.gz | Fastqsanger.gz | |||
| SRR15108238.fastq.gz | Fastqsanger.gz | |||
| SRR15108239.fastq.gz | Fastqsanger.gz | |||
| SRR15108240.fastq.gz | Fastqsanger.gz |
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Project description:The present study aimed to investigate the role of Thbs4 in skin regeneration and elucidate its effects on cellular responses. Here we show that Thbs4 expression is upregulated in healing skin wounds and wound healing can be promoted by the application of recombinant Thbs4 protein. Thbs4 was shown to promote keratinocyte proliferation and fibroblast migration by activating β-catenin signalling cascade. This indicates that incorporating Thbs4 into novel wound healing therapies can be a promising therapeutic strategy for hard-to-heal chronic wounds.
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Project description:Thrombosponin-4 (THBS4) is a non-structural extracellular matrix molecule associated with tissue regeneration and a variety of pathological processes characterized by increased cell proliferation and migration. However, the mechanisms of how THBS4 regulates cell behaviour as well as the pathways contributing to its effects have remained largely unexplored. In the present study we investigated the role of THBS4 in skin regeneration both in vitro and in vivo. We found that THBS4 expression was upregulated in the dermal compartment of healing skin wounds in humans as well as in mice. Application of recombinand THBS4 protein promoted cutaneous wound healing in mice and selectively stimulated migration of primary fibroblasts as well as proliferation of keratinocytes in vitro. By using a combined proteotranstriptomic pathway analysis approach we discovered that beta-catenin acted as a hub for THBS4-dependent cell signaling and likely plays a key role in promoting its downstream effects. Out results suggest that THBS4 is an important contributor to wound healing and its incorporation into novel wound healing therapies may be a promising strategy for treatment of hard-to-heal wounds.
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Project description:Thrombospondin-4 (THBS4) is a non-structural extracellular matrix molecule associated with tissue regeneration and a variety of pathological processes characterized by increased cell proliferation and migration. However, the mechanisms of how THBS4 regulates cell behavior as well as the pathways contributing to its effects have remained largely unexplored. In the present study we investigated the role of THBS4 in skin regeneration both in vitro and in vivo. We found that THBS4 expression was upregulated in the dermal compartment of healing skin wounds in humans as well as in mice. Application of recombinant THBS4 protein promoted cutaneous wound healing in mice and selectively stimulated migration of primary fibroblasts as well as proliferation of keratinocytes in vitro. By using a combined proteotranscriptomic pathway analysis approach we discovered that β-catenin acted as a hub for THBS4-dependent cell signaling and likely plays a key role in promoting its downstream effects. Our results suggest that THBS4 is an important contributor to wound healing and its incorporation into novel wound healing therapies may be a promising strategy for treatment of cutaneous wounds.
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