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In vitro significance of SOCS-3 and SOCS-4 and potential mechanistic links to wound healing

Feng, Yi ORCID:, Sanders, Andrew J. ORCID:, Morgan, Liam D. ORCID:, Owen, Sioned, Ruge, Fiona, Harding, Keith G and Jiang, Wen Guo ORCID: 2017. In vitro significance of SOCS-3 and SOCS-4 and potential mechanistic links to wound healing. Scientific Reports 7 (1) , 6715. 10.1038/s41598-017-06886-6

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Wound healing and the management of chronic wounds represent a significant burden on the NHS. Members of the suppressor of cytokine signalling (SOCS) family have been implicated in the regulation of a range of cellular processes. The current study aims to explore the importance of SOCS-3 and SOCS-4 in regulating cellular traits associated with wound healing. SOCS-3 over-expression and SOCS-4 knockdown mutant lines were generated and verified using q-PCR and western blotting in human keratinocytes (HaCaT) and endothelial cells (HECV). Over-expression of SOCS-3 resulted in a significantly reduced proliferative rate in HaCaT keratinocytes and also enhanced the tubule formation capacity of HECV cells. SOCS-4 knockdown significantly reduced HaCaT migration and HECV cell tubule formation. Suppression of SOCS-4 influenced the responsiveness of HaCaT and HECV cells to EGF and TGFβ and resulted in a dysregulation of phospho-protein expression in HaCaT cells. SOCS-3 and SOCS-4 appear to play regulatory roles in a number of keratinocyte and endothelial cellular traits associated with the wound healing process and may also be able to regulate the responsiveness of these cells to EGF and TGFβ. This implies a potential regulatory role in the wound healing process and, thus highlights their potential as novel therapies.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Publisher: Nature Publishing Group
ISSN: 2045-2322
Funders: GlaxoSmithKline (GSK), Cancer Research Wales and Life Sciences Research Network for Wales (LSRNW)
Date of First Compliant Deposit: 27 July 2017
Date of Acceptance: 22 June 2017
Last Modified: 02 Oct 2023 05:50

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