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

Abstract

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.

Mechanistic insights of epithelial protein lost in neoplasm in prostate cancer metastasis

“…Protein was extracted from PC‐3 EPLIN EXP and PC‐3 pEF6 cells and quantified by fluorometric protein quantification, as reported previously, and subsequently sent to Kinexus™ Bioinformatics (Kinexus Bioinformatics, Vancouver, British Columbia, Canada). Data were analyzed using several parameters including Globally Normalized Signal Intensity, z ratio and % change from control (CFC).…”

Therapeutic Effects and Underlying Mechanism of SOCS-com Gene-Transfected ADMSCs in Pressure Ulcer Mouse Models

“…Several studies have investigated the regulation of SOCS expression and its effects on wound healing. SOCS-1 and SOCS-5 modulate IL-4 signaling to regulate re-epithelialization and the tissue remodeling phase of wound healing [26,30,31], while SOCS-3 plays a role in regulating the inflammatory phase [40]. As SOCS-1, -3, and -5 are important factors involved in different phases of wound healing, the co-transfection of these genes is expected to improve the wound-healing function of MSCs.…”

“…SOC-1, -3, and -5 play important roles in the wound-healing process. Claire et al demonstrated that SOCS-1 plays a significant role in inflammatory inhibition [30], and Feng et al showed that overexpression of SOCS-3 is crucial for wound healing [21,31]. SOCS-5 also acts as a negative regulator of inflammatory cytokines [19].…”

Evaluation of Potential Risks to Human Health and Ecosystems During Exposure to Discarded Laboratory Chemical Mixtures by In Vitro Multimodel Approach

“…13 HECV cells, available from several cellular banks, were used since they share the same origin of HUVECs and are considered a bloodstream model. [14][15][16][17][18][19] No antibiotic or antifungal solutions were added to standard or experimental medium to avoid any potential interference of these drugs with the cell culture. [20][21][22][23][24][25] All cell cultures were found to be mycoplasma-free on regular checks with Reagent Mycoplasma Set (Euroclone).…”