Abstract
Objective: Wound healing without fibrosis remains a clinical challenge and a new strategy to promote the optimal wound healing is needed. Mesenchymal stem cells (MSCs) can completely regenerate tissue injury due to the robust MSCs ability in controlling inflammation niche leading to granulation tissue formation, particularly through a release of various growth factors including transforming growth factor-β (TGF-β). In response to TGF-β stimulation, fibroblasts differentiate into myofibroblast, marked by alpha-smooth muscle actin (α-SMA) that leads to wound healing acceleration. On the other hand, sustained activation of TGF-β in wound areas may contribute to fibrosis-associated scar formation. The aim of this study was to evaluate the α-SMA expression of myofibroblast induced by MSC-released TGF-β during wound healing process. Materials and Methods: Twenty-four full-thickness excisional rat wound models were randomly divided into four groups: sham (Sh), Control (C), and MSCs treatment groups; topically treated by the MSCs at doses 2x106 cells (T1) and 1x106 cells (T2), respectively. While the control group was treated with NaCl. TGF-β level was determined using ELISA assay, α-SMA expression of myofibroblast was analyzed by immunofluorescence staining, and wound size measurement was calculated using a standard caliper. Results: This study showed a significant increase in TGF-β levels in all treatment groups on days 3 and 6. This finding was consistent with a significant increase of α-SMA expression of myofibroblast at day 6 and wound closure percentage, indicating that MSCs might promote an increase of wound closure. Conclusion: MSCs regulated the release of TGF-β to induce α-SMA expression of myofibroblast for accelerating an optimal wound healing.
Highlights
An open wound healing is a highly organized physiological process to restore the integrity of the skin involving a complex interplay between various populations of cells surrounding cutaneous and immune cell[1]
The release of platelet-derived growth factor (PDGF), epidermal growth factor (EGF), and transforming growth factor-β (TGF-β) may promote a granulation tissue formation characterized by an active fibroblast known as myofibroblast expressing alpha-smooth muscle actin (α-SMA)
We found a significant increase of TGF-β levels in all treatment groups at day 3 (Figure 2a)
Summary
An open wound healing is a highly organized physiological process to restore the integrity of the skin involving a complex interplay between various populations of cells surrounding cutaneous and immune cell[1]. Under certain conditions such as diabetes and old patients, the wound healing is susceptible to interruption or failure which can lead nonhealing wounds[2]. The release of platelet-derived growth factor (PDGF), epidermal growth factor (EGF), and transforming growth factor-β (TGF-β) may promote a granulation tissue formation characterized by an active fibroblast known as myofibroblast expressing alpha-smooth muscle actin (α-SMA). The TGF-β may induce myofibroblast to produce an excessive extracellular matrix (ECM) that potentially causes a scar formation[5].
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
