THYMOSIN BETA 4 AFFECTS MATRIX METALLOPROTEINASE AND TISSUE INHIBITOR OF MATRIX METALLOPROTEINASE EXPRESSION, LAMININ-5 SECRETION, AND KERATINOCYTE MIGRATION IN MODELS OF CUTANEOUS WOUND HEALING.

2004 ◽  
Vol 52 ◽  
pp. S113
Author(s):  
E. L. Fine ◽  
H. K. Kleinman
Keyword(s):  
Wound Healing ◽  
Matrix Metalloproteinase ◽  
Cutaneous Wound Healing ◽  
Tissue Inhibitor ◽  
Laminin 5 ◽  
Cutaneous Wound ◽  
Thymosin Beta 4 ◽  
Keratinocyte Migration

scholarly journals MicroRNA-200b/c-3p regulate epithelial plasticity and inhibit cutaneous wound healing by modulating TGF-β-mediated RAC1 signaling

2020 ◽  
Vol 11 (10) ◽  
Author(s):  
Huiyi Tang ◽  
Xueer Wang ◽  
Min Zhang ◽  
Yuan Yan ◽  
Simin Huang ◽  
...  
Keyword(s):  
Wound Healing ◽  
Luciferase Reporter ◽  
Skin Wounds ◽  
Cutaneous Wound Healing ◽  
Mirna Regulation ◽  
Cutaneous Wound ◽  
Cutaneous Wounds ◽  
Keratinocyte Migration ◽  
Epithelial Plasticity ◽  
Tgf Β1

Abstract Cutaneous wound healing is pivotal for human skin to regain barrier function against pathogens. MicroRNAs (miRNAs) have been found to play regulatory roles in wound healing. However, the mechanism of miRNA regulation remains largely unknown. In this study, we focused on microRNA-200b/c-3p (miR-200b/c-3p) whose expression was abundant in intact epidermis, but dramatically decreased in skin wounds. In silico prediction identified RAC1 as a potential miR-200b/c-3p target. Luciferase reporter assay confirmed that miR-200b/c-p repressed RAC1 by direct targeting to its mRNA 3′UTR. Consistently, miR-200b/c-3p expression was discordantly related to RAC1 protein level during wound healing. Forced miR-200b/c-3p expression repressed RAC1 and inhibited keratinocyte migration as well as re-epithelialization in a mouse back skin full-thickness wound healing model. Mechanistically, miR-200b/c-3p modulated RAC1 to inhibit cell migration by repressing lamellipodia formation and intercellular adhesion dissolution in keratinocytes. Furthermore, we found that TGF-β1, which was highly expressed in skin wounds, contributed to the downregulation of miR-200b/c-3p in wound edge keratinocytes. Taken together, miR-200b/c-3p-mediated RAC1 repression inhibited keratinocyte migration to delay re-epithelialization. TGF-β1 induction attenuated miR-200b/c-3p regulation of RAC1 signaling in cutaneous wounds and the repression of miR-200b/c-3p accelerated keratinocyte migration to promote wound healing. Our data provide new insight into how miR-200b/c-3p affects keratinocyte migration and highlight the potential of miR-200b/c-3p targeting for accelerating wound healing.

scholarly journals Ectodomain Shedding of Epidermal Growth Factor Receptor Ligands Is Required for Keratinocyte Migration in Cutaneous Wound Healing

2000 ◽  
Vol 151 (2) ◽  
pp. 209-220 ◽  
Author(s):  
Sho Tokumaru ◽  
Shigeki Higashiyama ◽  
Takeshi Endo ◽  
Takatoshi Nakagawa ◽  
Jun-ichiro Miyagawa ◽  
...  
Keyword(s):  
Wound Healing ◽  
Growth Factor ◽  
Growth Factor Receptor ◽  
Cutaneous Wound Healing ◽  
Cutaneous Wound ◽  
Keratinocyte Migration ◽  
Egfr Ligands ◽  
Egfr Ligand ◽  
Epidermal Growth

Keratinocyte proliferation and migration are essential to cutaneous wound healing and are, in part, mediated in an autocrine fashion by epidermal growth factor receptor (EGFR)–ligand interactions. EGFR ligands are initially synthesized as membrane-anchored forms, but can be processed and shed as soluble forms. We provide evidence here that wound stimuli induce keratinocyte shedding of EGFR ligands in vitro, particularly the ligand heparin-binding EGF-like growth factor (HB-EGF). The resulting soluble ligands stimulated transient activation of EGFR. OSU8-1, an inhibitor of EGFR ligand shedding, abrogated the wound-induced activation of EGFR and caused suppression of keratinocyte migration in vitro. Soluble EGFR–immunoglobulin G-Fcγ fusion protein, which is able to neutralize all EGFR ligands, also suppressed keratinocyte migration in vitro. The application of OSU8-1 to wound sites in mice greatly retarded reepithelialization as the result of a failure in keratinocyte migration, but this effect could be overcome if recombinant soluble HB-EGF was added along with OSU8-1. These findings indicate that the shedding of EGFR ligands represents a critical event in keratinocyte migration, and suggest their possible use as an effective clinical treatment in the early phases of wound healing.

Recombinant thymosin beta 4 can promote full-thickness cutaneous wound healing

2007 ◽  
Vol 56 (2) ◽  
pp. 229-236 ◽  
Author(s):  
Xiankui Li ◽  
Lishu Zheng ◽  
Fuwang Peng ◽  
Chengyu Qi ◽  
Xiaoguang Zhang ◽  
...  
Keyword(s):  
Wound Healing ◽  
Cutaneous Wound Healing ◽  
Full Thickness ◽  
Cutaneous Wound ◽  
Thymosin Beta 4
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