Smad3 deficiency accelerates tongue wound healing via epithelial cell-extracellular matrix interactions
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Abstract
Aberrant wound closure occurs in a broad range of wounds and scars, and the altered regulation of transcription factors in wound areas can account for both of those conditions. This study aimed to explore the function of the transcription factor Smad3 in wound healing using a tongue wound model in Smad3 knockout (Smad3?/?) mice and with Smad3 small interfering RNA (siRNA) transfected human gingival fibroblasts (HGFs). Smad3?/?mice were used to examine the extent of repair in tongue wounds. Cell migration was evaluated in HGFs using wound healing assays. The mRNA expression levels of Sox2, E-cadherin, fibronectin, and vimentin were examined in HGFs using reverse transcription-quantitative polymerase chain reaction. Histopathological analysis of wound closure in Smad3?/? mice showed rapid re-epithelialization and remodeling in tongue wound repair compared with Smad3+/+ mice. Increased numbers of neutrophils were identified in the wounds of Smad3?/? mice. Sox2 and phospho-E-cadherin expression levels were increased in Smad3?/? mice. Smad3 knockdown by siRNA increased cell migration of HGFs. In addition, Sox2, E-cadherin, fibronectin, and vimentin mRNA levels were significantly increased in Smad3 siRNA-transfected HGFs compared with controls. Collectively, these findings demonstrate that a Smad3 deficiency can expedite wound healing and increase immune reactions and extracellular matrix formation after tongue injuries, boosting recovery through Sox2 and E-cadherin. Consequently, Smad3 inhibition would help stimulate tongue wound healing.
키워드
E-cadherin; Fibronectin; Wound healing
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