在小鼠模型中,瞬时受体电位香草素4通过调节角质形成细胞和成纤维细胞的迁移以及成纤维细胞中胶原的产生来促进皮肤伤口愈合。

IF 4.6
Bayarmaa Taivanbat , Sahori Yamazaki , Bolor Nasanbat , Akihiko Uchiyama , Syahla Nisaa Amalia , Munkhjargal Nasan-Ochir , Yuta Inoue , Mai Ishikawa , Keiji Kosaka , Akiko Sekiguchi , Sachiko Ogino , Yoko Yokoyama , Ryoko Torii , Mari Hosoi , Koji Shibasaki , Sei-ichiro Motegi
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引用次数: 0

摘要

背景:瞬时受体电位香草素4(TRPV4)是一种阳离子通道,在不同的细胞中表达,它调节不同疾病的发展。我们最近发现TRPV4在受伤的皮肤区域有高表达。然而,TRPV4在皮肤伤口愈合中的作用尚不清楚。目的:探讨TRPV4在小鼠皮肤创伤愈合中的作用。方法:在WT和TRPV4 KO小鼠之间进行皮肤创伤愈合实验和组织病理学研究。体外检测TRPV4拮抗剂和激动剂对细胞迁移、增殖和分化的影响。结果:TRPV4在皮肤损伤区表达增强。与WT小鼠相比,TRPV4 KO小鼠的皮肤伤口愈合受损。此外,它们显著抑制了皮肤伤口中上皮再上皮化和肉芽组织的形成、胶原沉积量和α-SMA阳性肌成纤维细胞的数量。qPCR显示KO小鼠在皮肤伤口中COL1A1和ACTA2的mRNA表达降低。在体外,用选择性TRPV4拮抗剂处理抑制了迁移能力,划痕刺激增强了角质形成细胞中磷酸ERK的表达,TGF-β刺激增强了成纤维细胞中COL1A1和ACTA2的mRNA表达。选择性TRPV4激动剂抑制角质形成细胞的细胞迁移,不增强增殖和迁移,但促进成纤维细胞的分化。结论:TRPV4介导角质形成细胞和成纤维细胞迁移,增加伤口胶原沉积,从而促进皮肤伤口愈合。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Transient receptor potential vanilloid 4 promotes cutaneous wound healing by regulating keratinocytes and fibroblasts migration and collagen production in fibroblasts in a mouse model

Background

Transient receptor potential vanilloid 4 (TRPV4), a cation ion channel, is expressed in different cells, and it regulates the development of different diseases. We recently found a high TRPV4 expression in the wounded skin area. However, the role of TRPV4 in cutaneous wound healing is unknown.

Objective

To investigate the role of TRPV4 in cutaneous wound healing in a mouse model.

Methods

Skin wound healing experiment and histopathological studies were performed between WT and TRPV4 KO mice. The effect of TRPV4 antagonist and agonist on cell migration, proliferation, and differentiation were examined in vitro.

Results

TRPV4 expression was enhanced in wounded area in the skin. TRPV4 KO mice had impaired cutaneous wound healing compared with the WT mice. Further, they had significantly suppressed re-epithelialization and formation of granulation tissue, amount of collagen deposition, and number of α-SMA-positive myofibroblasts in skin wounds. qPCR revealed that the KO mice had decreased mRNA expression of COL1A1 and ACTA2 in skin wounds. In vitro, treatment with selective TRPV4 antagonist suppressed migrating capacity, scratch stimulation enhanced the expression of phospho-ERK in keratinocytes, and TGF-β stimulation enhanced the mRNA expression of COL1A1 and ACTA2 in fibroblasts. Selective TRPV4 agonist suppressed cell migration in keratinocytes, and did not enhance proliferation and migration, but promoted differentiation in fibroblasts.

Conclusion

TRPV4 mediates keratinocytes and fibroblasts migration and increases collagen deposition in the wound area, thereby promoting cutaneous wound healing.

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