Lack of transient receptor potential ankyrin 1 (TRPA1) retards cutaneous wound healing in mice: A preliminary study.
Lack of transient receptor potential ankyrin 1 (TRPA1) retards cutaneous wound healing in mice: A preliminary study.
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DOI：
10.1016/j.bbrep.2022.101322
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发表时间：
2022-09
影响因子：
2.7
通讯作者：
Yamada, Hiroshi
中科院分区：
文献类型：
--
作者：
Murata, Shizumasa;Yamanaka, Manabu;Taniguchi, Wataru;Kajioka, Daiki;Suzuki, Kentaro;Yamada, Gen;Okada, Yuka;Saika, Shizuya;Yamada, Hiroshi
关键词：
创面愈合是各种疾病的重要过程，阐明创面愈合的潜在机制是制定治疗策略的关键。我们研究了瞬时受体潜能锚蛋白1(TRPA1)的缺失是否影响小鼠皮肤伤口的愈合过程。我们评估了由肌成纤维细胞和巨噬细胞形成的肉芽组织、再上皮化和相关基因的表达。采用TRPA1基因缺失(KO)和野生型(WT)C57BL/6小鼠建立创伤模型。全麻下于小鼠背部皮肤制作两个圆形全层切除创面，直径5.0 mm。在特定的时间间隔后，通过大体观察、组织学、免疫组织化学和实时逆转录聚合酶链式反应(RT-PCR)来评估愈合情况。TRPA1 KO可延缓皮肤创面愈合过程中肉芽组织的形成和再上皮化。此外，TRPA1KO可抑制小鼠皮肤成纤维细胞的出现、巨噬细胞的浸润以及αSMA、F4/80和COL-1α2mRNA的表达。这些结果表明，TRPA1是小鼠皮肤创面愈合所必需的。TRPA1的缺失阻碍了巨噬细胞的浸润和随后的纤维化组织的形成，这可能进一步损害成纤维细胞的纤维化行为。瞬时受体潜在锚蛋白1(TRPA1)在创伤愈合过程中起着至关重要的作用。TRPA-1基因缺陷小鼠的早期皮肤伤口愈合延迟。TRPA1的缺失可延缓创面新肉芽组织的形成。缺乏TRPA1会抑制巨噬细胞的浸润和肌成纤维细胞的形成。TRPA1缺乏可抑制转化生长因子-β-1、α-SMA、F4/80和胶原1-α-2mRNA的表达。
Wound healing is an important process in various diseases, and elucidating the underlying mechanism is essential for developing therapeutic strategies. We investigated whether the loss of transient receptor potential ankyrin 1 (TRPA1) affects the cutaneous wound healing process in mice. We assessed the formation of granulation tissue by myofibroblasts and macrophages, re-epithelialization, and related gene expression. TRPA1-null (KO) and wild-type (WT) C57BL/6 mice were used for establishing the wound model. Two round full-thickness excision wounds (diameter, 5.0 mm) were produced in the dorsal skin of mice under general anesthesia. After specific intervals, healing was evaluated using macroscopic observation, histology, immunohistochemistry, and real-time reverse transcription-polymerase chain reaction (RT-PCR). TRPA1 KO retarded the formation of granulation tissue and re-epithelialization in the healing of cutaneous wound. Furthermore, TRPA1 KO suppressed the appearance of myofibroblasts, macrophage infiltration, and mRNA expression of αSMA, F4/80, and Col-1α2. These findings indicate that TRPA1 is required for cutaneous wound healing in mice. The lack of TRPA1 retards macrophage infiltration and the subsequent fibrotic tissue formation, which might further impair the fibrogenic behavior of fibroblasts. Transient receptor potential ankyrin 1 (TRPA1) is essential for wound healing. Early cutaneous wound healing was delayed in TRPA-1-deficient mice. Loss of TRPA1 retards formation of new granulation tissue in the wound. Lack of TRPA1 inhibits macrophage infiltration and myofibroblast formation. TRPA1 deficiency inhibits expression of TGF-β1, αSMA, F4/80, and collagen 1α2 mRNA.
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影响因子：
3.3
作者：
Yamanaka M;Taniguchi W;Nishio N;Hashizume H;Yamada H;Yoshida M;Nakatsuka T
通讯作者：
Nakatsuka T
影响因子：
2.9
作者：
Lichtman, Michael K.;Otero-Vinas, Marta;Falanga, Vincent
通讯作者：
Falanga, Vincent
影响因子：
3
作者：
Shinozaki, Maki;Okada, Yuka;Shinozaki, Masahiro
通讯作者：
Shinozaki, Masahiro
影响因子：
24.8
作者：
Wei JJ;Kim HS;Spencer CA;Brennan-Crispi D;Zheng Y;Johnson NM;Rosenbach M;Miller C;Leung DH;Cotsarelis G;Leung TH
通讯作者：
Leung TH
DOI：
10.1073/pnas.0705924104
发表时间：
2007-08-14
影响因子：
11.1
作者：
McNamara, Colleen R.;Mandel-Brehm, Josh;Fanger, Christopher M.
通讯作者：
Fanger, Christopher M.