Impaired healing of cornea incision injury in a TRPV1-deficient mouse.
Impaired healing of cornea incision injury in a TRPV1-deficient mouse.
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DOI：
10.1007/s00441-018-2878-y
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发表时间：
2018-11
影响因子：
3.6
通讯作者：
Saika S
中科院分区：
文献类型：
--
作者：
Nidegawa-Saitoh Y;Sumioka T;Okada Y;Reinach PS;Flanders KC;Liu CY;Yamanaka O;Kao WW;Saika S
本研究试图阐明TRPV 1阳离子通道受体在小鼠角膜切口伤早期修复中的作用。以往的研究表明，阻断TRPV 1可抑制培养的角膜细胞或眼成纤维细胞中肌成纤维细胞的形成和转化生长因子β1（TGFβ1）的表达。雄性C57 BL/6（野生型; WT）小鼠和雄性C57 BL/6 Trpv 1-null（KO）小鼠在全身和局部麻醉下，用手术刀片在一只眼睛的中央角膜中造成全层切口损伤（1.8 mm长，利姆布斯至利姆布斯）。伤口没有缝合。在第0、5和10天，摘除眼睛，进行组织学、免疫组织化学和实时RT-PCR基因表达分析，以评估TRPV 1缺失对原发性愈合的影响。电镜观察TRPV 1缺失对角膜基质细胞超微结构的影响。结果表明，Trpv 1基因缺失导致角膜基质切口闭合延迟，肌成纤维细胞转分化沿着受阻，胶原Ia 1和TGFβ1表达下降。炎性细胞浸润不受TRPV 1缺失的影响。与WT角膜细胞相比，TRPV 1缺失角膜细胞的超微结构内质网更广泛地扩张，表明TRPV 1基因敲除对蛋白分泌的损害。这些结果表明，损伤相关TRPV 1信号通过选择性刺激TGFβ诱导的肉芽组织形成参与小鼠角膜中基质切口损伤的愈合。
The present study attempts to elucidate the role of TRPV1 cation channel receptor on primary repair in an incision-wounded mouse cornea in vivo. Previous study revealed that blocking TRPV1 suppressed myofibroblast formation and expression of transforming growth factor β1 (TGFβ1) in cultured keratocytes or ocular fibroblasts. Male C57BL/6 (wild-type; WT) mice and male C57BL/6 Trpv1-null (KO) mice incurred a full-thickness incision injury (1.8 mm in length, limbus to limbus) in the central cornea of one eye with a surgical blade under general and topical anesthesia. The injury was not sutured. On days 0, 5, and 10, the eyes were enucleated, processed for histology, immunohistochemistry, and real-time RT-PCR gene expression analysis to evaluate the effects of the loss of TRPV1 on primary healing. Electron microscopy observation was also performed to know the effect of the loss of TRPV1 on ultrastructure of keratocytes. The results showed that the loss of Trpv1 gene delayed closure of corneal stromal incision with hindered myofibroblast transdifferentiation along with declines in the expression of collagen Ia1 and TGFβ1. Inflammatory cell infiltration was not affected by the loss of TRPV1. Ultrastructurally endoplasmic reticulum of TRPV1-null keratocytes was more extensively dilated as compared with WT keratocytes, suggesting an impairment of protein secretion by TRPV1-gene knockout. These results indicate that injury-related TRPV1 signal is involved in healing of stromal incision injury in a mouse cornea by selectively stimulating TGFβ-induced granulation tissue formation.
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DOI：
10.1007/bf00918845
发表时间：
1993-04-01
影响因子：
2.7
作者：
SAIKA, S;UENOYAMA, K;HIKITA, M
通讯作者：
HIKITA, M
影响因子：
3.3
作者：
GARCIAHIRSCHFELD, J;LOPEZBRIONES, LG;VALDEOLMILLOS, M
通讯作者：
VALDEOLMILLOS, M
影响因子：
2.8
作者：
SAIKA, S;KOBATA, S;YAMANAKA, O
通讯作者：
YAMANAKA, O
光聚合产生的微地形特征通过 TRPV1 招募 RhoA/ROCK 来指导细胞和神经突生长。
影响因子：
14
作者：
Li, Shufeng;Tuft, Bradley W.;Xu, Linjing;Polacco, Marc A.;Clarke, Joseph C.;Guymon, C. Allan;Hansen, Marlan R.
通讯作者：
Hansen, Marlan R.
影响因子：
6
作者：
Okada, Yuka;Reinach, Peter S.;Saika, Shizuya
通讯作者：
Saika, Shizuya