Suppression of In Vivo Neovascularization by the Loss of TRPV1 in Mouse Cornea.

Suppression of In Vivo Neovascularization by the Loss of TRPV1 in Mouse Cornea.
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DOI:
10.1155/2015/706404
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发表时间:
2015
影响因子:
1.9
通讯作者:
Saika S
Saika S
中科院分区:
医学4区
文献类型:
--
作者:
Tomoyose K;Okada Y;Sumioka T;Miyajima M;Flanders KC;Shirai K;Morii T;Reinach PS;Yamanaka O;Saika S

文献摘要

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目的 研究瞬时受体电位香草酸受体 1 (TRPV1) 缺失对小鼠角膜基质新生血管形成的影响。阻断 TRPV1 受体并不影响细胞培养中 VEGF 依赖性新血管形成。缺乏 TRPV1 会抑制烧灼后角膜基质中的新血管形成。免疫组织化学显示,在两种基因型小鼠烧灼部位的上皮下基质中均检测到活性形式的 TGFβ1 和 VEGF 的免疫反应性,但在缺乏 TRPV1 的小鼠中,免疫反应性似乎不太明显。小鼠角膜中 VEGF 和 TGFβ1 的 mRNA 表达因 TRPV1 的缺失而受到抑制。 TRPV1 基因消融不影响烧灼小鼠角膜中中性粒细胞和巨噬细胞的侵袭。阻断 TRPV1 信号不会影响体外 HUVEC 的血管生成作用。然而,TRPV1 信号参与烧灼小鼠角膜中血管生成生长因子的表达,并且是体内角膜基质中新血管形成所必需的。
To investigate the effects of loss of transient receptor potential vanilloid receptor 1 (TRPV1) on the development of neovascularization in corneal stroma in mice. Blocking TRPV1 receptor did not affect VEGF-dependent neovascularization in cell culture. Lacking TRPV1 inhibited neovascularization in corneal stroma following cauterization. Immunohistochemistry showed that immunoreactivity for active form of TGFβ1 and VEGF was detected in subepithelial stroma at the site of cauterization in both genotypes of mice, but the immunoreactivity seemed less marked in mice lacking TRPV1. mRNA expression of VEGF and TGFβ1 in a mouse cornea was suppressed by the loss of TRPV1. TRPV1 gene ablation did not affect invasion of neutrophils and macrophage in a cauterized mouse cornea. Blocking TRPV1 signal does not affect angiogenic effects by HUVECs in vitro. TRPV1 signal is, however, involved in expression of angiogenic growth factors in a cauterized mouse cornea and is required for neovascularization in the corneal stroma in vivo.