周细胞中Cyp1b1的靶向缺失导致视网膜新生血管的衰减和小梁网发育不良。

Trends in developmental biology Pub Date : 2019-01-01
Juliana Falero-Perez, Michele C Larsen, Leandro B C Teixeira, Hao F Zhang, Volkhard Lindner, Christine M Sorenson, Colin R Jefcoate, Nader Sheibani
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引用次数: 0

摘要

细胞色素P450 1B1 (CYP1B1)基因突变在原发性先天性青光眼患者中有报道。在氧诱导的缺血性视网膜病变(OIR)中,Cyp1b1缺陷(Cyp1b1-/-)小鼠表现出小梁网(TM)组织发育不良和视网膜新生血管的衰减。尽管包括内皮细胞(EC)、周细胞(PC)、星形胶质细胞(AC)和TM内皮细胞在内的视网膜血管细胞表达CYP1B1,但CYP1B1对视网膜新生血管的衰减和TM组织发育不良的细胞自主贡献尚不清楚。本研究确定了EC、PC或AC中CYP1B1表达缺乏对视网膜新生血管和TM组织完整性的影响。我们在EC (Cyp1b1 EC)、PC (Cyp1b1 PC)和AC (Cyp1b1 AC)中产生了血管细胞特异性靶向Cre+缺失的Cyp1b1转基因小鼠。病理视网膜新生血管在OIR期间评估视网膜整体胶原IV染色。透射电镜观察TM组织的结构形态。视网膜新生血管的评估表明,与对照小鼠相比,只有Cyp1b1 PC小鼠的视网膜新生血管簇显著减少。TEM评估显示,Cyp1b1 PC小鼠也表现出与Cyp1b1-/-小鼠相似的TM组织形态和完整性缺陷。因此,Cyp1b1在PC中的表达在视网膜新生血管和TM组织的完整性中起着重要作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Targeted deletion of Cyp1b1 in pericytes results in attenuation of retinal neovascularization and trabecular meshwork dysgenesis.

Targeted deletion of Cyp1b1 in pericytes results in attenuation of retinal neovascularization and trabecular meshwork dysgenesis.

Targeted deletion of Cyp1b1 in pericytes results in attenuation of retinal neovascularization and trabecular meshwork dysgenesis.

Targeted deletion of Cyp1b1 in pericytes results in attenuation of retinal neovascularization and trabecular meshwork dysgenesis.

Mutations in cytochrome P450 1B1 (CYP1B1) gene are reported in patients with primary congenital glaucoma. Cyp1b1-deficient (Cyp1b1-/-) mice show dysgenesis of the trabecular meshwork (TM) tissue and attenuation of retinal neovascularization during oxygen-induced ischemic retinopathy (OIR). Although retinal vascular cells, including endothelial cells (EC), pericytes (PC), astrocytes (AC), and TM endothelial cells express CYP1B1, the cell autonomous contribution of CYP1B1 to attenuation of retinal neovascularization and TM tissue dysgenesis remains unknown. Here we determined the impact lack of CYP1B1 expression in EC, PC or AC has on retinal neovascularization and TM tissue integrity. We generated Cyp1b1-transgenic mice with vascular cell-specific targeted Cre+-deletion in EC (Cyp1b1 EC), in PC (Cyp1b1 PC) and in AC (Cyp1b1 AC). Pathologic retinal neovascularization during OIR was evaluated by collagen IV staining of retinal wholemounts. Structural morphology of TM tissue was examined by transmission electron microscopy (TEM). The assessment of retinal neovascularization indicated a significant decrease in retinal neovascular tufts only in Cyp1b1 PC mice compared with control mice. TEM evaluation demonstrated Cyp1b1 PC mice also exhibited a defect in TM tissue morphology and integrity similar to that reported in Cyp1b1-/- mice. Thus, Cyp1b1 expression in PC plays a significant role in retinal neovascularization and the integrity of TM tissue.

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