Meng Li-Hui, Cheng Shi-Yu, Chen He, Wang Yue-Lin, Zhang Wen-Fei, Chen Huan, Zhao Xin-Yu, Chen You-Xin
Department of Ophthalmology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China.
Key Lab of Ocular Fundus Diseases, Chinese Academy of Medical Sciences, Beijing 100730, China.
Int J Ophthalmol. 2024 Jan 18;17(1):16-24. doi: 10.18240/ijo.2024.01.03. eCollection 2024.
To investigate the impacts of angiotensin II (Ang II) on retinal artery changes in apolipoprotein E deficient () mice.
male mice were infused by minipumps with Ang II at 1000 ng/kg·min (Ang II group) or saline (control group) for 28d. They were underwent ophthalmic fundus examination on day 0, 14, and 28 of infusion. Histopathologic examination, ribonucleic acid (RNA) sequencing and local Ang II measurement of retinas were conducted.
Ophthalmic fundus examination showed Ang II infusion promoted the formation of retinal arterial aneurysm-like lesions on day 28. Optical coherence tomography revealed the ganglion cell and inner plexiform layer (GCIPL) thickness in the control group was significantly thinner than that in Ang II group (<0.001). Hematoxylin-eosin staining demonstrated diffused swelling of GCIPL layer and its disordered structure in Ang II group. Transmission electron microscopy showed Ang II infusion caused aggravation of atherosclerotic lesions, including increased swelling, roughness, disorganization of the retinal vasculature, and vacuoles formation. RNA-sequencing and gene ontology enrichment analysis demonstrated that the structure and function of cellular membrane might be disturbed and visual function might be compromised by Ang II. The local level of Ang II was higher in Ang II infusion group but did not show significant differences compared to the control group (=0.086).
Ang II infusion promotes the formation of retinal arterial aneurysm-like lesions in mice, causing aggravation of atherosclerotic lesions, more severe disorganization of the retinal vasculature and disturbance of the cellular membrane.
研究血管紧张素II(Ang II)对载脂蛋白E缺乏()小鼠视网膜动脉变化的影响。
雄性小鼠通过微型泵以1000 ng/kg·min的剂量输注Ang II(Ang II组)或生理盐水(对照组),持续28天。在输注的第0、14和28天对它们进行眼底检查。对视网膜进行组织病理学检查、核糖核酸(RNA)测序和局部Ang II测量。
眼底检查显示,输注Ang II在第28天促进了视网膜动脉动脉瘤样病变的形成。光学相干断层扫描显示,对照组的神经节细胞和内网状层(GCIPL)厚度明显薄于Ang II组(<0.001)。苏木精-伊红染色显示Ang II组GCIPL层弥漫性肿胀且结构紊乱。透射电子显微镜显示,输注Ang II导致动脉粥样硬化病变加重,包括视网膜血管肿胀增加、粗糙度增加、结构紊乱和空泡形成。RNA测序和基因本体富集分析表明,Ang II可能会干扰细胞膜的结构和功能,并损害视觉功能。Ang II输注组的局部Ang II水平较高,但与对照组相比无显著差异(=0.086)。
输注Ang II促进小鼠视网膜动脉动脉瘤样病变的形成,导致动脉粥样硬化病变加重、视网膜血管结构更严重紊乱和细胞膜紊乱。