Liu Gaoqin, Lu Peirong, Chen Lei, Zhang Wenpeng, Wang Mengjiao, Li Dan, Zhang Xueguang
Department of Ophthalmology, the First Affiliated Hospital of Soochow University, Suzhou, China.
Jiangsu Key Laboratory of Clinical Immunology, the First Affiliated Hospital of Soochow University, Suzhou, China.
Eye (Lond). 2018 Jul;32(7):1220-1231. doi: 10.1038/s41433-018-0039-x. Epub 2018 Mar 8.
Corneal neovascularization (CrNV) arises from many causes including corneal inflammatory, infectious, or traumatic insult, and frequently leads to impaired vision. This study seeks to determine the role of B-cell leukemia/lymphoma 10 (BCL-10) in the development of experimental CrNV.
Corneas from BCL-10 knockout (KO) mice and wild-type (WT) mice were burned by sodium hydroxide (NaOH) to create the CrNV model and neovascular formation in the corneas was assessed 2 weeks later. Intracorneal macrophage accumulation and the expression of angiogenic factors were quantified by flow cytometric analysis (FCM) and real-time PCR, respectively.
The amount of CrNV was determined 2 weeks after alkali burn. Compared to WT mice, the amount of CrNV in BCL-10 KO mice was significantly decreased. FCM revealed that F4/80-positive macrophages were markedly decreased in BCL-10 KO mice compared with WT mice. Reverse transcription PCR showed that the mRNA expression levels of intracorneal vascular endothelial growth factor-A (VEGF-A), basic fibroblast growth factor (bFGF) and monocyte chemotactic protein 1 were reduced in BCL-10 KO mice compared with WT mice.
BCL-10 KO mice exhibited reduced alkali-induced CrNV by suppressing intracorneal macrophage infiltration, which subsequently led to decreased VEGF-A and bFGF expression, suggesting that BCL-10 may become a potential clinical intervening target of CrNV.
角膜新生血管形成（CrNV）由多种原因引起，包括角膜炎症、感染或创伤性损伤等，且常导致视力受损。本研究旨在确定B细胞白血病/淋巴瘤10（BCL-10）在实验性CrNV发生发展中的作用。
用氢氧化钠（NaOH）烧灼B细胞白血病/淋巴瘤10基因敲除（KO）小鼠和野生型（WT）小鼠的角膜以建立CrNV模型，2周后评估角膜新生血管的形成情况。分别通过流式细胞术分析（FCM）和实时聚合酶链反应定量角膜内巨噬细胞的积聚情况以及血管生成因子的表达。
碱烧伤2周后测定CrNV的量。与野生型小鼠相比，BCL-10基因敲除小鼠的CrNV量显著减少。流式细胞术分析显示，与野生型小鼠相比，BCL-10基因敲除小鼠中F4/80阳性巨噬细胞明显减少。逆转录聚合酶链反应显示，与野生型小鼠相比，BCL-10基因敲除小鼠角膜内血管内皮生长因子-A（VEGF-A）、碱性成纤维细胞生长因子（bFGF）和单核细胞趋化蛋白1的mRNA表达水平降低。
BCL-10基因敲除小鼠通过抑制角膜内巨噬细胞浸润，表现出碱诱导的CrNV减少，这随后导致VEGF-A和bFGF表达降低，提示BCL-10可能成为CrNV潜在的临床干预靶点。
