Department of Ophthalmology, Affiliated Hospital of Nantong University, No. 20 Xisi Road, Nantong, 226001, Jiangsu Province, China.
Department of Trauma Center, Affiliated Hospital of Nantong University, No. 20 Xisi Road, Nantong, 226001, Jiangsu Province, China.
BMC Ophthalmol. 2022 Jun 15;22(1):267. doi: 10.1186/s12886-022-02481-0.
Corneal neovascularization (CRNV) is a severe threat to the vision of people. MicroRNA-335 (miR-335) has the function of facilitating angiogenesis. However, whether miR-335 regulates the progression of CRNV remains unclear.
The miR-335 expressions in CRNV rats induced by corneal suture and HUVECs induced by b-FGF were detected by quantitative real-time PCR. For the miR-335 function, wound healing and tube formation assays were performed. For the miR-335 mechanism, a dual-luciferase reporter gene assay was conducted. Besides, for the epidermal growth factor receptor (EGFR) function, Cell Counting Kit-8 and wound healing assays were performed. Meanwhile, the rescue assay was used to assess the miR-335/EGFR function in the migration and angiogenesis of b-FGF-treated HUVECs.
Functionally, the miR-335 knockdown weakened the migration and angiogenesis of b-FGF-treated HUVECs, while the miR-335 overexpression showed an opposite trend. Mechanistically, miR-335 interacted with EGFR and negatively regulated the expression of EGFR. The rescue assay illustrated that miR-335 regulated the migration and angiogenesis of b-FGF-treated HUVECs through EGFR.
In general, our data confirmed that miR-335 facilitated the process of CRNV by targeting EGFR.
角膜新生血管（CRNV）严重威胁着人们的视力。微小 RNA-335（miR-335）具有促进血管生成的功能。然而，miR-335 是否调节 CRNV 的进展尚不清楚。
通过实时定量 PCR 检测角膜缝线诱导的 CRNV 大鼠和 b-FGF 诱导的 HUVECs 中的 miR-335 表达。为了研究 miR-335 的功能，进行了划痕愈合和管形成实验。为了研究 miR-335 的机制，进行了双荧光素酶报告基因实验。此外，为了研究表皮生长因子受体（EGFR）的功能，进行了细胞计数试剂盒-8 和划痕愈合实验。同时，还进行了挽救实验，以评估 miR-335/EGFR 在 b-FGF 处理的 HUVECs 迁移和血管生成中的功能。
功能上，miR-335 的敲低削弱了 b-FGF 处理的 HUVECs 的迁移和血管生成能力，而 miR-335 的过表达则呈现相反的趋势。在机制上，miR-335 与 EGFR 相互作用并负调控 EGFR 的表达。挽救实验表明，miR-335 通过 EGFR 调节 b-FGF 处理的 HUVECs 的迁移和血管生成。
总的来说，我们的数据证实，miR-335 通过靶向 EGFR 促进了 CRNV 的发生。
