TEAD1 mRNA inhibits the repair process of traumatic optic nerve cell injury via miR-671-5p

Abstract Objectives This study aims to investigate the diagnostic value of TEAD1 mRNA in traumatic optic neuropathy (TON) and its regulatory role in damaged optic nerve cells. Methods A total of 240 patients were enrolled, including 122 with TON. 5 mL of peripheral venous blood was collected from patients. A TON mouse model was established via ocular trauma surgery, and damaged retinal ganglion cells (RGCs) were isolated. Gene expression was assessed via reverse transcription quantitative polymerase chain reaction (RT-qPCR), apoptosis was examined by flow cytometry, and inflammatory cytokine expression was measured by enzyme-linked immunosorbent assay (ELISA). Dual luciferase reporter assays and RNA immunoprecipitation validated interactions between the target gene and its regulatory partners. Results TEAD1 mRNA was significantly upregulated in TON patients and RGC cells. TEAD1 mRNA may represent a potential risk factor for TON development and hold diagnostic value. si- TEAD1 reduced RGC apoptosis, primarily manifested by decreased expression of the apoptotic genes Bax and Caspase-3 , alongside upregulation of the anti-apoptotic gene Bcl-2 . Furthermore, TEAD1 mRNA silencing also diminished inflammatory levels in damaged RGCs. Secondly, miR-671-5p was downregulated in TON patients and damaged RGCs, and served as a downstream target gene of TEAD1 mRNA. The miR inhibitor counteracted the reduced apoptosis and inflammation induced by TEAD1 mRNA silencing. Conclusions TEAD1 mRNA silencing alleviates TON by reducing apoptosis and inflammation in damaged RGCs through miR-671-5p upregulation.