Posterior capsular opacification (PCO) is the main reason affecting the long-term postoperative result of cataract patient, and it is well accepted that fibrotic PCO is driven by transforming growth factor beta (TGFβ) signaling. Ferroptosis, closely related to various ocular diseases, but has not been explored in PCO. RNA sequencing (RNA-seq) was performed on both TGF-β2 treated and untreated primary lens epithelial cells (pLECs). Differentially expressed genes (DEGs) associated with ferroptosis were analyzed using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) to investigate their biological function. Additionally, protein-to-protein interactions among selected ferroptosis-related genes by PPI network and the top 10 genes with the highest score (MCC algorithm) were selected as the hub genes. The top 20 genes with significant fold change values were validated using quantitative real-time polymerase chain reaction (qRT-PCR). Our analysis revealed 1253 DEGs between TGF-β2 treated and untreated pLECs, uncovering 38 ferroptosis-related genes between two groups. Among these 38 ferroptosis-related genes,the most prominent GO enrichment analysis process involved in the response to oxidative stress (BPs), apical part of cell (CCs),antioxidant activity (MFs). KEGG were mainly concentrated in fluid shear stress and atherosclerosis, IL-17 and TNF signaling pathways, and validation of top 20 genes with significant fold change value were consistent with RNA-seq. Our RNA-Seq data identified 38 ferroptosis-related genes in TGF-β2 treated and untreated pLECs, which is the first observation of ferroptosis related genes in primary human lens epithelial cells under TGF-β2 stimulation. Our study initially observed ferroptosis related genes in primary human lens epithelial cells stimulated by TGF-β2. These findings may improve the understanding of the molecular mechanisms of PCO and provide a new direction for exploring the potential mechanisms of PCO

中文翻译：

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后囊膜混浊发育过程中 TGFβ 诱导晶状体上皮向间质转化中铁死亡相关基因的转录组探索

后囊膜混浊（PCO）是影响白内障患者术后长期结果的主要原因，人们普遍认为纤维化的PCO是由转化生长因子β（TGFβ）信号驱动的。铁死亡与多种眼部疾病密切相关，但在 PCO 中尚未得到探索。对 TGF-β2 处理和未处理的原代晶状体上皮细胞 (pLEC) 进行 RNA 测序 (RNA-seq)。使用基因本体论（GO）和京都基因和基因组百科全书（KEGG）分析与铁死亡相关的差异表达基因（DEG）以研究其生物学功能。此外，通过PPI网络选择的铁死亡相关基因之间的蛋白质间相互作用以及得分最高的前10个基因（MCC算法）被选为枢纽基因。使用定量实时聚合酶链反应 (qRT-PCR) 验证了具有显着倍数变化值的前 20 个基因。我们的分析显示，TGF-β2 处理和未处理的 pLEC 之间有 1253 个 DEG，揭示了两组之间的 38 个与铁死亡相关的基因。在这38个铁死亡相关基因中,最突出的GO富集分析过程涉及氧化应激反应(BPs)、细胞顶端部分(CCs)、抗氧化活性(MFs)。 KEGG主要集中在流体剪切应力和动脉粥样硬化、IL-17和TNF信号通路上，对倍数变化值显着的前20个基因的验证与RNA-seq一致。我们的RNA-Seq数据在TGF-β2处理和未处理的pLEC中鉴定出38个铁死亡相关基因，这是在TGF-β2刺激下原代人晶状体上皮细胞中首次观察到铁死亡相关基因。我们的研究最初在 TGF-β2 刺激的原代人晶状体上皮细胞中观察到铁死亡相关基因。这些发现可能提高对PCO分子机制的理解，为探索PCO潜在机制提供新方向