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Long Non-Coding RNA H19 Regulates Human Lens Epithelial Cells Function

机译：长非编码RNA H19调节人晶状体上皮细胞功能

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Background/Aims Age-related cataract (ARC) remains the leading cause of visual impairment among the elderly population. Long non-coding RNAs (lncRNAs) have emerged as potential regulators in many ocular diseases. However, the role of lncRNAs in nuclear ARC, a subtype of ARC, requires further elucidation. Methods LncRNA sequencing was performed to identify differentially expressed lncRNAs between the capsules of transparent and nuclear ARC lenses. Expression validation was confirmed by qRT-PCR. MTT assay, Calcein-AM and propidium iodide double staining, Rhodamine 123 and Hoechst double staining, EdU and transwell assay were used to determine the role of H19 or miR-675 in the viability, apoptosis, proliferation and migration of primary cultured human lens epithelial cells (HLECs). Bioinformatics and luciferase reporter assays were used to identify the binding target of miR-675. Results Sixty-three lncRNAs are differentially expressed between the capsules of transparent and nuclear ARC lenses. One top abundantly expressed lncRNA, H19, is significantly up-regulated in the nuclear ARC lens capsules and positively associated with nuclear ARC grade. H19 knockdown accelerates apoptosis development and reduces the proliferation and migration of HLECs upon oxidative stress. H19 is the precursor of miR-675, and a reduction of H19 inhibits miR-675 expression. miR-675 regulates CRYAA expression by targeting the binding site within the 3’UTR. Moreover, miR-675 increases the proliferation and migration while decreasing the apoptosis of HLECs upon oxidative stress. Conclusion H19 regulates HLECs function through miR-675-mediated CRYAA expression. This finding would provide a novel insight into the pathogenesis of nuclear ARC.
机译：背景/目的年龄相关性白内障（ARC）仍然是老年人视觉障碍的主要原因。长的非编码RNA（lncRNA）已成为许多眼科疾病的潜在调节剂。但是，lncRNA在ARC的亚型核ARC中的作用需要进一步阐明。方法进行LncRNA测序，以鉴定透明和核ARC晶状体囊之间差异表达的lncRNA。通过qRT-PCR确认表达验证。用MTT法，钙黄绿素-AM和碘化丙啶双染色，若丹明123和Hoechst双染色，EdU和transwell法测定H19或miR-675在原代培养的人晶状体上皮细胞的活力，凋亡，增殖和迁移中的作用。细胞（HLEC）。使用生物信息学和萤光素酶报告基因测定法来鉴定miR-675的结合靶标。结果透明和核ARC晶状体囊之间有63个lncRNA差异表达。在核ARC晶状体囊中，一种表达最丰富的lncRNA H19被显着上调，并且与核ARC级呈正相关。 H19敲低加速了细胞凋亡的发展，并减少了氧化应激时HLEC的增殖和迁移。 H19是miR-675的前体，H19的减少会抑制miR-675的表达。 miR-675通过靶向3’UTR中的结合位点来调节CRYAA的表达。此外，miR-675在氧化应激下增加HLECs的增殖和迁移，同时减少其凋亡。结论H19通过miR-675介导的CRYAA表达调节HLEC的功能。这一发现将为核ARC的发病机理提供新颖的见解。

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