RESUMEN
Objective: To explore the possible mechanism of silent information regulator 1 (SIRT1) in regulating the function of human trabecular meshwork cells (HTMCs). Methods: Experimental study. HTMCs were transfected with SIRT1-overexpressed lentivirus and control lentivirus at the optimal multiplicity of infection, respectively. The total RNA was extracted, and the long non-coding RNA (lncRNA) microarray was used to detect the expression of lncRNAs. The differentially expressed lncRNAs were analyzed by bioinformatics. Real-time PCR was used to verify the microarray results. Student's t-test was used for comparison between groups. Results: Compared with the control group, there were 636 up-regulated lncRNAs and 2 246 down-regulated lncRNAs in the SIRT1 overexpressed group (all P<0.05). Gene ontology analysis showed that SIRT1 regulated extracellular matrix, cell metabolism, proliferation and apoptosis of HTMCs. Kyoto encyclopedia of genes and genomics pathway analysis indicated that differential lncRNAs induced by SIRT1 were involved in 19 signal pathways, including Notch signaling pathway, mitogen-activated protein kinase signaling pathway, inflammatory mediator regulation of tyrosinase-associated protein channels and extracellular matrix-receptor interaction. Conclusion: SIRT1 could have effects on the function of HTMCs through regulating lncRNAs in multiple signaling pathways, including Notch signaling pathway, mitogen-activated protein kinase signaling pathway, etc. (Chin J Ophthalmol, 2021, 57: 215-222).