Journal of diabetes investigation · 2025
Dysregulation of lncRNA OIP5-AS1 participants in the progression of diabetic retinopathy and affects the proliferation in retinal vascular endothelial cell.
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Yin Ziwen, Dong Jingyun, Meng Yachao, Yang Zhiqiang, Zhao Chunhong, Wu Qiuyun
Аннотация
AIMS: This study was to ascertain the clinical performance of OIP5-AS1 in diabetic retinopathy (DR) and its molecular mechanism in the disease progression.
MATERIALS AND METHODS: Subjects included 85 healthy controls, 79 patients with type 2 diabetes mellitus (T2DM), and 114 T2DM-DR patients. qRT-PCR was conducted to measure the relative abundances of OIP5-AS1 and miR-181a-5p in the research subjects. Receiver operating characteristic (ROC) and logistic regression analyses were employed for the diagnostic capability and risk factor prediction. Cell activities were assessed using CCK-8 and transwell assays. Luciferase reporter assay was used for the correlation confirmation of OIP5-AS1 and miR-181a-5p. Bioinformatic analysis was applied to predict the potential targets of miR-181a-5p.
RESULTS: A significant decrease of OIP5-AS1 was detected in serum from patients with T2MD and T2DM-DR (P < 0.001), exhibiting a high diagnostic value for detecting T2DM (AUC = 0.973) and T2DM-DR patients (AUC = 0.913). OIP5-AS1 was an independent protective indicator for the onset of T2DM-proliferative DR (T2DM-PDR; P = 0.021, OR = 0.306, 95%CI = 0.112-0.837). OIP5-AS1 was markedly reduced in human retinal vascular endothelial cells (HRVECs) with high glucose (HG) (P < 0.001). Overexpression of OIP5-AS1 could significantly suppress the cell growth of HRVECs (P < 0.001). OIP5-AS1 was negatively correlated with miR-181a-5p (r = -0.5327, P < 0.001). Additionally, the impacts caused by OIP5-AS1 on cell events were canceled by transfection of miR-181a-5p mimic (P < 0.001). The possible targets of miR-181a-5p were mined, suggesting mainly enriched in cellular senescence and the MAPK signaling pathway.
CONCLUSIONS: OIP5-AS1 was downregulated in T2DM-DR patients and regulated cellular functions via targeting miR-181a-5p. It might offer a new therapeutic target for the disease.
MATERIALS AND METHODS: Subjects included 85 healthy controls, 79 patients with type 2 diabetes mellitus (T2DM), and 114 T2DM-DR patients. qRT-PCR was conducted to measure the relative abundances of OIP5-AS1 and miR-181a-5p in the research subjects. Receiver operating characteristic (ROC) and logistic regression analyses were employed for the diagnostic capability and risk factor prediction. Cell activities were assessed using CCK-8 and transwell assays. Luciferase reporter assay was used for the correlation confirmation of OIP5-AS1 and miR-181a-5p. Bioinformatic analysis was applied to predict the potential targets of miR-181a-5p.
RESULTS: A significant decrease of OIP5-AS1 was detected in serum from patients with T2MD and T2DM-DR (P < 0.001), exhibiting a high diagnostic value for detecting T2DM (AUC = 0.973) and T2DM-DR patients (AUC = 0.913). OIP5-AS1 was an independent protective indicator for the onset of T2DM-proliferative DR (T2DM-PDR; P = 0.021, OR = 0.306, 95%CI = 0.112-0.837). OIP5-AS1 was markedly reduced in human retinal vascular endothelial cells (HRVECs) with high glucose (HG) (P < 0.001). Overexpression of OIP5-AS1 could significantly suppress the cell growth of HRVECs (P < 0.001). OIP5-AS1 was negatively correlated with miR-181a-5p (r = -0.5327, P < 0.001). Additionally, the impacts caused by OIP5-AS1 on cell events were canceled by transfection of miR-181a-5p mimic (P < 0.001). The possible targets of miR-181a-5p were mined, suggesting mainly enriched in cellular senescence and the MAPK signaling pathway.
CONCLUSIONS: OIP5-AS1 was downregulated in T2DM-DR patients and regulated cellular functions via targeting miR-181a-5p. It might offer a new therapeutic target for the disease.