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Iran J Immunol ; 20(2): 202-210, 2023 05 31.
Artículo en Inglés | MEDLINE | ID: mdl-37209045

RESUMEN

Background: Retinopathy of diabetes is a chronic diabetes mellitus complication affecting retinal vessels, and some ocular complications' molecular mechanisms remain obscure. Objective: To evaluate the expression of HLA-G1, HLA-G5, miRNA-181a, and miRNA-34a in the lens epithelial cells of patients with retinopathy of diabetes. Methods: In a case-control study, 30 diabetic patients with retinopathy, 30 diabetic patients without retinopathy, and 30 cataract patients without diabetes mellitus as the control group were enrolled after a full description with details about the study methods and objectives. The expression of HLA G1, HLA G5, miRNA-181a, and miRNA-34a in lens epithelial cells was assessed by quantitative RT PCR. Moreover, the levels of HLA-G protein in aqueous humor were evaluated by the ELISA method. Results: HLA-G1 expression was significantly upregulated in the retinopathy group (P=0.003). The aqueous humor of diabetic retinopathy patients contained significantly higher levels of HLA-G protein compared with the non-diabetic patients (P=0.001). miRNA-181a was significantly downregulated in the diabetic retinopathy group compared with the patients without diabetes (P=0.001). In addition, miRNA-34a was upregulated in the retinopathy group (P=0.009). Conclusion: Taken together, the present results showed that HLA-G1 and miRNA-34a can be valuable markers for diabetic retinopathy. Our data offers new perspectives for improving the control of inflammation in the lens epithelial cells by considering HLA-G and miRNA.


Asunto(s)
Diabetes Mellitus , Retinopatía Diabética , MicroARNs , Humanos , Humor Acuoso/metabolismo , Estudios de Casos y Controles , Diabetes Mellitus/metabolismo , Retinopatía Diabética/genética , Retinopatía Diabética/complicaciones , Retinopatía Diabética/metabolismo , Células Epiteliales/metabolismo , Antígenos HLA-G/genética , Antígenos HLA-G/metabolismo , MicroARNs/genética , MicroARNs/metabolismo , Regulación hacia Arriba
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