MiR-326 antagomir delays the progression of age-related cataract by upregulating FGF1-mediated expression of betaB2-crystallin
- Department of Laboratory Diagnosis, Changhai Hospital, The Second Military Medical University, Shanghai 200433 (China)
- Department of Ophthalmology, Changhai Hospital, The Second Military Medical University, Shanghai 200433 (China)
- Department of Gynaecology and Obstetrics, Changhai Hospital, The Second Military Medical University, Shanghai 200433 (China)
- Department of Clinical Laboratory, The Second Hospital of Shandong University, Shandong 250033 (China)
- Interdisciplinary Research Center on Biology and Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai, 201210 (China)
Highlights: • FGF-1 upregulates the expression of an anti-cataract protein βB2. • miR-326 inhibits FGF-1 expression and thereby decreases βB2 level. • miR-326 antagomir delay cataract progression via the function of miR-326. Age-related cataract, the most common cause of blindness worldwide, has been found closely associated with β-crystallin B2 (βB2 or CRYBB2). MicroRNAs (miRNAs) are the primary epigenetic regulators important for various biological processes. However, the role of miRNAs in the progression of lens cataract remains to be elucidated. In this study, we found a novel signal cascade miR-326–fibroblast growth factor 1 (FGF1)–βB2 modulating the progression of lens cataract. In brief, miR-326 exacerbated but its antagomirs attenuated H{sub 2}O{sub 2}-induced apoptosis of HLEC-B3 human lens epithelial cells. Dual-luciferase reporter assay and Western blot showed that miR-326 inhibited FGF1 expression by directly targeting its mRNA 3′-UTR. Consistent with this result, miR-326 antagomir enhanced FGF1 protein level. In addition to FGF1, miR-326 antagomir also enhanced βB2 expression and this enhancement was abolished by transfection of HLEC-B3 cells with FGF1 shRNA. These data demonstrated that miR-326 antagomir increased βB2 expression via upregulating FGF1, which was further confirmed by the studies in a rat model of selenite-induced cataract. This work suggests that miR-326 antagomir might be a promising candidate to prevent progression of age-related cataract.
- OSTI ID:
- 23134139
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 505, Issue 2; Other Information: Copyright (c) 2018 Elsevier Inc. All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
Similar Records
MiR-205–5p suppresses angiogenesis in gastric cancer by downregulating the expression of VEGFA and FGF1
miR-92a is upregulated in cervical cancer and promotes cell proliferation and invasion by targeting FBXW7