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MicroRNA‐4328 promotes lens epithelial cell apoptosis by targeting NLR family, apoptosis inhibitory protein in age‐related cataract.
- Source :
-
Cell Biochemistry & Function . Mar2020, Vol. 38 Issue 2, p149-157. 9p. - Publication Year :
- 2020
-
Abstract
- Cataract is the leading cause of blindness in the world while the molecular mechanisms of cataracts pathogenesis are not well elucidated. Dysregulated microRNA (miRNA) expressions have been implicated in cataract. However, the precise role of miR‐4328 in cataract is still unknown. We compared the expression level of total miR‐4328 between clinical samples from healthy people and cataract patient and between UV‐irradiated and control lens epithelial cells. We determined the effect of miR‐4328 on lens epithelial cell proliferation and apoptosis by suppressing miR‐4328. We further predicted NLR Family Apoptosis Inhibitory Protein (NAIP) as potential target of miR‐4328 and continued to evaluate the effects of NAIP on cell proliferation and apoptosis. MiR‐4328 was up‐regulated in cataract sample and in UV‐irradiated lens epithelial cells. Suppressing MiR‐4328 promoted cell proliferation and inhibited apoptosis. MiR‐4328 targeted NAIP and suppressed its expression. Knocking down NAIP abolished the effects of miR‐4328 on cell proliferation and inhibited apoptosis. MiR‐4328 promotes lens epithelial cell apoptosis by targeting NAIP in age‐related cataract. Significance of the study: MiR‐4328 targeted NAIP and suppressed its expression. Knocking down NAIP abolished the effects of miR‐4328 on cell proliferation and inhibited apoptosis. MiR‐4328 promotes lens epithelial cell apoptosis by targeting NAIP in age‐related cataract. [ABSTRACT FROM AUTHOR]
- Subjects :
- *EPITHELIAL cells
*CATARACT
*APOPTOSIS
*CELL proliferation
*PATHOLOGY
Subjects
Details
- Language :
- English
- ISSN :
- 02636484
- Volume :
- 38
- Issue :
- 2
- Database :
- Academic Search Index
- Journal :
- Cell Biochemistry & Function
- Publication Type :
- Academic Journal
- Accession number :
- 142949368
- Full Text :
- https://doi.org/10.1002/cbf.3453