Open Access


Read more
image01

Online Manuscript Submission


Read more
image01

Submitted Manuscript Trail


Read more
image01

Online Payment


Read more
image01

Online Subscription


Read more
image01

Email Alert



Read more
image01

Original Research Article | OPEN ACCESS

Mechanism of lncRNA FOXD3-AS1 targeting miR-338-3p in human lens epithelial cell injury in diabetic cataract

QingWei Du1, LiLun Wang2, Mei Li3

1Department of Ophthalmology, Yanan University Affiliated Hospital, Yanan, Shaanxi Province, 716000, China; 2Department of Ophthalmology, Yanan University Affiliated Hospital, Yanan, Shaanxi Province, 716000, China; 3Yan"An Peoples Hospital, 57 Qilipu Street, Baota District, Yanan City, Shaanxi Province, 716000, China.

For correspondence:-  Mei Li   Email: yub95882@126.com

Accepted: 12 March 2023        Published: 31 March 2023

Citation: Du Q, Wang L, Li M. Mechanism of lncRNA FOXD3-AS1 targeting miR-338-3p in human lens epithelial cell injury in diabetic cataract. Trop J Pharm Res 2023; 22(3):535-542 doi: 10.4314/tjpr.v22i3.10

© 2023 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To explore the influence of lncRNA FOXD3-AS1 on high glucose (HG)-stimulated human lens epithelial cell injury in diabetic cataract.
Methods: Lens epithelial cell HLEB3 were cultured in vitro and transfected with si-FOXD3-AS1, miR-338-3p mimic or miR-338-3p inhibitor, followed by HG (40 mmol/L) treatment. FOXD3-AS1, miR-338-3p, cleaved caspases3 and cleaved caspases9 expression were analyzed by RT-qPCR or western blot. SOD and CAT activities and MDA production in cells were determined using special kits. Cell apoptotic rate was quantified by flow cytometry. Regulatory relationship of FOXD3-AS1 and miR-338-3p was investigated by mechanism assay.
Results: HG enhanced FOXD3-AS1 expression but repressed miR-338-3p (P<0.05) in HLEB3 cells. FoxD3-AS1 depletion or miR-338-3p introduction promoted SOD and CAT activities, decreased MDA content, apoptosis rate, and cleaved caspases3 and cleaved caspases9 protein production in HG-induced HLEB3 cells (P<0.05). FOXD3-AS1 could target and negatively regulate miR-338-3p. FOXD3-AS1-mediated influence on HG-induced HLEB3 cells was rescued by miR-338-3p inhibitors.
Conclusion: FOXD3-AS1 silenced upregulated miR-338-3p expression to alleviate HG-induced oxidative stress and apoptosis of HLEB3 cells.

Keywords: Apoptosis; Diabetic cataract; FOXD3-AS1; miR-338-3p; oxidative stress

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

Article Tools

Share this article with



Article status: Free
Fulltext in PDF
Similar articles in Google
Similar article in this Journal:

Archives

2024; 23: 
1,   2,   3,   4. 
2023; 22: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12. 
2022; 21: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12. 
2021; 20: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12. 
2020; 19: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12. 
2019; 18: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12. 
2018; 17: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12. 
2017; 16: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12. 
2016; 15: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12. 
2015; 14: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12. 
2014; 13: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12. 
2013; 12: 
1,   2,   3,   4,   5,   6. 
2012; 11: 
1,   2,   3,   4,   5,   6. 
2011; 10: 
1,   2,   3,   4,   5,   6. 
2010; 9: 
1,   2,   3,   4,   5,   6. 
2009; 8: 
1,   2,   3,   4,   5,   6. 
2008; 7: 
1,   2,   3,   4. 
2007; 6: 
1,   2,   3,   4. 
2006; 5: 
1,   2. 
2005; 4: 
1,   2. 
2004; 3: 
1. 
2003; 2: 
1,   2. 
2002; 1: 
1,   2. 

News Updates