lncRNA LENGA sponges miR-378 to promote myocardial fibrosis in atrial fibrillation

lncRNA LENGA sponges miR-378 to promote myocardial fibrosis in atrial fibrillation

miR-378 is known to suppress myocardial fibrosis, while its upstream regulators have not been identified. lncRNA LENGA is a recently identified lncRNA in cancer biology. We observed the altered expression of LENGA in atrial fibrillation (AF) patients and predicted its interaction with miR-378. We th...

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Bibliographic Details
Published in:Open medicine (Warsaw, Poland) Vol. 18; no. 1; p. 20230831
Main Authors: Wu, Liting, Gao, Bingjing, Shen, Mengyuan, Wei, Lu, Li, Zhumeng, Zhuang, Wenfang
Format: Journal Article
Language:English
Published: Warsaw De Gruyter 14-11-2023
Walter de Gruyter GmbH
Subjects:
atrial fibrillation
Cardiac arrhythmia
Fibroblasts
LENGA
miR-378
myocardial fibrosis
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Summary:miR-378 is known to suppress myocardial fibrosis, while its upstream regulators have not been identified. lncRNA LENGA is a recently identified lncRNA in cancer biology. We observed the altered expression of LENGA in atrial fibrillation (AF) patients and predicted its interaction with miR-378. We then explored the interaction between LENGA and miR-378 in AF. Angiotensin-II (Ang-II)-induced human atrial cardiac fibroblasts and human atrial muscle tissues were collected and the expression of LENGA and miR-378 was determined by RT-qPCR. The interaction between LENGA and miR-378 was analyzed through bioinformatics analysis and confirmed by RNA pulldown assay. Cell proliferation and collagen production were analyzed through assay to analyze the role of LENGA and miR-378 in MF. AF patients showed increased expression of LENGA and deceased expression of miR-378 compared to the sinus rhythm group. LENGA and miR-378 interacted with each other, while they are not closely correlated with each other. Overexpression assay showed that LENGA and miR-378 overexpression failed to affect each other’s expression. LENGA promoted collagen production and proliferation of Ang-II-induced atrial fibroblasts, while miR-378 played opposite roles. Moreover, LENGA suppressed the function of miR-378. Therefore, LENGA may sponge miR-378 to promote MF in AF.
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content type line 23
ISSN:2391-5463
2391-5463
DOI:10.1515/med-2023-0831