METTL3-mediated m6A modification involved in electrical remodeling of atrial cardiomyocytes under high hydrostatic pressure
- Author:
Pan-Yue LIU
1
;
Fei-Fei XIAO
1
;
Pan-Yue LIU
2
;
Long ZENG
2
;
Hai-Yin XIAO
2
;
Fei-Fei XIAO
2
;
Rui ZHU
2
;
Hui YANG
2
;
Su-Juan KUANG
2
;
Chun-Yu DENG
2
;
Fang RAO
2
;
Wei WEI
2
Author Information
- Publication Type:Journal Article
- Keywords: atrial cloctriral remodeling; atrial fibrillation; high hydiDstatic pressure; Ivtypc calcium channrl; m6A; METTI3
- From: Chinese Pharmacological Bulletin 2023;39(12):2258-2265
- CountryChina
- Language:Chinese
- Abstract: To investigate the regulation of N6- methyladenosine ( m6A ) modification on L-type calcium channels in atrial myocytes under high hydrostatic pressure, mediated by methyltransferase-like protein 3 ( METTL3 ). Methods C57BL/6J mice were randomly assigned to the control group and the hypertension group ( treated with continuous administration of angiotensin for four weeks ). Masson staining was used to observe the fibrosis of mouse atrial tissue, while dot blot assay and Western blot were used to detect the levels of m6A, METTL3, and Cavi1 2 in the atrial tissue. A high hydrostatic pressure model was constructed using the HL-1 cell line cultured in vitro, and METTL3 was intervened to observe changes in m6A expression levels, METTL3 and Cavi1 2 levels in cells,and action potential duration ( APD ) and L-type calcium current ( I
