Open AccessTWEAK /Fn14 mediates atrial‐derived HL ‐1 myocytes hypertrophy via JAK 2/ STAT 3 signalling pathway
Author(s) -
Hao Li,
Ren Manyi,
Rong Bing,
Xie Fei,
Lin Mingjie,
Zhao Yachao,
Yue Xin,
Han Wenqiang,
Zhong Jingquan
Publication year - 2018
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13724
Subject(s) - myocyte , medicine , gene knockdown , muscle hypertrophy , endocrinology , atrial natriuretic peptide , atrial fibrillation , chemistry , signal transduction , microbiology and biotechnology , biology , gene , biochemistry
Atrial myocyte hypertrophy is one of the most important substrates in the development of atrial fibrillation ( AF ). The TWEAK /Fn14 axis is a positive regulator of cardiac hypertrophy in cardiomyopathy. This study therefore investigated the effects of Fn14 on atrial hypertrophy and underlying cellular mechanisms using HL ‐1 atrial myocytes. In patients with AF , Fn14 protein levels were higher in atrial myocytes from atrial appendages, and expression of TWEAK was increased in peripheral blood mononuclear cells, while TWEAK serum levels were decreased. In vitro, Fn14 expression was up‐regulated in response to TWEAK treatment in HL ‐1 atrial myocytes. TWEAK increased the expression of ANP and Troponin T, and Fn14 knockdown counteracted the effect. Inhibition of JAK 2, STAT 3 by specific si RNA attenuated TWEAK ‐induced HL ‐1 atrial myocytes hypertrophy. In conclusion, TWEAK /Fn14 axis mediates HL ‐1 atrial myocytes hypertrophy partly through activation of the JAK 2/ STAT 3 pathway.