TWEAK /Fn14 mediates atrial‐derived HL ‐1 myocytes hypertrophy via JAK 2/ STAT 3 signalling pathway

Autor: Xin Yue, Manyi Ren, Bing Rong, Yachao Zhao, Mingjie Lin, Fei Xie, Li Hao, Wenqiang Han, Jing-Quan Zhong
Rok vydání: 2018
Předmět:
Male
0301 basic medicine
Cardiomyopathy
Muscle hypertrophy
Mice
TWEAK
Atrial Fibrillation
Myocyte
Myocytes
Cardiac

RNA
Small Interfering

STAT3
biology
Cytokine TWEAK
Atrial fibrillation
Middle Aged
Hedgehog signaling pathway
TWEAK Receptor
cardiovascular system
Molecular Medicine
Female
Original Article
hypertrophy
Atrial Natriuretic Factor
Signal Transduction
STAT3 Transcription Factor
medicine.medical_specialty
Primary Cell Culture
Atrial Appendage
Cardiomegaly
03 medical and health sciences
Troponin T
Internal medicine
medicine
Animals
Humans
Heart Atria
cardiovascular diseases
Aged
business.industry
JAK2/STAT3
Fn14
Original Articles
HL‐1 atrial myocytes
Cell Biology
Janus Kinase 2
medicine.disease
Troponin
Disease Models
Animal

030104 developmental biology
Endocrinology
Gene Expression Regulation
Case-Control Studies
Leukocytes
Mononuclear

biology.protein
business
Zdroj: Journal of Cellular and Molecular Medicine
ISSN: 1582-4934
1582-1838
Popis: 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 JAK2, STAT3 by specific siRNA attenuated TWEAK‐induced HL‐1 atrial myocytes hypertrophy. In conclusion, TWEAK/Fn14 axis mediates HL‐1 atrial myocytes hypertrophy partly through activation of the JAK2/STAT3 pathway.
Databáze: OpenAIRE