Preliminary Investigation into the Mechanism of Cardiomyocyte Hypertrophy Induced by Visfatin_Journal of Biomedical Engineering

Authors：

LIJunli , LIAOYanbiao , LULihui , FENGJun , WUWenchao ,  LIUXiaojing

Laboratory of Cardiovascular Diseases, Regenerative Medicine Research Center, West China Hospital, Sichuan University, Chengdu 610041, China;

Corresponding author：

LIUXiaojing, Email: liuxq@scu.edu.cn

Keywords：

visfatin; cardiomyocyte hypertrophy; endoplasmic reticulum stress

DOI：

10.7507/1001-5515.20140071

Video：

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The aim of the current study is to investigate the effect of visfatin on cardiomyocyte hypertrophy. Cultured H9c2 cardiomyocytes were exposed to visfatin at different concentrations for different periods of time, and the markers of cardiomyocyte hypertrophy were detected. Moreover, pravastatin, the inhibitor of endoplasmic reticulum stress (ERS) or thapsigargin, an ERS agonist was used respectively to pre-treat the cells before visfatin stimulation. F-actin staining was performed to measure the cell surface change. The mRNA expressions of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP)and ERS markers including glucose-regulated protein 78(GRP78), C/EPB homologous protein (CHOP) and activating transcription factor 6 (ATF6) were assessed by real time RT-PCR. The change of protein level of GRP78 and CHOP was detected by Western blot. The experimental data demonstrated that exposure to 100 or 150 ng/mL concentrations of visfatin for 24 h, or 100 ng/mL of visfatin for 24 or 48 h, significantly increased the expression of markers for cardiomyocyte hypertrophy. Visfatin stimulation provoked ERS in H9c2 cells. Furthermore, pre-treatment with pravastatin partially inhibited the visfatin-induced mRNA expression of ANP and BNP in H9c2 cells, whereas thapsigargin promoted the visfatin-induced expression of cardiomyocyte hypertrophy markers. The results suggest that visfatin might induce cardiomyocyte hypertrophy via ERS -dependent pathways.

Citation： LIJunli, LIAOYanbiao, LULihui, FENGJun, WUWenchao, LIUXiaojing. Preliminary Investigation into the Mechanism of Cardiomyocyte Hypertrophy Induced by Visfatin. Journal of Biomedical Engineering, 2014, 31(2): 379-384. doi: 10.7507/1001-5515.20140071 Copy

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7.	JEONG K,KWON H,MIN C,et al.Modulation of the caveolin-3 localization to caveolae and STAT3 to mitochondria by catecholamine-induced cardiac hypertrophy in H9c2 cardiomyoblasts[J].Exp Mol Med,2009,41(4):226-235.
8.	WATKINS S J,BORTHWICK G M,ARTHUR H M.The H9c2 cell line and primary neonatal cardiomyocyte cells show similar hypertrophic responses in vitro[J].In Vitro Cell Dev Biol Anim,2011,47(2):125-131.
9.	ROMACHO T,AZCUTIA V,VAZQUEZ-BELLA M,et al.Extracellular PBEF/NAMPT/visfatin activates pro-inflammatory signalling in human vascular smooth muscle cells through nicotinamide phosphoribosyltransferase activity[J].Diabetologia,2009,52(11):2455-2463.
10.	BAE M K,SU-RYUN K,SOO-KYUNG B.Visfatin enhances ICAM-1 and VCAM-1 expression through ROS-dependent NF-kappa B activation in endothelial cells[J].Febs J,2009,276:187-188.
11.	DICKHOUT J G,CARLISLE R E,AUSTIN R C.Interrelationship between cardiac hypertrophy,heart failure,and chronic kidney disease endoplasmic reticulum stress as a mediator of pathogenesis[J].Circ Res,2011,108(5):629-642.
12.	CAKIR I,CYR N E,PERELLO M,et al.Obesity induces hypothalamic endoplasmic reticulum stress and impairs proopiomelanocortin (POMC) post-translational processing[J].J Biol Chem,2013,288(24):17675-17688.

1. FERNANNDEZ-TWⅡNN D S,BLACKMORE H L,SIGGENS L,et al.The programming of cardiac hypertrophy in the offspring by maternal obesity is associated with hyperinsulinemia,AKT,ERK,and mTOR activation[J].Endocrinology,2012,153(12):5961-5971.
2. FUKUHARA A,MATSUDA M,NISHIZAWA M,et al.Visfatin:a protein secreted by visceral fat that mimics the effects of insulin[J].Science,2005,307(5708):426-430.
3. USLU S,KEBAPC1 N,KARA M,et al.Relationship between adipocytokines and cardiovascular risk factors in patients with type 2 diabetes mellitus[J].Exp Ther Med,2012,4(1):113-120.
4. CHANG L,YANG R,WANG M,et al.Angiotensin Ⅱ type-1 receptor-JAK/STAT pathway mediates the induction of visfatin in angiotensin Ⅱ-induced cardiomyocyte hypertrophy[J].Am J Medi Sci,2012,343(3):220-226.
5. SCHULZE P C,BIOLO A,GOPAL D,et al.Dynamics in insulin resistance and plasma levels of adipokines in patients with acute decompensated and chronic stable heart failure[J].J Card Fail,2011,17(12):1004-1011.
6. MINAMINO T,KOMURO I,KITAKAZE M.Endoplasmic reticulum stress as a therapeutic target in cardiovascular disease[J].Circ Res,2010,107(9):1071-1082.
7. JEONG K,KWON H,MIN C,et al.Modulation of the caveolin-3 localization to caveolae and STAT3 to mitochondria by catecholamine-induced cardiac hypertrophy in H9c2 cardiomyoblasts[J].Exp Mol Med,2009,41(4):226-235.
8. WATKINS S J,BORTHWICK G M,ARTHUR H M.The H9c2 cell line and primary neonatal cardiomyocyte cells show similar hypertrophic responses in vitro[J].In Vitro Cell Dev Biol Anim,2011,47(2):125-131.
9. ROMACHO T,AZCUTIA V,VAZQUEZ-BELLA M,et al.Extracellular PBEF/NAMPT/visfatin activates pro-inflammatory signalling in human vascular smooth muscle cells through nicotinamide phosphoribosyltransferase activity[J].Diabetologia,2009,52(11):2455-2463.
10. BAE M K,SU-RYUN K,SOO-KYUNG B.Visfatin enhances ICAM-1 and VCAM-1 expression through ROS-dependent NF-kappa B activation in endothelial cells[J].Febs J,2009,276:187-188.
11. DICKHOUT J G,CARLISLE R E,AUSTIN R C.Interrelationship between cardiac hypertrophy,heart failure,and chronic kidney disease endoplasmic reticulum stress as a mediator of pathogenesis[J].Circ Res,2011,108(5):629-642.
12. CAKIR I,CYR N E,PERELLO M,et al.Obesity induces hypothalamic endoplasmic reticulum stress and impairs proopiomelanocortin (POMC) post-translational processing[J].J Biol Chem,2013,288(24):17675-17688.

Journal of Biomedical Engineering

Preliminary Investigation into the Mechanism of Cardiomyocyte Hypertrophy Induced by Visfatin

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