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AICAR and cardiomyocyte hypertrophy

Xiao-Yu Liu, Hai-Han Liao, Hong Feng, Nan Zhang, Jing-Jing Yang, Wen-Jing Li, Si Chen, Wei Deng, Qi-Zhu Tang
Icariside II (ICA II), a flavonoid derived from Epimediumbrevicormum Maxin in, has multiple biological activities in Chinese traditional medicine. Our study aimed to investigate the potential activity of ICA II against cardiac remodeling and the underlying mechanism. Mice received aorta banding (AB) or sham surgery, and then were randomly divided into ICA II or vehicle (veh) group for 6 weeks. After echocardiography and pressure-volume loop examination, hearts were harvested for histopathological analysis and molecular mechanism investigation...
September 4, 2018: Journal of Pharmacological Sciences
Yapeng Li, Dianhong Zhang, Lingyao Kong, Huiting Shi, Xinyu Tian, Lu Gao, Yuzhou Liu, Leiming Wu, Binbin Du, Zhen Huang, Cui Liang, Zheng Wang, Rui Yao, Yanzhou Zhang
Metabolic dysfunction is a hallmark of cardiac hypertrophy and heart failure. During cardiac failure, the metabolism of cardiomyocyte switches from fatty acid oxidation to glycolysis. However, the roles of key metabolic enzymes in cardiac hypertrophy are not understood fully. Here in the present work, we identified Aldolase A (AldoA) as a core regulator of cardiac hypertrophy. The mRNA and protein levels of AldoA were significantly up-regulated in transverse aortic constriction (TAC)- and isoproterenol (ISO)-induced hypertrophic mouse hearts...
September 1, 2018: Experimental Cell Research
Florence Mailleux, Christophe Beauloye, Jean-Luc Balligand, Sandrine Horman, Luc Bertrand
Pathological cardiac hypertrophy, which is a compensatory mechanism established to maintain cardiac function in response to neurohormonal or mechanical stresses, becomes maladaptive with time and frequently leads to heart failure. AMP-activated protein kinase (AMPK) has been extensively described in the literature to act as a break in cardiac hypertrophy development. Its anti-hypertrophic action mostly correlates with the inhibition of several important players of cardiac hypertrophy including protein synthesis and pro-hypertrophic gene expression pathways involving the transcription factor nuclear factor of activated T cells (NFAT) and the mitogen-activated protein kinases ERK1/2...
2018: Methods in Molecular Biology
Baolin Chen, Qiang Wu, Zhaojun Xiong, Yuedong Ma, Sha Yu, Dandan Chen, Shengwen Huang, Yugang Dong
Control of cardiac muscle mass is thought to be determined by a dynamic balance of protein synthesis and degradation. Recent studies have demonstrated that atrophy-related forkhead box O 3a (FOXO3a)/muscle atrophy F-box (MAFbx) signaling pathway plays a central role in the modulation of proteolysis and exert inhibitory effect on cardiomyocyte hypertrophy. In this study, we tested the hypothesis that adenosine monophosphate-activated protein kinase (AMPK) activation attenuates cardiomyocyte hypertrophy by regulating FOXO3a/MAFbx signaling pathway and its downstream protein degradation...
September 2016: Acta Biochimica et Biophysica Sinica
Sheng Xie, Yan Deng, Yue-Ying Pan, Jie Ren, Meng Jin, Yu Wang, Zhi-Hua Wang, Die Zhu, Xue-Ling Guo, Xiao Yuan, Jin Shang, Hui-Guo Liu
Autophagy is tightly regulated to maintain cardiac homeostasis. Impaired autophagy is closely associated with pathological cardiac hypertrophy. However, the relationship between autophagy and cardiac hypertrophy induced by chronic intermittent hypoxia (CIH) is not known. In the present study, we measured autophagy-related genes and autophagosomes during 10 weeks of CIH in rats, and 6 days in H9C2 cardiomyocytes, and showed that autophagy was impaired. This conclusion was confirmed by the autophagy flux assay...
September 15, 2016: Archives of Biochemistry and Biophysics
Zhenhua Zeng, Qiuju Huang, Zhaohui Shu, Peiqing Liu, Shaorui Chen, Xuediao Pan, Linquan Zang, Sigui Zhou
Short-chain acyl-CoA dehydrogenase (SCAD), a key enzyme of fatty acid β-oxidation, plays an important role in cardiac hypertrophy. However, its effect on the cardiomyocyte apoptosis remains unknown. We aimed to determine the role of SCAD in tert-butyl hydroperoxide (tBHP)-induced cardiomyocyte apoptosis. The mRNA and protein expression of SCAD were significantly down-regulated in the cardiomyocyte apoptosis model. Inhibition of SCAD with siRNA-1186 significantly decreased SCAD expression, enzyme activity and ATP content, but obviously increased the content of free fatty acids...
July 2016: Journal of Cellular and Molecular Medicine
Ke Yang, Xinli Xu, Ling Nie, Tangli Xiao, Xu Guan, Ting He, Yanlin Yu, Liang Liu, Yunjian Huang, Jingbo Zhang, Jinghong Zhao
As a typical protein-bound uremic toxin, indoxyl sulfate is considered to be able to induce cardiomyocytes hypertrophy by promoting oxidative stress in chronic kidney disease (CKD). Uncoupling protein 2 (UCP2), a member of the uncoupling protein family, may protect cardiomyocytes from oxidative stress by suppressing mitochondrial reactive oxygen species (ROS). In the present study, we aimed to determine whether UCP2 was involved in indoxyl sulfate-induced cardiomyocytes hypertrophy. We demonstrated that indoxyl sulfate could increase the ROS levels in a time and dose-dependent manner in cultured neonatal rat cardiomyocytes...
April 16, 2015: Toxicology Letters
Jiaojiao Wang, Zhiping Liu, Xiaojun Feng, Si Gao, Suowen Xu, Peiqing Liu
Cardiac hypertrophy, an adaptive growth process that occurs in response to various pathophysiological stimuli, constitutes an important risk factor for the development of heart failure. However, the molecular mechanisms that regulate this cardiac growth response are not completely understood. Here we revealed that ING3 (inhibitor of growth family, member 3), a type II tumor suppressor, plays a critical role in the regulation of cardiac hypertrophy. ING3 expression was present in relatively high abundance in the heart, and was prominently upregulated in hypertrophic agonists angiotensin II (Ang II), phenylephrine (PE), or isoproterenol (ISO)-stimulated cardiomyocytes and in hearts of rat undergoing abdominal aortic constriction (AAC) surgery...
November 15, 2014: Archives of Biochemistry and Biophysics
Yanh Li, Cong Chen, Fengj Yao, Qiao Su, Dan Liu, Ruic Xue, Gang Dai, Rong Fang, Juny Zeng, Yil Chen, Huil Huang, Yued Ma, Wenw Li, Lil Zhang, Chen Liu, Yug Dong
AMPK, a serine/threonine protein kinase, has proven to be an important positive regulator of autophagy, which is a key factor in the regulation of cardiac hypertrophy. Thus, we explored whether AMPK could inhibit cardiac hypertrophy by regulating autophagy. In pressure overload induced cardiac hypertrophy, decreased autophagy was detected. Administration of AMPK activators (AICAR and metformin) significantly blocked hypertrophy, accompanied by enhanced autophagy level in the hearts. Furthermore, AMPK activation resulted in enhanced autophagosome formation and unimpaired lysosomal function...
September 15, 2014: Archives of Biochemistry and Biophysics
Yukiko Hasumi, Masaya Baba, Hisashi Hasumi, Ying Huang, Martin Lang, Rachel Reindorf, Hyoung-bin Oh, Sebastiano Sciarretta, Kunio Nagashima, Diana C Haines, Michael D Schneider, Robert S Adelstein, Laura S Schmidt, Junichi Sadoshima, W Marston Linehan
Cardiac hypertrophy, an adaptive process that responds to increased wall stress, is characterized by the enlargement of cardiomyocytes and structural remodeling. It is stimulated by various growth signals, of which the mTORC1 pathway is a well-recognized source. Here, we show that loss of Flcn, a novel AMPK-mTOR interacting molecule, causes severe cardiac hypertrophy with deregulated energy homeostasis leading to dilated cardiomyopathy in mice. We found that mTORC1 activity was upregulated in Flcn-deficient hearts, and that rapamycin treatment significantly reduced heart mass and ameliorated cardiac dysfunction...
November 1, 2014: Human Molecular Genetics
Yingmei Zhang, Shou-Ling Mi, Nan Hu, Thomas A Doser, Aijun Sun, Junbo Ge, Jun Ren
Cardiac aging is associated with compromised myocardial function and morphology although the underlying mechanism remains elusive. Aldehyde dehydrogenase 2 (ALDH2), an essential mitochondrial enzyme governing cardiac function, displays polymorphism in humans. This study was designed to examine the role of ALDH2 in aging-induced myocardial anomalies. Myocardial mechanical and intracellular Ca(2+) properties were examined in young (4-5 months) and old (26-28 months) wild-type and ALDH2 transgenic mice. Cardiac histology, mitochondrial integrity, O2(-) generation, apoptosis, and signaling cascades, including AMPK activation and Sirt1 level were evaluated...
June 2014: Free Radical Biology & Medicine
John T Fassett, Xinli Hu, Xin Xu, Zhongbing Lu, Ping Zhang, Yingjie Chen, Robert J Bache
Cell hypertrophy requires increased protein synthesis and expansion of the cytoskeletal networks that support cell enlargement. AMPK limits anabolic processes, such as protein synthesis, when energy supply is insufficient, but its role in cytoskeletal remodeling is not known. Here, we examined the influence of AMPK in cytoskeletal remodeling during cardiomyocyte hypertrophy, a clinically relevant condition in which cardiomyocytes enlarge but do not divide. In neonatal cardiomyocytes, activation of AMPK with 5-aminoimidazole carboxamide ribonucleotide (AICAR) or expression of constitutively active AMPK (CA-AMPK) attenuated cell area increase by hypertrophic stimuli (phenylephrine)...
March 1, 2013: American Journal of Physiology. Heart and Circulatory Physiology
Sandra Marisa Oliveira, Yin-Hua Zhang, Raquel Sancho Solis, Henrik Isackson, Mohamed Bellahcene, Arash Yavari, Katalin Pinter, Joanna K Davies, Ying Ge, Houman Ashrafian, Jeffery W Walker, David Carling, Hugh Watkins, Barbara Casadei, Charles Redwood
RATIONALE: AMP-activated protein kinase (AMPK) is an important regulator of energy balance and signaling in the heart. Mutations affecting the regulatory γ2 subunit have been shown to cause an essentially cardiac-restricted phenotype of hypertrophy and conduction disease, suggesting a specific role for this subunit in the heart. OBJECTIVE: The γ isoforms are highly conserved at their C-termini but have unique N-terminal sequences, and we hypothesized that the N-terminus of γ2 may be involved in conferring substrate specificity or in determining intracellular localization...
April 27, 2012: Circulation Research
Rongsen Meng, Zhaohui Pei, Aixia Zhang, Yutian Zhou, Xingming Cai, Baolin Chen, Guanjie Liu, Weiyi Mai, Jianrui Wei, Yugang Dong
Activation of adenosine monophosphate-activated protein kinase (AMPK) has been shown to inhibit cardiac hypertrophy through peroxisome proliferators-activated receptor-α (PPARα) signaling pathway, but the detailed mechanism remains unclear. A rat model of cardiac hypertrophy created by transaortic constriction (TAC) was used to investigate the mechanism involved in regulation of PPARα activity by AMPK. It was observed that treatment with AICAR (5-aminoimidazole 1 carboxamide ribonucleoside), an AMPK activator, significantly inhibited cardiac hypertrophy in vivo and in vitro...
July 2011: Archives of Biochemistry and Biophysics
Bao-lin Chen, Yue-dong Ma, Rong-sen Meng, Zhao-jun Xiong, Hai-ning Wang, Jun-yi Zeng, Chen Liu, Yu-gang Dong
AIM: To examine the inhibitory effects of adenosine monophosphate-activated protein kinase (AMPK) activation on cardiac hypertrophy in vitro and to investigate the underlying molecular mechanisms. METHODS: Cultured neonatal rat cardiomyocytes were treated with the specific AMPK activator 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) and the specific AMPK antagonist Compound C, and then stimulated with phenylephrine (PE). The Muscle RING finger 1 (MuRF1)-small interfering RNA (siRNA) was transfected into cardiomyocytes using Lipofectamine 2000...
July 2010: Acta Pharmacologica Sinica
Rong-Sen Meng, Zhao-Hui Pei, Ran Yin, Cheng-Xi Zhang, Bao-Lin Chen, Yang Zhang, Dan Liu, An-Long Xu, Yu-Gang Dong
The activation of adenosine monophosphate (AMP)-activated protein kinase (AMPK) has been shown to inhibit cardiac hypertrophy, however, the mechanism remains unclear. Rat models of cardiac hypertrophy were created with transaortic constriction (TAC) to investigate the mechanistic role of AMPK involved. RT-PCR and Western blot analyses indicated that hypertrophy marker genes ANP and beta-MHC expression were up-regulated in the myocardium of TAC rats. We also observed that the expressions of peroxisome proliferator-activated receptor-alpha (PPARalpha) and its target genes, carnitine palmitoyl transferase-capital I, Ukrainian (CPT-capital I, Ukrainian) and medium-chain acyl-COA dehydrogenases (MCAD), were down-regulated, and the fatty acid oxidation was decreased in TAC rats...
October 12, 2009: European Journal of Pharmacology
Sabzali Javadov, Venkatesh Rajapurohitam, Ana Kilić, Asad Zeidan, Angel Choi, Morris Karmazyn
Although Na(+)-H(+) exchanger 1 (NHE-1) inhibition has been demonstrated to have anti-hypertrophic effect indirectly through mitochondria, the detailed cellular mechanisms mediating this effect remain elusive. In this study we sought to determine whether NHE-1 inhibition exerts an anti-hypertrophic effect by modulating the mitochondrial permeability transition pore (mPTP) opening through the AMP-activated protein kinase (AMPK)/glycogen synthase kinase 3beta (GSK-3beta) pathway during hypertrophy in cardiomyocytes...
June 2009: Journal of Molecular and Cellular Cardiology
Jaetaek Kim, Adam R Wende, Sandra Sena, Heather A Theobald, Jamie Soto, Crystal Sloan, Benjamin E Wayment, Sheldon E Litwin, Martin Holzenberger, Derek LeRoith, E Dale Abel
The receptors for IGF-I (IGF-IR) and insulin (IR) have been implicated in physiological cardiac growth, but it is unknown whether IGF-IR or IR signaling are critically required. We generated mice with cardiomyocyte-specific knockout of IGF-IR (CIGF1RKO) and compared them with cardiomyocyte-specific insulin receptor knockout (CIRKO) mice in response to 5 wk exercise swim training. Cardiac development was normal in CIGF1RKO mice, but the hypertrophic response to exercise was prevented. In contrast, despite reduced baseline heart size, the hypertrophic response of CIRKO hearts to exercise was preserved...
November 2008: Molecular Endocrinology
Bettina Johanna Stuck, Matthias Lenski, Michael Böhm, Ulrich Laufs
Angiotensin II induces cardiomyocyte hypertrophy, but its consequences on cardiomyocyte metabolism and energy supply are not completely understood. Here we investigate the effect of angiotensin II on glucose and fatty acid utilization and the modifying role of AMP-activated protein kinase (AMPK), a key regulator of metabolism and proliferation. Treatment of H9C2 cardiomyocytes with angiotensin II (Ang II, 1 microm, 4 h) increased [(3)H]leucine incorporation, up-regulated the mRNA expression of the hypertrophy marker genes MLC, ANF, BNP, and beta-MHC, and decreased the phosphorylation of the negative mTOR-regulator tuberin (TSC-2)...
November 21, 2008: Journal of Biological Chemistry
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