نتایج جستجو برای: nuclear hypertrophy

تعداد نتایج: 279538  

Journal: :Arteriosclerosis, thrombosis, and vascular biology 2007
Xiangbin Xu Chang-Hoon Ha Chelsea Wong Weiye Wang Angelika Hausser Klaus Pfizenmaier Eric N Olson Timothy A McKinsey Zheng-Gen Jin

BACKGROUND Angiotensin II (Ang II) induces the phenotypic modulation and hypertrophy of vascular smooth muscle cells (VSMCs), which is implicated in the pathogenesis of hypertension, atherosclerosis, and diabetes. In this study, we tested the hypothesis that histone deacetylases 5 (HDAC5) and its signal pathway play a role in Ang II-induced VSMC hypertrophy. METHODS AND RESULTS VSMCs were iso...

2014
Ci Chen Liang Shen Shiping Cao Xixian Li Wanling Xuan Jingwen Zhang Xiaobo Huang Jianping Bin Dingli Xu Guofeng Li Masafumi Kitakaze Yulin Liao

The gene ankyrin repeat domain 1 (Ankrd1) is an enigmatic gene and may exert pleiotropic function dependent on its expression level, subcellular localization and even types of pathological stress, but it remains unclear how these factors influence the fate of cardiomyocytes. Here we attempted to investigate the role of CARP on cardiomyocyte hypertrophy. In neonatal rat ventricular cardiomyocyte...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2006
Yasuyuki Tsujita John Muraski Isao Shiraishi Takahiro Kato Jan Kajstura Piero Anversa Mark A Sussman

The serine/threonine kinase Akt regulates cellular survival, proliferation, gene transcription, protein translation, metabolism, and differentiation. Although Akt substrates are found throughout the cell, activated Akt normally accumulates in the nucleus, suggesting that biologically relevant targets are located there. Consequences of nuclear Akt signaling in cardiomyocytes were explored by usi...

Journal: :Circulation 2014
Senka Ljubojevic Snjezana Radulovic Gerd Leitinger Simon Sedej Michael Sacherer Michael Holzer Claudia Winkler Elisabeth Pritz Tobias Mittler Albrecht Schmidt Michael Sereinigg Paulina Wakula Spyros Zissimopoulos Egbert Bisping Heiner Post Gunther Marsche Julie Bossuyt Donald M Bers Jens Kockskämper Burkert Pieske

BACKGROUND A hallmark of heart failure is impaired cytoplasmic Ca(2+) handling of cardiomyocytes. It remains unknown whether specific alterations in nuclear Ca(2+) handling via altered excitation-transcription coupling contribute to the development and progression of heart failure. METHODS AND RESULTS Using tissue and isolated cardiomyocytes from nonfailing and failing human hearts, as well a...

2017
Yuezhang Chen Jie Yuan Guoliang Jiang Jianbing Zhu Yunzeng Zou Qianzhou Lv

Previous studies have demonstrated that lercanidipine, a calcium channel blocker, may protect against cardiac hypertrophy; however, the underlying mechanisms remain unclear. In the present study, the effects of lercanidipine on hypertrophy and the mechanisms involved were investigated. Cardiomyocytes isolated from neonatal rats were cultured and treated with angiotensin II (Ang II) in the prese...

Journal: :Hypertension 2000
Y Aihara M Kurabayashi Y Saito Y Ohyama T Tanaka S Takeda K Tomaru K Sekiguchi M Arai T Nakamura R Nagai

CARP, a cardiac doxorubicin (adriamycin)-responsive protein, has been identified as a nuclear protein whose expression is downregulated in response to doxorubicin. In the present study, we tested the hypothesis that CARP serves as a reliable genetic marker of cardiac hypertrophy in vivo and in vitro. CARP expression was markedly increased in 3 distinct models of cardiac hypertrophy in rats: con...

2011
Ying Li Jian Ma Huaqing Zhu Manpreet Singh David Hill Peter A. Greer J. Malcolm Arnold E. Dale Abel Tianqing Peng

OBJECTIVE Recently we have shown that calpain-1 activation contributes to cardiomyocyte apoptosis induced by hyperglycemia. This study was undertaken to investigate whether targeted disruption of calpain would reduce myocardial hypertrophy and fibrosis in mouse models of type 1 diabetes. RESEARCH DESIGN AND METHODS Diabetes in mice was induced by injection of streptozotocin (STZ), and OVE26 m...

2017
Philipp Schlegel Julia Reinkober Eric Meinhardt Henrike Tscheschner Erhe Gao Sarah M Schumacher Ancai Yuan Johannes Backs Patrick Most Thomas Wieland Walter J Koch Hugo A Katus Philip W Raake

The increase in protein activity and upregulation of G-protein coupled receptor kinase 2 (GRK2) is a hallmark of cardiac stress and heart failure. Inhibition of GRK2 improved cardiac function and survival and diminished cardiac remodeling in various animal heart failure models. The aim of the present study was to investigate the effects of GRK2 on cardiac hypertrophy and dissect potential molec...

2012
Qinghang Liu Yi Chen Mannix Auger-Messier Jeffery D. Molkentin

Rationale: Both nuclear factors of activated T cells (NFAT) and nuclear factorB (NF B) are Rel homology domain (RHD)-containing transcription factors whose independent activities are critically involved in regulating cardiac hypertrophy and failure. Objective: To determine the potential functional interaction between NFAT and NF B signaling pathways in cardiomyocytes and its role in cardiac hyp...

Journal: :Circulation research 2012
Qinghang Liu Yi Chen Mannix Auger-Messier Jeffery D Molkentin

RATIONALE Both nuclear factors of activated T cells (NFAT) and nuclear factor-κB (NFκB) are Rel homology domain (RHD)-containing transcription factors whose independent activities are critically involved in regulating cardiac hypertrophy and failure. OBJECTIVE To determine the potential functional interaction between NFAT and NFκB signaling pathways in cardiomyocytes and its role in cardiac h...

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