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The Role of Human Antigen R (HuR) in Pathological Cardiac RemodelingGreen, Lisa 24 May 2022 (has links)
No description available.
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Class III PI3K-Mediated Prolonged Activation of Autophagy Plays a Critical Role in the Transition of Cardiac Hypertrophy to Heart FailureYu, Peng, Zhang, Yangyang, Li, Chuanfu, Li, Yuehua, Jiang, Surong, Zhang, Xiaojin, Ding, Zhengnian, Tu, Fei, Wu, Jun, Gao, Xiang, Li, Liu 01 July 2015 (has links)
Pathological cardiac hypertrophy often leads to heart failure. Activation of autophagy has been shown in pathological hypertrophic hearts. Autophagy is regulated positively by Class III phosphoinositide 3-kinase (PI3K). However, it is unknown whether Class III PI3K plays a role in the transition of cardiac hypertrophy to heart failure. To address this question, we employed a previously established cardiac hypertrophy model in heat shock protein 27 transgenic mice which shares common features with several types of human cardiomyopathy. Age-matched wild-type mice served as control. Firstly, a prolonged activation of autophagy, as reflected by autophagosome accumulation, increased LC3 conversion and decreased p62 protein levels, was detected in hypertrophic hearts from adaptive stage to maladaptive stage. Moreover, morphological abnormalities in myofilaments and mitochondria were presented in the areas accumulated with autophagosomes. Secondly, activation of Class III PI3K Vacuolar protein sorting 34 (Vps34), as demonstrated by upregulation of Vps34 expression, increased interaction of Vps34 with Beclin-1, and deceased Bcl-2 expression, was demonstrated in hypertrophic hearts from adaptive stage to maladaptive stage. Finally, administration with Wortmaninn, a widely used autophagy inhibitor by suppressing Class III PI3K activity, significantly decreased autophagy activity, improved morphologies of intracellular apartments, and most importantly, prevented progressive cardiac dysfunction in hypertrophic hearts. Collectively, we demonstrated that Class III PI3K plays a central role in the transition of cardiac hypertrophy to heart failure via a prolonged activation of autophagy in current study. Class III PI3K may serve as a potential target for the treatment and management of maladaptive cardiac hypertrophy.
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Tollip Attenuated the Hypertrophic Response of Cardiomyocytes Induced by IL-1betaHu, Yulong, Li, Ting, Wang, Yongmei, Li, Jing, Guo, Lin, Wu, Meiling, Shan, Xiaohong, Que, Lingli, Ha, Tuanzhu, Chen, Qi, Kelley, Jim, Li, Yuehua 01 January 2009 (has links)
We examined the role of Tollip in the hypertrophic response of cardiomyocytes. C57BL/6 mice were subjected to transverse aortic constriction (TAC) for 2 weeks and age-matched sham surgical operated mice served as control. TAC significantly reduced the association of Tollip with IRAK-1 by 66.4 percent and increased NF-kappaB binding activity by 86.5 percent and the levels of phosphop38 by 114.6 percent in the myocardium compared with sham control, respectively. In vitro experiments showed that IL-1beta stimulation also significantly reduced the association of Tollip with IRAK-1 and increased NFkappaB binding activity in neonatal cardiomyocytes. Tollip overexpression by transfection of cardiac myocytes significantly attenuated the IL-1beta-induced hypertrophic response of cardiac myocytes as evidenced by reduced cell size (16.4 percent) and decreased ANP expression (33.3 percent). Overexpression of Tollip also reduced NFkappaB binding activity by 30.7 percent and phospho-p38 by 47.1 percent, respectively. The results suggest that Tollip could be a negative regulator during the development of cardiac hypertrophy. The negative regulation of cardiac hypertrophy by Tollip may involve downregulation of the MyD88-dependent NF-kappaB activation pathway.
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Reduced Cardiac Hypertrophy in Toll-Like Receptor 4-Deficient Mice Following Pressure OverloadHa, Tuanzhu, Li, Yuehua, Hua, Fang, Ma, Jinag, Gao, Xiang, Kelley, Jim, Zhao, Aiqiu, Haddad, Georges E., Williams, David L., Browder, I. William, Kao, Race L., Li, Chuanfu 01 November 2005 (has links)
Objective: We have previously demonstrated that nuclear factor kappa B (NFκB) activation is needed for the development of cardiac hypertrophy in vivo. NFκB is a downstream transcription factor in the Toll-like receptor (TLR)-mediated signaling pathway; therefore, we investigated a role of TLR4 in cardiac hypertrophy in vivo. Methods: TLR4-deficient mice (C.C3H-Tlr4 lps-d, n = 6), wild-type (WT) genetic background mice (BALB/c, n = 6), TLR4-deleted strain (C57BL/10ScCr, n = 8), and WT controls (C57BL/10ScSn, n = 8) were subjected to aortic banding for 2 weeks. Age-matched surgically operated mice served as controls. In a separate experiment, rapamycin (2 mg/kg, daily) was administered to TLR4-deficient mice and WT mice immediately following aortic banding. The ratio of heart weight/body weight (HW / BW) was calculated, and cardiac myocyte size was examined by FITC-labeled wheat germ agglutinin staining of membranes. NFκB binding activity and the levels of phospho-p70S6K in the myocardium were also examined. Results: Aortic banding significantly increased the ratio of HW / BW by 33.9% (0.601 ± 0.026 vs. 0.449 ± 0.004) and cell size by 68.4% in WT mice and by 10.00% (0.543 ± 0.011 vs. 0.495 ± 0.005) and by 11.8% in TLR4-deficient mice, respectively, compared with respective sham controls. NFκB binding activity and phospho-p70S6K levels were increased by 182.6% and 115.2% in aortic-banded WT mice and by 78.0% and 162.0% in aortic-banded TLR4-deficient mice compared with respective sham controls. In rapamycin-treated aortic-banded mice, the ratio of HW / BW was increased by 18.0% in WT mice and by 3.5% in TLR4-deficient mice compared with respective sham controls. Conclusion: Our results demonstrate that TLR4 is a novel receptor contributing to the development of cardiac hypertrophy in vivo and that both the TLR4-mediated pathway and PI3K/Akt/mTOR signaling are involved in the development of cardiac hypertrophy in vivo.
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The Role of Tsg101 in the Development of Physiological Cardiac Hypertrophy and Cardio-Protection from Endotoxin-Induced Cardiac DysfunctionEssandoh, Kobina 19 November 2019 (has links)
No description available.
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TRANSCRIPTIONAL REGULATION OF CARDIAC HYPERTROPHY AND HEART FAILUREXU, JIAN 13 July 2006 (has links)
No description available.
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The Role of Profilin1 Gene in the Development of Cardiovascular Diseases: Insights From Profilin1 Transgenic Mouse ModelHessein Hassona, Mohamed Darwish January 2010 (has links)
No description available.
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Transplanted embryonic stem cells inhibit cardiac fibrosis and hypertrophy in type 1 diabetesAbrahan, Dennrik 01 January 2009 (has links)
Cell therapy is a novel potential approach to treat many diseases including diabetes. Embryonic stem cells have been examined in various diabetic and non-diabetic heart studies. However, the role of pancreas transcription factor 1 alpha (ptfla) over expressing embryonic stem (ES) cells has not been defined. We hypothesize that transplanted over expressing ptfla-ES cells in streptozotocin (STZ) induced diabetic mice will attenuate cardiac hypertrophy, fibrosis, and improve cardiac function. In this investigation we divided C57/bl6 mice into three groups: Control, STZ, and STZ + ptflaES cells. Diabetes was induced with STZ (lO0mg/kg, body weight), with two separate injections on day 1 (D1) and D2. Following STZ injections, mice were transplanted with 1.2 million ptfla-ES cells in three days. Control group received normal saline. After injections, animals were examined for glucose levels, cardiac hypertrophy, fibrosis, and heart function. Our data shows that glucose levels were significantly increased following STZ injections, suggesting diabetes, and this increase was reversed with transplanted ptfl a-ES cell. Our H&E qualitative data suggest that there was increase in cardiac hypertrophy in STZ-induced diabetic animals compared with control. Moreover, Massan's trichrome staining shows increased amount of cardiac fibrosis in STZ-induced diabetic animals compared with control. This data suggests that animals have developed diabetic cardiomyopathy. Interestingly, the increased cardiac hypertrophy and fibrosis was attenuated in the animals transplanted with ptfl a-ES cells. Furthermore, cardiac function examined by echocardiography was reduced in the STZ treated animals which was reversed following ptfla-ES cell treatment. In conclusion, our data suggests that
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Einfluss körperlichen Übergewichts auf die Entwicklung einer kardialen Hypertrophie und die kardialen Umbauprozesse nach experimenteller Myokardischämie / Impact of overweight on the development of cardiac hypertrophy and cardiac remodeling resulting from myocardial infarctionBremen, Eva Sabine 19 October 2011 (has links)
No description available.
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Effet de l'hypertrophie cardiaque physiologique et pathologique sur la régulation du pore de perméabilité transitionnelleMarcil, Mariannick January 2008 (has links)
Thèse numérisée par la Division de la gestion de documents et des archives de l'Université de Montréal.
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