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Transverse aortic constriction

Xuelian Li, GuoYuan Wang, MuGe QiLi, HaiHai Liang, TianShi Li, XiaoQiang E, Ying Feng, Ying Zhang, Xiao Liu, Ming Qian, BoZhi Xu, ZhiHang Shen, Samuel Chege Gitau, DanDan Zhao, HongLi Shan
BACKGROUND/AIMS: Cardiac interstitial fibrosis is an abnormality of various cardiovascular diseases, including myocardial infarction, hypertrophy, and atrial fibrillation, and it can ultimately lead to heart failure. However, there is a lack of practical therapeutic approaches to treat fibrosis and reverse the damage to the heart. The purpose of this study was to investigate the effect of long-term aspirin administration on pressure overload-induced cardiac fibrosis in mice and reveal the underlying mechanisms of aspirin treatment...
March 2, 2018: Cellular Physiology and Biochemistry
Lifang Lv, Tianyu Li, Xuelian Li, Chaoqian Xu, Qiushuang Liu, Hua Jiang, Yingnan Li, Yingqi Liu, He Yan, Qihe Huang, Yuhong Zhou, Mingyu Zhang, Hongli Shan, Haihai Liang
Cardiac hypertrophy accompanied by maladaptive cardiac remodeling is the uppermost risk factor for the development of heart failure. Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have various biological functions, and their vital role in the regulation of cardiac hypertrophy still needs to be explored. In this study, we demonstrated that lncRNA Plscr4 was upregulated in hypertrophic mice hearts and in angiotensin II (Ang II)-treated cardiomyocytes. Next, we observed that overexpression of Plscr4 attenuated Ang II-induced cardiomyocyte hypertrophy...
March 2, 2018: Molecular Therapy. Nucleic Acids
Qing Liu, Hui Hu, Tingting Hu, Ting Han, Ahui Wang, Lijie Huang, Qiwen Tan, Wen Tan
Right heart failure and pulmonary artery remodeling resulting from increased left heart pressure are prevalent in a clinical setting, and the specific pathological feature exhibits cancer-like cell proliferation in lung. STVNa has been previously demonstrated its anti-proliferation property. In this study, we want to verify the therapeutic effect of STVNa against right ventricle hypertrophy and pulmonary artery remodeling in rats induced by transverse aortic constriction (TAC). The results show that TAC surgery increased mean right ventricle pressure (mRVP) less in the STVNa group than that in the vehicle group (11...
February 27, 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
Yongzheng Guo, Zhen Wang, Xinghua Qin, Jie Xu, Zuoxu Hou, Hongyan Yang, Xuechao Mao, Wenjuan Xing, Xiaoliang Li, Xing Zhang, Feng Gao
Aims: Heart failure is characterized by reduced fatty acid (FA) utilization associated with mitochondrial dysfunction. Recent evidence has shown that enhancing FA utilization may provide cardioprotection against heart failure. Our aim was to investigate the effects and the underlying mechanisms of cardiac FA utilization on cardiac function in response to pressure overload. Methods and Results: Transverse aortic constriction (TAC) was used in C57 mice to establish pressure overload-induced heart failure...
February 27, 2018: Cardiovascular Research
Peter P Rainer, Peihong Dong, Matteo Sorge, Justyna Fert-Bober, Ronald J Holewinski, Yuchuan Wang, Catherine Foss, Steven S An, Alessandra Baracca, Giancarlo Solaini, Charles Glabe, Martin G Pomper, Jennifer E Van Eyk, Gordon F Tomaselli, Nazareno Paolocci, Giulio Agnetti
<u>Rationale:</u> Disrupted proteostasis is one major pathological trait that heart failure (HF) shares with other organ proteinopathies, such as Alzheimer's and Parkinson's diseases. Yet, differently from the latter, whether and how cardiac preamyloid oligomers (PAOs) develop in acquired forms of HF is unclear. <u>Objective:</u> We previously reported a rise in mono-phosphorylated, aggregate-prone desmin in canine and human HF. We now tested if mono-phosphorylated desmin acts as the seed nucleating PAOs formation and determined if positron emission tomography (PET) is able to detect myocardial PAOs in non-genetic HF...
February 26, 2018: Circulation Research
Arti V Shinde, Ya Su, Brad A Palanski, Kana Fujikura, Mario J Garcia, Nikolaos G Frangogiannis
Tissue transglutaminase (tTG) is a multifunctional protein with a wide range of enzymatic and non-enzymatic functions. We have recently demonstrated that tTG expression is upregulated in the pressure-overloaded myocardium and exerts fibrogenic actions promoting diastolic dysfunction, while preventing chamber dilation. Our current investigation dissects the in vivo and in vitro roles of the enzymatic effects of tTG on fibrotic remodeling in pressure-overloaded myocardium. Using a mouse model of transverse aortic constriction, we demonstrated perivascular and interstitial tTG activation in the remodeling pressure-overloaded heart...
February 23, 2018: Journal of Molecular and Cellular Cardiology
Simon M Bryant, Cherrie H T Kong, Judy J Watson, Hanne C Gadeberg, Andrew F James, Mark B Cannell, Clive H Orchard
BACKGROUND: Previous work has shown redistribution of L-type Ca current (ICa ) from the t-tubules to the surface membrane of rat ventricular myocytes following myocardial infarction. However, whether this occurs in all species and in response to other insults, the relationship of this redistribution to the severity of the pathology, and the underlying mechanism, are unknown. We have therefore investigated the response of mouse hearts and myocytes to pressure overload induced by transverse aortic constriction (TAC)...
February 23, 2018: Experimental Physiology
Soichi Sano, Kosei Oshima, Ying Wang, Susan MacLauchlan, Yasufumi Katanasaka, Miho Sano, María A Zuriaga, Minoru Yoshiyama, David Goukassian, Matthew A Cooper, José J Fuster, Kenneth Walsh
BACKGROUND: Recent studies have shown that hematopoietic stem cells can undergo clonal expansion secondary to somatic mutations in leukemia-related genes, thus leading to an age-dependent accumulation of mutant leukocytes in the blood. This somatic mutation-related clonal hematopoiesis is common in healthy older individuals, but it has been associated with an increased incidence of future cardiovascular disease. The epigenetic regulator TET2 is frequently mutated in blood cells of individuals exhibiting clonal hematopoiesis...
February 27, 2018: Journal of the American College of Cardiology
Ilona Schirmer, Tippaporn Bualeong, Heidi Budde, Diana Cimiotti, Avinash Appukuttan, Nicole Klein, Philip Steinwascher, Peter Reusch, Andreas Mügge, Rainer Meyer, Yury Ladilov, Kornelia Jaquet
AIMS: In contrast to the membrane bound adenylyl cyclases, the soluble adenylyl cyclase (sAC) is activated by bicarbonate and divalent ions including calcium. sAC is located in the cytosol, nuclei and mitochondria of several tissues including cardiac muscle. However, its role in cardiac pathology is poorly understood. Here we investigate whether sAC is involved in hypertrophic growth using two different model systems. METHODS AND RESULTS: In isolated adult rat cardiomyocytes hypertrophy was induced by 24 h β1-adrenoceptor stimulation using isoprenaline (ISO) and a β2-adrenoceptor antagonist (ICI118,551)...
2018: PloS One
Wei Sheng Tan, Thomas P Mullins, Melanie Flint, Sarah L Walton, Helle Bielefeldt-Ohmann, David A Carter, Meera R Gandhi, Hayley R McDonald, Joan Li, Karen M Moritz, Melissa E Reichelt, Linda A Gallo
There is an increased incidence of heart failure in individuals with diabetes mellitus (DM). The co-existence of kidney disease in DM exacerbates the cardiovascular prognosis. Researchers have attempted to combine the critical features of heart failure, using transverse aortic constriction, with DM in mice but variable findings have been reported. Furthermore, kidney outcomes have not been assessed in this setting thus its utility as a model of heart failure in DM and kidney disease is unknown. We generated a mouse model of obesity, hyperglycemia and mild kidney pathology by feeding male C57BL/6J mice a high fat diet (HFD)...
February 14, 2018: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
Su Ming, Wang Shui-Yun, Qiu Wei, Li Jian-Hui, Hui Ru-Tai, Song Lei, Jia Mei, Wang Hui, Wang Ji-Zheng
Hypertrophic cardiomyopathy (HCM) is a serious monogenic disease characterized by cardiac hypertrophy, fibrosis, sudden cardiac death and heart failure. Previously, we identified that miR-139-5p was downregulated in HCM patients. However, the regulatory effects of miR-139-5p remain unclear. Thus, we investigated the role of miR-139-5p in the regulation of cardiac hypertrophy. The expression of miR-139-5p in left ventricular tissues in HCM patients and mice subjected to transverse aortic constriction (TAC) was significantly downregulated...
February 12, 2018: Bioscience Reports
Cheng-Lin Zhang, Qian Zhao, Hui Liang, Xue Qiao, Jin-Yu Wang, Dan Wu, Li-Ling Wu, Li Li
Cardiac fibrosis is characterized by excessive deposition of extracellular matrix (ECM) proteins in the myocardium and results in decreased ventricular compliance and diastolic dysfunction. Cartilage intermediate layer protein-1 (CILP-1), a novel identified cardiac matricellular protein, is upregulated in most conditions associated with cardiac remodeling, however, whether CILP-1 is involved in pressure overload-induced fibrotic response is unknown. Here, we investigated whether CILP-1 was critically involved in the fibrotic remodeling induced by pressure overload...
February 10, 2018: Journal of Molecular and Cellular Cardiology
Yue Ji, Ming Qiu, Yejiao Shen, Li Gao, Yaqing Wang, Wei Sun, Xinli Li, Yan Lu, Xiangqing Kong
MicroRNA (miRNA/miR) dysregulation has been reported to be fundamental in the development and progression of cardiac hypertrophy and fibrosis. In the present study, miR-327 levels in fibroblasts were increased in response to cardiac hypertrophy induced by transverse aortic constriction with prominent cardiac fibrosis, particularly when compared with the levels in unstressed cardiomyocytes. In neonatal rat cardiac fibroblasts, induced expression of miR-327 upregulated fibrosis-associated gene expression and activated angiotensin II-induced differentiation into myofibroblasts, as assessed via α-smooth muscle actin staining...
January 25, 2018: International Journal of Molecular Medicine
Ryan Lahey, Andrew N Carley, Xuerong Wang, Carley E Glass, Kevin Accola, Scott C Silvestry, J M O'Donnell, E Douglas Lewandowski
Rationale: Metabolic remodeling in hypertrophic hearts includes inefficient glucose oxidation via increased anaplerosis fueled by pyruvate carboxylation. Pyruvate carboxylation to malate through elevated malic enzme-1 (ME1) consumes NADPH necessary for reduction of glutathione and maintenance of intracellular redox state. Objective: To elucidate upregulated ME1 as a potential maladaptive mechanism for inefficient glucose oxidation and compromised redox state in hypertrophied hearts. Methods and Results: ME1 expression was selectively inhibited, in vivo, via non-native miRNA specific to ME1 (miR-ME1) in pressure-overloaded rat hearts...
January 31, 2018: Circulation Research
Juan Tang, Hui Zhang, Lingjuan He, Xiuzhen Huang, Yan Li, Wenjuan Pu, Wei Yu, Libo Zhang, Dongqing Cai, Kathy O Lui, Bin Zhou
<u>Rationale:</u> Endocardium is the major source of coronary endothelial cells in the fetal and neonatal hearts. It remains unclear whether endocardium in the adult stage is also the main origin of neovascularization after cardiac injury. <u>Objective:</u> To define the vascular potential of adult endocardium in homeostasis and after cardiac injuries by fate mapping studies. <u>Methods and Results:</u> We generate an inducible adult endocardial Cre line ( Npr3-CreER ) and show that Npr3-CreER efficiently and specifically labels endocardial cells but not coronary blood vessels in the adult heart...
January 26, 2018: Circulation Research
Rong-Rong Zhao, Matthew Ackers-Johnson, Justus Stenzig, Chen Chen, Tao Ding, Yue Zhou, Peipei Wang, Shi Ling Ng, Peter Y Li, Gavin Teo, Pauline M Rudd, James W Fawcett, Roger S Y Foo
Background -Heart failure (HF) is a leading cause of mortality and morbidity, and the search for novel therapeutic approaches continues. In the monogenic disease mucopolysaccharidosis (MPS) VI, loss of function mutations in arylsulfatase B (ASB) leads to myocardial accumulation of chondroitin sulfate (CS) glycosaminoglycans (GAGs), manifesting as a myriad of cardiac symptoms. Here, we studied changes in myocardial CS in non-MPS failing hearts, and assessed its generic role in pathological cardiac remodeling...
January 25, 2018: Circulation
Bianca C Bernardo, Kate L Weeks, Thawin Pongsukwechkul, Xiaoming Gao, Helen Kiriazis, Nelly Cemerlang, Esther Jh Boey, Yow Keat Tham, Chad J Johnson, Hongwei Qian, Xiao-Jun Du, Paul Gregorevic, Julie R McMullen
We previously showed that medium chain acyl-coenzyme A dehydrogenase (MCAD, key regulator of fatty acid oxidation) is positively modulated in the heart by the cardioprotective kinase, phosphoinositide 3-kinase [PI3K(p110α)]. Disturbances in cardiac metabolism are a feature of heart failure patients, and targeting metabolic defects is considered a potential therapeutic approach. The specific role of MCAD in the adult heart is unknown. To examine the role of MCAD in the heart and to assess the therapeutic potential of increasing MCAD in the failing heart, we developed a gene therapy tool using recombinant adeno-associated viral vectors (rAAV) encoding MCAD...
January 22, 2018: Clinical Science (1979-)
Fatih Yalcin, Nagehan Kucukler, Oscar H Cingolani, Blaid Mbiyangandu, Lars Sorensen, Aurelio Pinherio, Roselle Abraham, Theodore P Abraham
LEFT VENTRICULAR HYPERTROPHY (LVH) is an adaptive response to physiologic or pathologic stimuli and distinguishing between the two has obvious clinical implications. However, asymmetric septal hypertrophy and preserved cardiac function are noted in early stages in both cases. We characterized the early anatomic and functional changes in a mouse model of physiologic and pathologic stress using serial echocardiography-based morphometry and tissue velocity imaging. Weight-matched CF-1 male mice were separated into CONTROLS (n=10), treadmill EXERCISE 1 hour daily x 5 days/week (n=7) and transverse aortic constriction (TAC, n=7)...
January 4, 2018: Journal of Applied Physiology
D M Schwab, L Tilemann, R Bauer, M Heckmann, A Jungmann, M Wagner, J Burgis, C Vettel, H A Katus, A El-Armouche, O J Müller
The downregulation of β-adrenergic receptors (β-AR) and decreased cAMP-dependent protein kinase activity in failing hearts results in decreased phosphorylation and inactivation of phosphatase-inhibitor-1 (I-1), a distal amplifier element of β-adrenergic signaling, leading to increased protein phosphatase 1 activity and dephosphorylation of key phosphoproteins, including phospholamban. Downregulated and hypophosphorylated I-1 likely contributes to β-AR desensitization; therefore its modulation is a promising approach in heart failure treatment...
January 2018: Gene Therapy
Beihua Zhong, Jack Rubinstein, Shuangtao Ma, Donna H Wang
Transient receptor potential vanilloid 1 (TRPV1) channels expressed in sensory nerves may regulate vascular tone and cardiovascular function via their anti-inflammatory effects by releasing neuropeptide calcitonin gene-related peptide (CGRP). Inflammation plays a role in the progression of cardiac hypertrophy and TRPV1 activation may be key to cardiac inflammatory processes. The aim of this study was to test the hypothesis that TRPV1 modulates inflammatory processes to protect the heart from pressure overload-induced hypertrophy and inflammatory responses...
January 12, 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
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