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Circulation Research

Worawan B Limpitikul, Ivy E Dick, David Tester, Nicole J Boczek, Pattraranee Limphong, Wanjun Yang, Myoung Hyun Choi, Jennifer Babich, Deborah DiSilvestre, Ronald J Kanter, Gordon F Tomaselli, Michael J Ackerman, David Yue
RATIONALE: Calmodulinopathies comprise a new category of potentially life-threatening genetic arrhythmia syndromes capable of producing severe long QT syndrome (LQTS) with mutations involving either CALM1, CALM2, or CALM3 The underlying basis of this form of LQTS is a disruption of Ca(2+)/CaM-dependent inactivation (CDI) of L-type Ca(2+) channels (LTCCs). OBJECTIVE: To gain insight into the mechanistic underpinnings of calmodulinopathies and devise new therapeutic strategies for the treatment of this form of LQTS...
October 20, 2016: Circulation Research
Karina Di Gregoli, Nur Najmi Mohamad Anuar, Rosaria Bianco, Stephen J White, Andrew C Newby, Sarah J George, Jason L Johnson
RATIONALE: Atherosclerosis and aneurysms are leading causes of mortality worldwide. MicroRNAs (miRs) are key determinants of gene and protein expression, and atypical miR expression has been associated with a number of cardiovascular diseases; although their contributory role to atherosclerotic plaque and abdominal aortic aneurysm (AAA) stability are poorly understood. OBJECTIVE: To investigate whether miR-181b regulates TIMP-3 expression and affects atherosclerosis and aneurysms Methods and Results: Here, we demonstrate that miR-181b was over-expressed in symptomatic human atherosclerotic plaques and abdominal aortic aneurysms, and correlated with decreased expression of predicted miR-181b targets, TIMP-3 and elastin...
October 18, 2016: Circulation Research
Jingjiang Pi, Ting Tao, Tao Zhuang, Huimin Sun, Xiaoli Chen, Jie Liu, Yu Cheng, Zuoren Yu, Helen H Zhu, Wei-Qiang Gao, Yuanzhen Suo, Xunbin Wei, Paul Chan, Xiangjian Zheng, Ying Tian, Edward Morrisey, Lin Zhang, Yuzhen Zhang
RATIONALE: Angiogenic hypersprouting and leaky vessels are essential for tumor growth. MicroRNAs have unique therapeutic advantages by targeting multiple pathways of tumor-associated angiogenesis, but the function of individual miRNAs of miR302-367cluster in angiogenesis and tumors has not yet been fully evaluated. OBJECTIVE: To investigate the functions of miR302-367 in developmental angiogenesis and tumor angiogenesis and explore the molecular mechanisms of microRNA for the treatment of pathological neovascularization-related diseases...
October 18, 2016: Circulation Research
Ann P Quick, Qiongling Wang, Leonne E Philippen, Giselle Barreto-Torres, David Y Chiang, David L Beavers, Guoliang Wang, Maha Khalid, Julia O Reynolds, Hannah M Campbell, Jordan Showell, Mark D McCauley, Arjen Scholten, Xander H Wehrens
RATIONALE: Junctional membrane complexes (JMC) in myocytes are critical microdomains, in which excitation-contraction coupling occurs. Structural and functional disruption of JMCs underlies contractile dysfunction in failing hearts. However, the role of newly identified JMC protein striated muscle preferentially expressed gene (SPEG) remains unclear. OBJECTIVE: To determine the role of SPEG in healthy and failing adult hearts. MMethods and Results: Proteomic analysis of immunoprecipatated JMC-proteins ryanodine receptor type-2 (RyR2) and junctophilin-2 (JPH2) followed by mass spectrometry identified the serine-threonine kinase SPEG as the only novel binding partner for both proteins...
October 11, 2016: Circulation Research
Wenbin Zhong, Guoping Pan, Lin Wang, Shiqian Li, Jingsong Ou, Mengyang Xu, Jiwei Li, Biying Zhu, Xiuye Cao, Hongling Ma, Chaowen Li, Jun Xu, Vesa M Olkkonen, Bart Staels, Daoguang Yan
RATIONALE: Macrophage survival within the arterial wall is a central factor contributing to atherogenesis. Oxysterols, major components of oxidized LDL (ox-LDL), exert cytotoxic effects on macrophages. OBJECTIVE: To determine whether ORP4L, an oxysterol-binding protein, affects macrophage survival and the pathogenesis of atherosclerosis. METHODS AND RESULTS: By hiring cell biological approaches and ORP4L(-/-) mice, we show that ORP4L co-expresses with and forms a complex with G&alphaq/11 and PLCβ3 in macrophages...
October 11, 2016: Circulation Research
Joyce Bischoff, Guillem Casanovas, Jill Wylie-Sears, Dae-Hee Kim, Philipp Bartko, J Guerrero, Jacob Dal-Bianco, Jonathan Beaudoin, Michael Garcia, Suzanne Sullivan, Margo Seybolt, Brittan Morris, Joshua Keegan, Whitney Irvin, Elena Aikawa, Robert Levine
RATIONALE: Ischemic mitral regurgitation (IMR), a complication after myocardial infarction (MI), induces adaptive mitral valve (MV) responses that may be initially beneficial, but eventually lead to leaflet fibrosis and MV dysfunction. We sought to examine the MV endothelial response and its potential contribution to IMR. OBJECTIVE: Endothelial, interstitial and hematopoietic cells in MVs from post-MI sheep were quantified. MV endothelial CD45, found post-MI, was analyzed in vitro...
October 6, 2016: Circulation Research
Natascha Luther, Fatemeh Shahneh, Melanie Brähler, Franziska Krebs, Sven Jäckel, Saravanan Subramaniam, Christian Stanger, Tanja Schönfelder, Bettina Kleis-Fischer, Christoph Reinhardt, Hans C Probst, Philip Wenzel, Katrin Schäfer, Christian Becker
RATIONALE: Immune cells play an important role during the generation and resolution of thrombosis. T cells are powerful regulators of immune and non-immune cell function, however their role in sterile inflammation in venous thrombosis has not been systematically examined. OBJECTIVE: This study investigated the recruitment, activation and inflammatory activity of T cells in deep vein thrombosis (DVT) and its consequences for venous thrombus resolution. METHODS AND RESULTS: CD4(+) and CD8(+) T cells infiltrate the thrombus and vein wall rapidly upon DVT induction and remain in the tissue throughout thrombus resolution...
October 5, 2016: Circulation Research
Aditi Khandekar, Steven Springer, Wei Wang, Stephanie Hicks, Carla J Weinheimer, Ramon Diaz-Trelles, Jeanne M Nerbonne, Stacey Rentschler
RATIONALE: Ventricular arrhythmias often arise from the Purkinje-myocyte junction and are a leading cause of sudden cardiac death. Notch activation reprograms cardiac myocytes to an "induced Purkinje-like" state characterized by prolonged action potential duration and expression of Purkinje enriched genes. OBJECTIVE: To understand the mechanism by which canonical Notch signaling causes action potential prolongation. METHODS AND RESULTS: We find that endogenous Purkinje cells have reduced peak K(+) current, Ito and IK,slow when compared with ventricular myocytes...
October 3, 2016: Circulation Research
Joel Chappell, Jennifer L Harman, Vagheesh M Narasimhan, Haixiang Yu, Kirsty Foote, Benjamin D Simons, Martin R Bennett, Helle F Jorgensen
RATIONALE: Vascular smooth muscle cell (VSMC) accumulation is a hallmark of atherosclerosis and vascular injury. However, fundamental aspects of proliferation and the phenotypic changes within individual VSMCs, which underlie vascular disease remain unresolved. In particular, it is not known if all VSMCs proliferate and display plasticity, or whether individual cells can switch to multiple phenotypes. OBJECTIVE: To assess whether proliferation and plasticity in disease is a general characteristic of VSMCs or a feature of a subset of cells...
September 28, 2016: Circulation Research
Esther A Warnert, Jonathan C Rodrigues, Amy E Burchell, Sandra Neumann, Laura E Ratcliffe, Nathan E Manghat, Ashley D Harris, Zoe H Adams, Angus K Nightingale, Richard G Wise, Julian F Paton, Emma C Hart
RATIONALE: Data from animal models of hypertension indicate that high blood pressure may develop as a vital mechanism to maintain adequate blood flow to the brain. We propose that congenital vascular abnormalities of the posterior cerebral circulation and cerebral hypoperfusion could partially explain the etiology of essential hypertension, which remains enigmatic in 95% of patients. OBJECTIVE: To evaluate the role of the cerebral circulation in the pathophysiology of hypertension...
September 26, 2016: Circulation Research
Sailesh C Harwani, Jason Ratcliff, Fayyaz S Sutterwala, Zuhair K Ballas, David K Meyerholz, Mark W Chapleau, Francois Abboud
RATIONALE: Renal inflammation contributes to the pathophysiology of hypertension. CD161a+ immune cells are dominant in the Spontaneously Hypertensive Rat (SHR) and expand in response to nicotinic cholinergic activation. OBJECTIVE: We aimed to phenotype CD161a+ immune cells in pre-hypertensive SHR following cholinergic activation with nicotine, and determine if these cells are involved in renal inflammation and the development of hypertension. METHODS AND RESULTS: Studies utilized young SHR and Wistar Kyoto (WKY) rats...
September 22, 2016: Circulation Research
Julio Gallego-Delgado, Thomas Walther, Ana Rodriguez
RATIONALE: A recently proposed hypothesis states that malaria may contribute to hypertension in endemic areas1, but the role of angiotensin (Ang) II, a major regulator of blood pressure, was not considered. Elevated levels of Ang II may confer protection against malaria morbidity and/or mortality, providing an alternative explanation for hypertension in malaria endemic areas. OBJECTIVE: To discuss a possible alternative cause for hypertension in populations that have been under the selective pressure of malaria...
September 22, 2016: Circulation Research
Aditya A Joshi, Joseph B Lerman, Tsion M Aberra, Mehdi Afshar, Heather L Teague, Justin A Rodante, Parasuram Krishnamoorthy, Qimin Ng, Tarek Z Aridi, Taufiq Salahuddin, Balaji Natarajan, Benjamin N Lockshin, Mark A Ahlman, Marcus Y Chen, Daniel J Rader, Muredach Reilly, Alan T Remaley, David A Bluemke, Martin P Playford, Joel M Gelfand, Nehal N Mehta
RATIONALE: GlycA, an emerging inflammatory biomarker, predicted cardiovascular events in population-based studies. Psoriasis, an inflammatory disease associated with increased cardiovascular risk, provides a model to study inflammatory biomarkers in cardiovascular disease (CVD). Whether GlycA associates with psoriasis and how it predicts subclinical CVD beyond hsCRP in psoriasis is unknown. OBJECTIVE: To investigate the relationships between GlycA and psoriasis, and between GlycA and subclinical CVD...
September 21, 2016: Circulation Research
Hou-Zao Chen, Fang Wang, Peng Gao, Jian-Fei Pei, Yue Liu, Ting-Ting Xu, Xiaoqiang Tang, Wen-Yan Fu, Jie Lu, Yun-Fei Yan, Xiao-Man Wang, Lei Han, Zhu-Qin Zhang, Ran Zhang, Ming-Hui Zou, De-Pei Liu
RATIONALE: Uncontrolled growth of abdominal aortic aneurysms (AAAs) is a life-threatening vascular disease without an effective pharmaceutical treatment. AAA incidence dramatically increases with advancing age in men. However, the molecular mechanisms by which aging predisposes individuals to AAAs remain unknown. OBJECTIVE: In this study, we investigated the role of Sirtuin 1 (SIRT1), a class Ⅲ histone deacetylase, in AAA formation and the underlying mechanisms linking vascular senescence and inflammation...
September 20, 2016: Circulation Research
Shufeng Liu, Leon J DeLalio, Brant E Isakson, Tony T Wang
RATIONALE: The mosquito-borne Zika virus (ZIKV) is now recognized as a blood-borne pathogen, raising an important question about how the virus gets into human bloodstream. The imminent threat of the ZIKV epidemic to the global blood supply also demands novel therapeutics to stop virus transmission though transfusion. OBJECTIVE: We intend to characterize ZIKV tropism for human endothelial cells (ECs) and provide potential targets for intervention. METHODS AND RESULTS: We conducted immunostaining, plaque assay, and quantitative RT-PCR of ZIKV RNA to evaluate the possible infection of ECs by ZIKV...
September 20, 2016: Circulation Research
Xaoyan Dai, Ye Ding, Zhaoyu Liu, Wencheng Zhang, Ming-Hui Zou
RATIONALE: Elevated levels of C/EBP homologous protein (CHOP), a member of the C/EBP transcription factor family, in advanced atherosclerotic plaques is reported to be associated with atherosclerotic plaque rupture in humans. However, the molecular mechanism by which CHOP accumulation occurs is poorly defined. OBJECTIVE: The aim of this study was to investigate if (1) macrophage AMP-activated kinase (AMPK) regulates cellular CHOP accumulation and (2) whole-body Ampk deletion leads to neointimal disruption...
September 20, 2016: Circulation Research
Matthew J Butcher, Adam R Filipowicz, Tayab C Waseem, Christopher McGary, Kevin J Crow, Nathaniel Magilnick, Mark Boldin, Patric S Lundberg, Elena Galkina
RATIONALE: Foxp3(+)T regulatory cells (Tregs) are key players in maintaining immune homeostasis. Evidence suggests that Tregs respond to environmental cues to permit or suppress inflammation. In atherosclerosis, Th1-driven inflammation affects Treg homeostasis, but the mechanisms governing this phenomenon are unclear. OBJECTIVE: Here, we address whether atherosclerosis impacts Treg plasticity and functionality in Apoe(-/-) mice, and what effect Treg plasticity might have on the pathology of atherosclerosis...
September 15, 2016: Circulation Research
Charles H Cunningham, Justin Y Lau, Albert P Chen, Benjamin J Geraghty, William J Perks, Idan Roifman, Graham A Wright, Kim A Connelly
RATIONALE: Altered cardiac energetics is known to play an important role in the progression towards heart failure. A non-invasive method for imaging metabolic markers that could be used in longitudinal studies would be useful for understanding therapeutic approaches that target metabolism. OBJECTIVE: To demonstrate the first hyperpolarized (13)C metabolic magnetic resonance imaging (MRI) of the human heart. METHODS AND RESULTS: Four healthy subjects underwent conventional proton cardiac MRI followed by (13)C imaging and spectroscopic acquisition immediately following intravenous administration of a 0...
September 15, 2016: Circulation Research
Meryl C Woodall, Benjamin P Woodall, Erhe Gao, Ancai Yuan, Walter J Koch
RATIONALE: G protein-coupled receptor kinase 2 (GRK2) is an important molecule upregulated after myocardial injury and during heart failure. Myocyte-specific GRK2 loss before and after myocardial ischemic injury improves cardiac function and remodeling. The cardiac fibroblast plays an important role in the repair and remodeling events following cardiac ischemia; the importance of GRK2 in these events has not been investigated. OBJECTIVE: The aim of this study is to elucidate the in vivo implications of deleting GRK2 in the cardiac fibroblast after ischemia/reperfusion (I/R) injury...
September 6, 2016: Circulation Research
Susan A Austin, Zvonimir S Katusic
RATIONALE: Alzheimer's disease (AD) has an unknown etiology; however, cardiovascular risk factors are associated with a higher incidence of AD. A defining feature of endothelial dysfunction induced by cardiovascular risk factors is reduced bioavailable endothelial nitric oxide (NO). We previously demonstrated endothelial NO acts as an important signaling molecule in neuronal tissue. OBJECTIVE: We sought to determine the relationship between the loss of endothelial nitric oxide synthase (eNOS) and tau phosphorylation in neuronal tissue...
September 6, 2016: Circulation Research
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