journal
MENU ▼
Read by QxMD icon Read
search

Basic Research in Cardiology

journal
https://www.readbyqxmd.com/read/28439731/il-10-improves-cardiac-remodeling-after-myocardial-infarction-by-stimulating-m2-macrophage-polarization-and-fibroblast-activation
#1
Mira Jung, Yonggang Ma, Rugmani Padmanabhan Iyer, Kristine Y DeLeon-Pennell, Andriy Yabluchanskiy, Michael R Garrett, Merry L Lindsey
Inflammation resolution is important for scar formation following myocardial infarction (MI) and requires the coordinated actions of macrophages and fibroblasts. In this study, we hypothesized that exogenous interleukin-10 (IL-10), an anti-inflammatory cytokine, promotes post-MI repair through actions on these cardiac cell types. To test this hypothesis, C57BL/6J mice (male, 3- to 6-month old, n = 24/group) were treated with saline or IL-10 (50 μg/kg/day) by osmotic mini-pump infusion starting at day (d) 1 post-MI and sacrificed at d7 post-MI...
May 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28439730/physiological-and-therapeutic-regulation-of-pcsk9-activity-in-cardiovascular-disease
#2
REVIEW
Simon Glerup, Rainer Schulz, Ulrich Laufs, Klaus-Dieter Schlüter
Ischemic heart disease is the main cause of death worldwide and is accelerated by increased levels of low-density lipoprotein cholesterol (LDL-C). Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a potent circulating regulator of LDL-C through its ability to induce degradation of the LDL receptor (LDLR) in the lysosome of hepatocytes. Only in the last few years, a number of breakthroughs in the understanding of PCSK9 biology have been reported illustrating how PCSK9 activity is tightly regulated at several levels by factors influencing its transcription, secretion, or by extracellular inactivation and clearance...
May 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28421341/insufficient-activation-of-akt-upon-reperfusion-because-of-its-novel-modification-by-reduced-pp2a-b55%C3%AE-contributes-to-enlargement-of-infarct-size-by-chronic-kidney-disease
#3
Toshiyuki Tobisawa, Toshiyuki Yano, Masaya Tanno, Takayuki Miki, Atsushi Kuno, Yukishige Kimura, Satoko Ishikawa, Hidemichi Kouzu, Keitaro Nishizawa, Hideaki Yoshida, Tetsuji Miura
Chronic kidney disease (CKD) increases myocardial infarct size by an unknown mechanism. Here we examined the hypothesis that impairment of protective PI3K-PDK1-Akt and/or mTORC-Akt signaling upon reperfusion contributes to CKD-induced enlargement of infarct size. CKD was induced in rats by 5/6 nephrectomy (SNx group) 4 weeks before myocardial infarction experiments, and sham-operated rats served as controls (Sham group). Infarct size as a percentage of area at risk after ischemia/reperfusion was significantly larger in the SNx group than in the Sham group (56...
May 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28409279/aquaporin-1-controls-the-functional-phenotype-of-pulmonary-smooth-muscle-cells-in-hypoxia-induced-pulmonary-hypertension
#4
Claudio Schuoler, Thomas J Haider, Caroline Leuenberger, Johannes Vogel, Louise Ostergaard, Grazyna Kwapiszewska, Malcolm Kohler, Max Gassmann, Lars C Huber, Matthias Brock
Vascular remodelling in hypoxia-induced pulmonary hypertension (PH) is driven by excessive proliferation and migration of endothelial and smooth muscle cells. The expression of aquaporin 1 (AQP1), an integral membrane water channel protein involved in the control of these processes, is tightly regulated by oxygen levels. The role of AQP1 in the pathogenesis of PH, however, has not been directly addressed so far. This study was designed to characterize expression and function of AQP1 in pulmonary vascular cells from human arteries and in the mouse model of hypoxia-induced PH...
May 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28389717/sex-difference-in-expression-and-function-of-beta-adrenoceptors-in-macrovessels-role-of-the-endothelium
#5
Suzan Al-Gburi, Andreas Deussen, Birgit Zatschler, Silvio Weber, Stephan Künzel, Ali El-Armouche, Kristina Lorenz, Maria Cybularz, Henning Morawietz, Irakli Kopaliani
Estrogen modulates adrenergic reactivity of macrovessels, resulting in weaker α-adrenergic vasoconstriction in females than males. However, the mechanisms governing this important sex-specific difference are not well understood. We hypothesized that vessels of females express more dilatory β-adrenoceptors, which counteract constrictive effects of α-adrenoceptors. This hypothesis was tested using aortas of normotensive (WKY) and hypertensive rats (SHR), along with human mammary artery. Selective blockade of β1 (CGP20712) or β3 (SR59230A), but not β2 (ICI118,551) adrenoceptors, greatly increased α-adrenergic constriction (norepinephrine) of aorta in female SHRs, but not in male SHRs at 12 weeks of age...
May 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28386775/intermittent-pacing-therapy-favorably-modulates-infarct-remodeling
#6
André Uitterdijk, Tirza Springeling, Kevin C M Hermans, Daphne Merkus, Vincent J de Beer, Charlotte Gorsse-Bakker, Eric Mokelke, Evangelos P Daskalopoulos, Piotr A Wielopolski, Jack P M Cleutjens, W Matthijs Blankesteijn, Frits W Prinzen, Willem J van der Giessen, Robert-Jan M van Geuns, Dirk J Duncker
Despite early revascularization, remodeling and dysfunction of the left ventricle (LV) after acute myocardial infarction (AMI) remain important therapeutic targets. Intermittent pacing therapy (IPT) of the LV can limit infarct size, when applied during early reperfusion. However, the effects of IPT on post-AMI LV remodeling and infarct healing are unknown. We therefore investigated the effects of IPT on global LV remodeling and infarct geometry in swine with a 3-day old AMI. For this purpose, fifteen pigs underwent 2 h ligation of the left circumflex coronary artery followed by reperfusion...
May 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28364353/mitochondrial-cx43-hemichannels-contribute-to-mitochondrial-calcium-entry-and-cell-death-in-the-heart
#7
Ashish Kumar Gadicherla, Nan Wang, Marco Bulic, Esperanza Agullo-Pascual, Alessio Lissoni, Maarten De Smet, Mario Delmar, Geert Bultynck, Dmitri V Krysko, Amadou Camara, Klaus-Dieter Schlüter, Rainer Schulz, Wai-Meng Kwok, Luc Leybaert
Mitochondrial connexin 43 (Cx43) plays a key role in cardiac cytoprotection caused by repeated exposure to short periods of non-lethal ischemia/reperfusion, a condition known as ischemic preconditioning. Cx43 also forms calcium (Ca(2+))-permeable hemichannels that may potentially lead to mitochondrial Ca(2+) overload and cell death. Here, we studied the role of Cx43 in facilitating mitochondrial Ca(2+) entry and investigated its downstream consequences. To that purpose, we used various connexin-targeting peptides interacting with extracellular (Gap26) and intracellular (Gap19, RRNYRRNY) Cx43 domains, and tested their effect on mitochondrial dye- and Ca(2+)-uptake, electrophysiological properties of plasmalemmal and mitochondrial Cx43 channels, and cell injury/cell death...
May 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28349259/effect-of-paroxetine-on-left-ventricular-remodeling-in-an-in-vivo-rat-model-of-myocardial-infarction
#8
Thomas Ravn Lassen, Jan Møller Nielsen, Jacob Johnsen, Steffen Ringgaard, Hans Erik Bøtker, Steen Buus Kristiansen
Left ventricular (LV) remodeling following a myocardial infarction (MI) involves formation of reactive oxygen species (ROS). Paroxetine, a selective serotonin reuptake inhibitor, has an antioxidant effect in the vascular wall. We investigated whether paroxetine reduces myocardial ROS formation and LV remodeling following a MI. In a total of 32 Wistar rats, MI was induced by a 30-min ligation of the left anterior descending artery followed by 7- or 28-day reperfusion. During the 28 days of reperfusion, LV remodeling was evaluated by magnetic resonance imaging (MRI) and echocardiography (n = 20)...
May 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28349258/role-of-bone-marrow-derived-cd11c-dendritic-cells-in-systolic-overload-induced-left-ventricular-inflammation-fibrosis-and-hypertrophy
#9
Huan Wang, Dongmin Kwak, John Fassett, Xiaohong Liu, Wu Yao, Xinyu Weng, Xin Xu, Yawei Xu, Robert J Bache, Daniel L Mueller, Yingjie Chen
Inflammatory responses play an important role in the development of left ventricular (LV) hypertrophy and dysfunction. Recent studies demonstrated that increased T-cell infiltration and T-cell activation contribute to LV hypertrophy and dysfunction. Dendritic cells (DCs) are professional antigen-presenting cells that orchestrate immune responses, especially by modulating T-cell function. In this study, we investigated the role of bone marrow-derived CD11c(+) DCs in transverse aortic constriction (TAC)-induced LV fibrosis and hypertrophy in mice...
May 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28343262/cavin-1-deficiency-modifies-myocardial-and-coronary-function-stretch-responses-and-ischaemic-tolerance-roles-of-nos-over-activity
#10
Mika Kaakinen, Melissa E Reichelt, Zhibin Ma, Charles Ferguson, Nick Martel, Enzo R Porrello, James E Hudson, Walter G Thomas, Robert G Parton, John P Headrick
Caveolae and associated cavin and caveolins may govern myocardial function, together with responses to mechanical and ischaemic stresses. Abnormalities in these proteins are also implicated in different cardiovascular disorders. However, specific roles of the cavin-1 protein in cardiac and coronary responses to mechanical/metabolic perturbation remain unclear. We characterised cardiovascular impacts of cavin-1 deficiency, comparing myocardial and coronary phenotypes and responses to stretch and ischaemia-reperfusion in hearts from cavin-1 (+/+) and cavin-1 (-/-) mice...
May 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28299467/cardiomyocyte-ogt-limits-ventricular-dysfunction-in-mice-following-pressure-overload-without-affecting-hypertrophy
#11
Sujith Dassanayaka, Robert E Brainard, Lewis J Watson, Bethany W Long, Kenneth R Brittian, Angelica M DeMartino, Allison L Aird, Anna M Gumpert, Timothy N Audam, Peter J Kilfoil, Senthilkumar Muthusamy, Tariq Hamid, Sumanth D Prabhu, Steven P Jones
The myocardial response to pressure overload involves coordination of multiple transcriptional, posttranscriptional, and metabolic cues. The previous studies show that one such metabolic cue, O-GlcNAc, is elevated in the pressure-overloaded heart, and the increase in O-GlcNAcylation is required for cardiomyocyte hypertrophy in vitro. Yet, it is not clear whether and how O-GlcNAcylation participates in the hypertrophic response in vivo. Here, we addressed this question using patient samples and a preclinical model of heart failure...
May 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28271186/suv39h1-mediated-sirt1-trans-repression-contributes-to-cardiac-ischemia-reperfusion-injury
#12
Guang Yang, Xinjian Zhang, Xinyu Weng, Peng Liang, Xin Dai, Sheng Zeng, Huihui Xu, Hailin Huan, Mingming Fang, Yuehua Li, Dachun Xu, Yong Xu
Ischemic reperfusion (I/R) contributes to deleterious cardiac remodeling and heart failure. The deacetylase SIRT1 has been shown to protect the heart from I/R injury. We examined the mechanism whereby I/R injury represses SIRT1 transcription in the myocardium. There was accumulation of trimethylated histone H3K9 on the proximal SIRT1 promoter in the myocardium in mice following I/R injury and in cultured cardiomyocytes exposed to hypoxia-reoxygenation (H/R). In accordance, the H3K9 trimethyltransferase SUV39H1 bound to the SIRT1 promoter and repressed SIRT1 transcription...
May 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28258299/vasopressors-induce-passive-pulmonary-hypertension-by-blood-redistribution-from-systemic-to-pulmonary-circulation
#13
Chunling Jiang, Hong Qian, Shuhua Luo, Jing Lin, Jerry Yu, Yajiao Li, Qi An, Nanfu Luo, Lei Du
Vasopressors are widely used in resuscitation, ventricular failure, and sepsis, and often induce pulmonary hypertension with undefined mechanisms. We hypothesize that vasopressor-induced pulmonary hypertension is caused by increased pulmonary blood volume and tested this hypothesis in dogs under general anesthesia. In normal hearts (model 1), phenylephrine (2.5 μg/kg/min) transiently increased right but decreased left cardiac output, associated with increased pulmonary blood volume (63% ± 11.8, P = 0...
May 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28258298/complement-factor-5-blockade-reduces-porcine-myocardial-infarction-size-and-improves-immediate-cardiac-function
#14
Soeren E Pischke, A Gustavsen, H L Orrem, K H Egge, F Courivaud, H Fontenelle, A Despont, A K Bongoni, R Rieben, T I Tønnessen, M A Nunn, H Scott, H Skulstad, A Barratt-Due, T E Mollnes
Inhibition of complement factor 5 (C5) reduced myocardial infarction in animal studies, while no benefit was found in clinical studies. Due to lack of cross-reactivity of clinically used C5 antibodies, different inhibitors were used in animal and clinical studies. Coversin (Ornithodoros moubata complement inhibitor, OmCI) blocks C5 cleavage and binds leukotriene B4 in humans and pigs. We hypothesized that inhibition of C5 before reperfusion will decrease infarct size and improve ventricular function in a porcine model of myocardial infarction...
May 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28238121/leukocyte-inos-is-required-for-inflammation-and-pathological-remodeling-in-ischemic-heart-failure
#15
Justin R Kingery, Tariq Hamid, Robert K Lewis, Mohamed Ameen Ismahil, Shyam S Bansal, Gregg Rokosh, Tim M Townes, Suzanne T Ildstad, Steven P Jones, Sumanth D Prabhu
In the failing heart, iNOS is expressed by both macrophages and cardiomyocytes. We hypothesized that inflammatory cell-localized iNOS exacerbates left ventricular (LV) remodeling. Wild-type (WT) C57BL/6 mice underwent total body irradiation and reconstitution with bone marrow from iNOS(-/-) mice (iNOS(-/-)c) or WT mice (WTc). Chimeric mice underwent coronary ligation to induce large infarction and ischemic heart failure (HF), or sham surgery. After 28 days, as compared with WTc sham mice, WTc HF mice exhibited significant (p < 0...
March 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28210871/repeated-doses-of-cardiac-mesenchymal-cells-are-therapeutically-superior-to-a-single-dose-in-mice-with-old-myocardial-infarction
#16
Yiru Guo, Marcin Wysoczynski, Yibing Nong, Alex Tomlin, Xiaoping Zhu, Anna M Gumpert, Marjan Nasr, Senthikumar Muthusamy, Hong Li, Michael Book, Abdur Khan, Kyung U Hong, Qianhong Li, Roberto Bolli
We have recently demonstrated that repeated administrations of c-kit(POS) cardiac progenitor cells (CPCs) have cumulative beneficial effects in rats with old myocardial infarction (MI), resulting in markedly greater improvement in left ventricular (LV) function compared with a single administration. To determine whether this paradigm applies to other species and cell types, mice with a 3-week-old MI received one or three doses of cardiac mesenchymal cells (CMCs), a novel cell type that we have recently described...
March 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28188434/bloodless-reperfusion-with-the-oxygen-carrier-hboc-201-in-acute-myocardial-infarction-a-novel-platform-for-cardioprotective-probes-delivery
#17
Jose M García-Ruiz, Carlos Galán-Arriola, Rodrigo Fernández-Jiménez, Jaume Aguero, Javier Sánchez-González, Ana García-Alvarez, Mario Nuno-Ayala, Gregory P Dubé, Zafiris Zafirelis, Gonzalo J López-Martín, Juan A Bernal, Enrique Lara-Pezzi, Valentín Fuster, Borja Ibáñez
Reperfusion, despite being required for myocardial salvage, is associated with additional injury. We hypothesize that infarct size (IS) will be reduced by a period of bloodless reperfusion with hemoglobin-based oxygen carriers (HBOC) before blood-flow restoration. In the pig model, we first characterized the impact of intracoronary perfusion with a fixed volume (600 ml) of a pre-oxygenated acellular HBOC, HBOC-201, on the healthy myocardium. HBOC-201 was administered through the lumen of the angioplasty balloon (i...
March 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28168403/carbon-monoxide-releasing-molecule-3-improves-myocardial-function-in-mice-with-sepsis-by-inhibiting-nlrp3-inflammasome-activation-in-cardiac-fibroblasts
#18
Wenbo Zhang, Aibin Tao, Ting Lan, Gediminas Cepinskas, Raymond Kao, Claudio M Martin, Tao Rui
The NLRP3 inflammasome is an intracellular multiple-protein complex that controls the maturation and release of interleukin (IL)-1β and IL-18. Endogenous carbon monoxide (CO) is anti-inflammatory. The aim of this study was to assess the effects/mechanisms of CO-releasing molecule-3 (CORM-3)-dependent modulation of the NLRP3 inflammasome in cardiac fibroblasts (CF) and its effect on myocardial function in sepsis. CF were treated with CORM-3 or inactive CORM-3 (iCORM-3) before NLRP3 inflammasome priming with lipopolysaccharides (LPS) or following activation with adenosine triphosphate (ATP)...
March 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28160133/cardioprotective-kinase-signaling-to-subsarcolemmal-and-interfibrillar-mitochondria-is-mediated-by-caveolar-structures
#19
Wylly Ramsés García-Niño, Francisco Correa, Julia Isabel Rodríguez-Barrena, Juan Carlos León-Contreras, Mabel Buelna-Chontal, Elizabeth Soria-Castro, Rogelio Hernández-Pando, José Pedraza-Chaverri, Cecilia Zazueta
The demonstration that caveolin-3 overexpression reduces myocardial ischemia/reperfusion injury and our own finding that multiprotein signaling complexes increase in mitochondria in association with caveolin-3 levels, led us to investigate the contribution of caveolae-driven extracellular signal-regulated kinases 1/2 (ERK1/2) on maintaining the function of cardiac mitochondrial subpopulations from reperfused hearts subjected to postconditioning (PostC). Rat hearts were isolated and subjected to ischemia/reperfusion and to PostC...
March 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28120038/compensatory-role-of-the-nbcn1-sodium-bicarbonate-cotransporter-on-ca-2-induced-mitochondrial-swelling-in-hypertrophic-hearts
#20
Lorena A Vargas, Fernanda Carrizo Velasquez, Bernardo V Alvarez
NBC Na(+)/HCO3(-) cotransporter (NBCn1) and NHE1 Na(+)/H(+) exchanger have been associated with cardiac disorders and recently located in coronary endothelial cells (CEC) and cardiomyocytes mitochondria, respectively. Mitochondrial NHE1 blockade delays permeability transition pore (MPTP) opening and reduces superoxide levels, two critical events exacerbated in cells of diseased hearts. Conversely, activation of NBCn1 prevented apoptosis in CEC subjected to ischemic stress. We characterized the role of the NHE1 and NBCn1 transporters in heart mitochondria from hypertrophic (SHR) and control (Wistar) rats...
March 2017: Basic Research in Cardiology
journal
journal
23071
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"