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iNOS cardiomyocyte

Aly Mohamed Ahmed
The left ventricular hypertrophy (LVH) occurs in response to the hemodynamic overload in some physiological and pathological conditions. This study was designed to investigate the possible cardioprotective effect of simvastatin (SIM) treatment against isoproterenol (ISO)-induced LVH and the probable underlying mechanism in adult male Wistar rats. Animals were allocated into 4 groups. Rats of control group received normal saline orally for 30 days and intraperitoneally for the last 7 days. Rats of SIM group received SIM orally (10 mg/kg/day in saline) for 30 days...
September 26, 2016: Folia Morphologica (Warsz)
Ernestina M De Francesco, Carmine Rocca, Francesco Scavello, Daniela Amelio, Teresa Pasqua, Damiano C Rigiracciolo, Andrea Scarpelli, Silvia Avino, Francesca Cirillo, Nicola Amodio, Maria C Cerra, Marcello Maggiolini, Tommaso Angelone
The use of Doxorubicin (Dox), a frontline drug for many cancers, is often complicated by dose-limiting cardiotoxicity in approximately 20% of patients. The G-protein estrogen receptor GPER/GPR30 mediates estrogen action as the cardioprotection under certain stressful conditions. For instance, GPER activation by the selective agonist G-1 reduced myocardial inflammation, improved immunosuppression, triggered pro-survival signaling cascades, improved myocardial mechanical performance and reduced infarct size after ischemia/reperfusion (I/R) injury...
September 8, 2016: Journal of Cellular Physiology
Sheng-An Su, Du Yang, Wei Zhu, Zhejun Cai, Na Zhang, Lina Zhao, Jian-An Wang, Meixiang Xiang
Interleukin-17A, a pro-inflammatory cytokine, has a direct proapoptotic effect on cardiomyocytes. However, the specific mechanism has not been clarified. In the present study, an in-vitro model of cardiomyocyte apoptosis induced by IL-17A stimulation was employed and the roles of iNOS and Stat3 involved were investigated. Our data showed that the neonatal mouse cardiomyocytes express IL-17 receptors: IL-17RA and IL-17RC, but did not express IL-17A. Exogenous IL-17A significantly induces iNOS expression and hence the cardiomyocyte apoptosis...
August 23, 2016: Biochimica et Biophysica Acta
Britta Mayer, Josefin Soppert, Sandra Kraemer, Sabrina Schemmel, Christian Beckers, Christian Bleilevens, Rolf Rossaint, Mark Coburn, Andreas Goetzenich, Christian Stoppe
Increasing evidence indicates that argon has organoprotective properties. So far, the underlying mechanisms remain poorly understood. Therefore, we investigated the effect of argon preconditioning in cardiomyocytes within the first and second window of preconditioning. Primary isolated cardiomyocytes from neonatal rats were subjected to 50% argon for 1 h, and subsequently exposed to a sublethal dosage of hypoxia (<1% O₂) for 5 h either within the first (0-3 h) or second window (24-48 h) of preconditioning...
2016: International Journal of Molecular Sciences
Chien-Hung Lin, Chung-Ching Lin
Glucagon-like peptide-1 (GLP-1) and GLP-1 receptors (GLP-1Rs) are responsible for glucose homeostasis, and have been shown to reduce inflammation in preclinical studies. The aim of the present study was to determine whether sitagliptin, an inhibitor of the enzyme dipeptidyl peptidase-4 (DPP-4), as a GLP-1 receptor agonist, exerts an anti-inflammatory effect on cardiomyoblasts during lipopolysaccharide (LPS) stimulation. Exposure to LPS increased the expression levels of tumor necrosis factor (TNF)-α, interleukin-6 (IL)-6 and IL-1β in H9c2 cells, and also resulted in elevations in cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expression and nuclear factor-κB (NF-κB) nuclear translocation...
June 2016: Experimental and Therapeutic Medicine
Xueli Li, Wenliang Li, Zhonghong Gao, Hailing Li
The role of iron in the etiology of diabetes complications is not well established. Thus, this study was performed to test whether the iron-induced increase of oxidative/nitrative damage is involved in SERCA2a-related diabetic heart complication. Four randomly divided groups of rats were used: normal control group; iron overload group; diabetes group, and diabetic plus iron overload group. Iron supplementation stimulated cardiomyocyte hypertrophy and led to an increase in cardiac protein carbonyls, nitrotyrosine (3-NT) formation, and iNOS protein expression, thus resulting in abnormal myocardium calcium homeostasis of diabetic rats...
August 2016: Biochimie
Wei-Dong Qin, Guo-Liang Liu, Juan Wang, Hao Wang, Jian-Ning Zhang, Fan Zhang, Yang Ma, Xin-Ying Ji, Chen Li, Ming-Xiang Zhang
Diabetic cardiomyopathy (DCM) is characterized by structural alterations such as cardiomyocyte hypertrophy, necrosis and focal fibrosis. Poly(ADP-ribose) polymerase 1 (PARP-1) is a nuclear enzyme which can be activated by DNA damage and plays a critical role in various diseases. We hypothesized that PARP-1 may play an important role in DCM and that its inhibition may protect cardiomyocytes from inflammation and apoptosis in DCM. H9c2 cardiomyocytes were treated with normal glucose, mannitol or high glucose (HG)...
March 24, 2016: Oncotarget
Hiroki Takanari, Keiko Miwa, XianMing Fu, Junichi Nakai, Akira Ito, Kousuke Ino, Hiroyuki Honda, Wataru Tonomura, Satoshi Konishi, Tobias Opthof, Marcel Ag van der Heyden, Itsuo Kodama, Jong-Kook Lee
Skeletal myoblast (SkMB) transplantation has been conducted as a therapeutic strategy for severe heart failure. However, arrhythmogenicity following transplantation remains unsolved. We developed an in vitro model of myoblast transplantation with "patterned" or "randomly-mixed" co-culture of SkMBs and cardiomyocytes enabling subsequent electrophysiological, and arrhythmogenic evaluation. SkMBs were magnetically labeled with magnetite nanoparticles and co-cultured with neonatal rat ventricular myocytes (NRVMs) on multi-electrode arrays...
October 2016: Journal of Cellular Physiology
E V Navolotskaya
The data on the properties and mechanism of action of the peptide octarphin (TPLVTLFK, the fragment 12-19 of β-endorphin)--a selective agonist of nonopioid (insensitive to the action of the opioid antagonist naloxone) β-endorphin receptor found on n immune cells (peritoneal macrophages, T and B lymphocytes of spleen and blood), endocrine (adrenal cortex, hypothalamus), cardiovascular (cardiomyocytes) systems are analyzed and systematized. Binding to the receptor octarphin increases increases the mitogen-induced pro- liferation of human and mouse T and B lymphocytes in vitro, activates murine peritoneal macrophages in vitro and in vivo, stimulates growth of human T-lymphoblast cell lines Jurkat and MT-4, inhibits adenylate cyclase activity of rat adrenal cortex membranes and suppresses the secretion of glucocorticoids from the adrenal gland into the blood...
September 2015: Bioorganicheskaia Khimiia
Qun Shao, Heng-Jie Cheng, Michael F Callahan, Dalane W Kitzman, Wei-Min Li, Che Ping Cheng
BACKGROUND: Altered nitric oxide synthase (NOS) has been implicated in the pathophysiology of heart failure (HF). Recent evidence links hypothyroidism to the pathology of HF. However, the precise mechanisms are incompletely understood. The alterations and functional effects of cardiac NOS in hypothyroidism are unknown. We tested the hypothesis that hypothyroidism increases cardiomyocyte inducible NOS (iNOS) expression, which plays an important role in hypothyroidism-induced depression of cardiomyocyte contractile properties, [Ca(2+)]i transient ([Ca(2+)]iT), and β-adrenergic hyporesponsiveness...
February 1, 2016: International Journal of Cardiology
Udesh Dhawan, Chia Hui Lee, Chun-Chung Huang, Ying Hao Chu, Guewha S Huang, Yan-Ren Lin, Wen-Liang Chen
BACKGROUND: Nitric oxide (NO) plays a very important role in the cardiovascular system as a major secondary messenger in signaling pathway. Its concentration regulates most of the important physiological indexes including the systemic blood pressure, blood flow, regional vascular tone and other cardiac functions. The effect of nanotopography on the NO secretion in cardiomyocytes has not been elucidated before. In this study, we report how the nanotopography can modulate the secretion profile of NO and attempt to elucidate the genetic pathways responsible for the same by using Tantalum Oxide nanodot arrays ranging from 10 to 200 nm...
2015: Journal of Nanobiotechnology
Muneyoshi Okada, Hideyuki Yamawaki
Levosimendan, a calcium sensitizer, known as an inotropic agent has a cytoprotective effect against apoptosis in cardiomyocytes. However, the cytoprotective effect of levosimendan on cardiac fibroblasts has not been clarified. The aim of this study was to examine whether levosimendan modulates interleukin (IL)-1β-induced apoptosis in adult rat cardiac fibroblast. Cardiac fibroblasts were isolated from adult male Wistar rats. Apoptosis of cardiac fibroblasts was evaluated by 4',6-diamidino-2-phenylindole staining and TdT-mediated d-UTP nick end labeling (TUNEL)-based staining...
December 15, 2015: European Journal of Pharmacology
Derya Karabulut, Hasan Basri Ulusoy, Emin Kaymak, Mehmet Fatih Sönmez
OBJECTIVE: Diabetes mellitus causes a decrease in cardiac output, arterial blood pressure, and heart rate. In this study, we aimed to investigate, at the molecular level, the effect of nitric oxide synthase (NOS) on heart pathology in type 1 diabetes and look at the therapeutic effect of pentoxifylline on this pathology. METHODS: In this experimental study, 50 Wistar albino male rats were used. The rats were divided into 5 groups: group C, control; group D, only diabetes; group D+PI and D+PII, diabetes + pentoxifylline; group P, only pentoxifylline...
May 2016: Anatolian Journal of Cardiology
Cristina Chimenti, Fernanda Scopelliti, Elisabetta Vulpis, Marco Tafani, Lidia Villanova, Romina Verardo, Ruggero De Paulis, Matteo A Russo, Andrea Frustaci
Cardiac dysfunction of Fabry disease (FD) has been associated with myofilament damage and cell death as result of α-galactosidase A deficiency and globotriaosylceramide accumulation. We sought to evaluate the role of oxidative stress in FD cardiomyocyte dysfunction. Myocardial tissue from 18 patients with FD was investigated for the expression of inducible nitric oxide synthase (iNOS) and nitrotyrosine by immunohistochemistry. Western blot analysis for nitrotyrosine was also performed. Oxidative damage to DNA was investigated by immunostaining for 8-hydroxydeoxyguanosine (8-OHdG), whereas apoptosis was evaluated by in situ ligation with hairpin probes...
November 2015: Human Pathology
Urszula Paslawska, Liliana Kiczak, Jacek Bania, Robert Paslawski, Adrian Janiszewski, Piotr Dzięgiel, Maciej Zacharski, Alicja Tomaszek, Katarzyna Michlik
BACKGROUND: The adverse effects of oxidative stress and the presence of proinflammatory factors in the heart have been widely demonstrated mainly on rodent models. However, larger clinical trials focusing on inflammation or oxidative stress in heart failure (HF) have not been carried out. This may be due to differences in the anatomy and physiology of the cardiovascular system between small rodents and large mammals. Thus, we investigated myocardial inflammatory factors, such as inducible NO synthase (iNOS) and oxidative stress indices in female pigs with chronic tachycardia-induced cardiomyopathy...
January 2016: Cardiovascular Pathology: the Official Journal of the Society for Cardiovascular Pathology
Bernadin Ndongson-Dongmo, Regine Heller, Dirk Hoyer, Michael Brodhun, Michael Bauer, Johannes Winning, Emilio Hirsch, Reinhard Wetzker, Peter Schlattmann, Reinhard Bauer
AIMS: Sepsis-induced myocardial depression (SIMD), an early and frequent event of infection-induced systemic inflammatory response syndrome (SIRS), is characterized by reduced contractility irrespective of enhanced adrenergic stimulation. Phosphoinositide-3 kinase γ (PI3Kγ) is known to prevent β-adrenergic overstimulation via its scaffold function by activating major cardiac phosphodiesterases and restricting cAMP levels. However, the role of PI3Kγ in SIRS-induced myocardial depression is unknown...
November 1, 2015: Cardiovascular Research
Hisashi Nagai, Ichiro Kuwahira, Daryl O Schwenke, Hirotsugu Tsuchimochi, Akina Nara, Sayoko Ogura, Takashi Sonobe, Tadakatsu Inagaki, Yutaka Fujii, Rutsuko Yamaguchi, Lisa Wingenfeld, Keiji Umetani, Tatsuo Shimosawa, Ken-Ichi Yoshida, Koichi Uemura, James T Pearson, Mikiyasu Shirai
Chronic intermittent hypoxia (IH) induces activation of the sympathoadrenal system, which plays a pivotal role in attenuating hypoxic pulmonary vasoconstriction (HPV) via central β1-adrenergic receptors (AR) (brain) and peripheral β2AR (pulmonary arteries). Prolonged hypercatecholemia has been shown to upregulate β3AR. However, the relationship between IH and β3AR in the modification of HPV is unknown. It has been observed that chronic stimulation of β3AR upregulates inducible nitric oxide synthase (iNOS) in cardiomyocytes and that IH exposure causes expression of iNOS in RAW264...
2015: PloS One
Huanxin Zhao, Rong Yang, Yujuan Shi, Wanfang Yang, Qun Zeng, Guoyi Zhao, Xiaoliang Wang
Apoptosis is a crucial mode of cell death induced by ischemia and reperfusion, and ischemic postconditioning (PostC) has been reported to inhibit cell apoptosis. Inducible nitric oxide synthase (iNOS) has been confirmed to play an important role in triggering and mediating the late cardio-protection against ischemia/hypoxia. In this study, we found that hypoxic PostC remarkably up-regulated the expression of iNOS and decreased cardiomyocyte apoptosis. Pre-treatment with 1400w (a highly selective inhibitor of iNOS) or iNOS siRNA weakened the anti-apoptotic effect of hypoxic PostC...
July 2015: Acta Biochimica et Biophysica Sinica
Yanshan Zhang, Liang Chen, Fan Li, Huijuan Wang, Yunyi Yao, Jiamei Shu, Ming-Zhong Ying
CONTEXT: The serious side effect of Adriamycin (ADR) is cardiomyopathy. Cryptotanshinone (CRY) is widely and safely used as antioxidant with MTD more than 5 mg/g in rats (p.o). OBJECTIVE: The objective of this study is to study the protection effects of CRY against ADR-induced mitochondrial dysfunction in cardiomyocytes. MATERIALS AND METHODS: The chemical administration lasted for 20 days with an effective dose of CRY (p.o.) at 50 mg/kg in rats...
2016: Pharmaceutical Biology
Eman Rashed, Paulo Lizano, Huacheng Dai, Andrew Thomas, Carolyn K Suzuki, Christophe Depre, Hongyu Qiu
OBJECTIVES: Stress-inducible heat shock protein 22 (Hsp22) confers protection against ischemia through induction of the inducible isoform of nitric oxide synthase (iNOS). Hsp22 overexpression in vivo stimulates cardiac mitochondrial respiration, whereas Hsp22 deletion in vivo significantly reduces respiration. We hypothesized that Hsp22-mediated regulation of mitochondrial function is dependent upon its mitochondrial translocation together with iNOS. METHODS AND RESULTS: Adenoviruses harboring either the full coding sequence of Hsp22 (Ad-WT-Hsp22) or a mutant lacking a N-terminal 20 amino acid putative mitochondrial localization sequence (Ad-N20-Hsp22) were generated, and infected in rat neonatal cardiomyocytes...
2015: PloS One
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