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https://www.readbyqxmd.com/read/28537917/microrna-210-suppresses-glucocorticoid-receptor-expression-in-response-to-hypoxia-in-fetal-rat-cardiomyocytes
#1
Shannalee R Martinez, Qingyi Ma, Chiranjib Dasgupta, Xianmei Meng, Lubo Zhang
Hypoxia is a common intrauterine stressor, often resulting in intrauterine growth restriction and increased risk for cardiovascular disease later in life. The aim of this work was to test the hypothesis that microRNA-210 (miR-210) mediates the detrimental suppression of glucocorticoid receptor (GR) in response to hypoxia in fetal rat cardiomyocytes. Cardiomyocytes isolated from gestational day 21 Sprague Dawley fetal rats showed increased miR-210 levels and reduced GR abundance after exposure to ex vivo hypoxia (1% O2)...
May 11, 2017: Oncotarget
https://www.readbyqxmd.com/read/28537760/caveolin-1-autophagy-pathway-mediated-cardiomyocyte-hypertrophy-induced-by-apelin-13
#2
Di Wu, Feng Xie, Ling Xiao, Fen Feng, Shifang Huang, Lu He, Meiqing Liu, Qun Zhou, Lanfang Li, Linxi Chen
Apelin, an endogenous ligand for apelin receptor (APJ), is reported to be involved in cardiomyocyte hypertrophy. In this study, we explored the mechanism of cardiomyocyte hypertrophy induced by apelin-13/APJ system. Left ventricular hypertrophy (LVH) rat model was established by constricting the abdominal aorta. Western blots were used for protein expression in LVH rats and cultured H9c2 cardiomyocytes. Transmission electron microscopy (TEM) was used to monitor morphological features of cells. In addition, the diameter and volume of H9c2 cells were detected by Scepter™ Handheld Automated Cell Counter...
May 24, 2017: DNA and Cell Biology
https://www.readbyqxmd.com/read/28534118/exercise-induced-circulating-extracellular-vesicles-protect-against-cardiac-ischemia-reperfusion-injury
#3
Yihua Bei, Tianzhao Xu, Dongchao Lv, Pujiao Yu, Jiahong Xu, Lin Che, Avash Das, John Tigges, Vassilios Toxavidis, Ionita Ghiran, Ravi Shah, Yongqin Li, Yuhui Zhang, Saumya Das, Junjie Xiao
Extracellular vesicles (EVs) serve an important function as mediators of intercellular communication. Exercise is protective for the heart, although the signaling mechanisms that mediate this cardioprotection have not been fully elucidated. Here using nano-flow cytometry, we found a rapid increase in plasma EVs in human subjects undergoing exercise stress testing. We subsequently identified that serum EVs were increased by ~1.85-fold in mice after 3-week swimming. Intramyocardial injection of equivalent quantities of EVs from exercised mice and non-exercised controls provided similar protective effects against acute ischemia/reperfusion (I/R) injury in mice...
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28526910/expression-and-regulation-of-type-2a-protein-phosphatases-and-alpha4-signalling-in-cardiac-health-and-hypertrophy
#4
Olga Eleftheriadou, Andrii Boguslavskyi, Michael R Longman, Jonathan Cowan, Asvi Francois, Richard J Heads, Brian E Wadzinski, Ali Ryan, Michael J Shattock, Andrew K Snabaitis
Cardiac physiology and hypertrophy are regulated by the phosphorylation status of many proteins, which is partly controlled by a poorly defined type 2A protein phosphatase-alpha4 intracellular signalling axis. Quantitative PCR analysis revealed that mRNA levels of the type 2A catalytic subunits were differentially expressed in H9c2 cardiomyocytes (PP2ACβ > PP2ACα > PP4C > PP6C), NRVM (PP2ACβ > PP2ACα = PP4C = PP6C), and adult rat ventricular myocytes (PP2ACα > PP2ACβ > PP6C > PP4C)...
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28526717/major-contribution-of-the-3-6-7-class-of-trpc-channels-to-myocardial-ischemia-reperfusion-and-cellular-hypoxia-reoxygenation-injuries
#5
Xiju He, Shoutian Li, Benju Liu, Sebastian Susperreguy, Karina Formoso, Jinghong Yao, Jinsong Kang, Anbing Shi, Lutz Birnbaumer, Yanhong Liao
The injury phase after myocardial infarcts occurs during reperfusion and is a consequence of calcium release from internal stores combined with calcium entry, leading to cell death by apoptopic and necrotic processes. The mechanism(s) by which calcium enters cells has(ve) not been identified. Here, we identify canonical transient receptor potential channels (TRPC) 3 and 6 as the cation channels through which most of the damaging calcium enters cells to trigger their death, and we describe mechanisms activated during the injury phase...
May 19, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28526709/acetylation-of-mitochondrial-proteins-by-gcn5l1-promotes-enhanced-fatty-acid-oxidation-in-the-heart
#6
Dharendra Thapa, Manling Zhang, Janet R Manning, Danielle Guimarães, Michael Stoner, Robert M O'Doherty, Sruti Shiva, Iain Scott
Lysine acetylation is a reversible post-translational modification, and is particularly important in the regulation of mitochondrial metabolic enzymes. Acetylation uses acetyl-CoA derived from fuel metabolism as a co-factor, thereby linking nutrition to metabolic activity. In this study, we investigated how mitochondrial acetylation status in the heart is controlled by food intake, and how these changes affect mitochondrial metabolism. We found that there was a significant increase in cardiac mitochondrial protein acetylation in mice fed a long-term high fat diet, and that this change correlated with an increase in the abundance of the mitochondrial acetyltransferase-related protein GCN5L1...
May 19, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28525945/the-protective-effect-of-luteolin-on-myocardial-ischemia-reperfusion-i-r-injury-through-tlr4-nf-%C3%AE%C2%BAb-nlrp3-inflammasome-pathway
#7
Xu Zhang, Qianming Du, Yan Yang, Jianing Wang, Shuai Dou, Chao Liu, Junguo Duan
The purpose of the present study was to investigate the effect of Luteolin(Lut) on myocardial ischemia reperfusion injury and explore the underlying mechanism. Myocardial ischemia reperfusion injury (I/R) model was induced with 30min of left anterior descending (LAD) occlusion followed by 24h of reperfusion. In vivo, the rats were randomly divided into 5 groups: (1)Sham, (2)I/R, (3)I/R+Lut(40mg/kg), (4)I/R+Lut(80mg/kg) and (5)I/R+Lut(160mg/kg). In vitro, the H9c2 cells were assigned to five groups: (1)control, (2)hypoxia-reoxygenation(H/R), (3)H/R+Lut(5μM), (4)H/R+Lut(10μM) and (5)H/R+Lut(20μM)...
May 15, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28500761/melatonin-ameliorates-myocardial-ischemia-reperfusion-injury-through-sirt3-dependent-regulation-of-oxidative-stress-and-apoptosis
#8
Mengen Zhai, Buying Li, Weixun Duan, Lin Jing, Bin Zhang, Meng Zhang, Liming Yu, Zhenhua Liu, Bo Yu, Kai Ren, Erhe Gao, Yang Yang, Hongliang Liang, Zhenxiao Jin, Shiqiang Yu
Sirtuins are a family of highly evolutionarily conserved nicotinamide adenine nucleotide-dependent histone deacetylases. Sirtuin-3 (SIRT3) is a member of the sirtuin family that is localized primarily to the mitochondria and protects against oxidative stress-related diseases, including myocardial ischemia/reperfusion (MI/R) injury. Melatonin has a favorable effect in ameliorating MI/R injury. We hypothesized that melatonin protects against MI/R injury by activating the SIRT3 signaling pathway. In this study, mice were pre-treated with or without a selective SIRT3 inhibitor and then subjected to MI/R operation...
May 13, 2017: Journal of Pineal Research
https://www.readbyqxmd.com/read/28500736/high-density-lipoprotein-hdl-reverses-palmitic-acid-induced-energy-metabolism-imbalance-by-switching-cd36-and-glut4-signaling-pathways-in-cardiomyocyte
#9
Su-Ying Wen, Bharath Kumar Velmurugan, Cecilia Hsuan Day, Chia-Yao Shen, Li-Chin Chun, Yi-Chieh Tsai, Yueh-Min Lin, Ray-Jade Chen, Chia-Hua Kuo, Chih-Yang Huang
In our previous study palmitic acid (PA) induced lipotoxicity and switches energy metabolism from CD36 to GLUT4 in H9c2 cells. Low level of high density lipoprotein (HDL) is an independent risk factor for cardiac hypertrophy. Therefore we in the present study investigated whether HDL can reverse PA induced lipotoxicity in H9c2 cardiomyoblast cells. In this study, we treated H9c2 cells with PA to create a hyperlipidemia model in vitro and analyzed for CD36 and GLUT4 metabolic pathway proteins. CD36 metabolic pathway proteins (phospho-AMPK, SIRT1, PGC1α, PPARα, CPT1β and CD36) were decreased by high PA (150 and 200 µg/µL) concentration...
May 13, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28499238/inhibition-of-inos-protects-cardiomyocytes-against-coxsackievirus-b3-induced-cell-injury-by-suppressing-autophagy
#10
Li Qi, Qi Xin, Jia Wenjun
BACKGROUND: Coxsackievirus B3 (CVB3), a member of the picornavirus family, is one of the major causative enteroviruses of viral myocarditis. The aim of the current study was to investigate the role and underlying mechanism of iNOS and autophagy in CVB3 infected cardiomyocytes. METHODS: Myocardial cell H9c2 were randomly divided into four groups: control group, CVB3 group, CVB3+L-NAME group and the CVB3+iNOS siRNA group. Cell proliferation was detected by MTT method and cell apoptosis was determined by flow cytometric...
May 9, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28494450/stachydrine-protects-against-pressure-overload-induced-cardiac-hypertrophy-by-suppressing-autophagy
#11
Tong-Tong Cao, Hui-Hua Chen, Zhiwei Dong, Yan-Wu Xu, Pei Zhao, Wei Guo, Hong-Chang Wei, Chen Zhang, Rong Lu
BACKGROUND: Autophagy is required for the maintenance of cardiomyocyte homeostasis. However, excessive autophagy plays a maladaptive role in pressure overload-induced heart failure. To identify mechanisms by which Stachydrine inhibits pressure overload-induced cardiac hypertrophy, we determined inhibitory activities against activation of NADPH oxidase, reactive oxygen species(ROS) production and excessive activation of autophagy. METHODS: Stachydrine was administered intragastrically to Wistar rats after Transverse aortic constriction(TAC) and H9c2 cells were treated with Stachydrine after Angiotension II stimulation...
May 11, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/28494360/fluoride-induces-apoptosis-in-h9c2-cardiomyocytes-via-the-mitochondrial-pathway
#12
Xiaoyan Yan, Lu Wang, Xia Yang, Yulan Qiu, Xiaolin Tian, Yi Lv, Fengjie Tian, Guohua Song, Tong Wang
Numerous studies have shown that chronic excessive fluoride intake can adversely affect different organ systems. In particular, the cardiovascular system is susceptible to disruption by a high concentration of fluoride. The objectives of this study were to explore the mechanism of apoptosis by detecting the toxic effects of different concentrations of sodium fluoride (NaF) in H9c2 cells exposed for up to 96 h. NaF not only inhibited H9c2 cell proliferation but also induced apoptosis and morphological damage...
May 1, 2017: Chemosphere
https://www.readbyqxmd.com/read/28491238/inhibition-of-mir-302-suppresses-hypoxia-reoxygenation-induced-h9c2-cardiomyocyte-death-by-regulating-mcl-1-expression
#13
Yao-Ching Fang, Chi-Hsiao Yeh
MicroRNAs play important roles in cell proliferation, differentiation, and apoptosis, and their expression influences cardiomyocyte apoptosis resulting from ischemia-induced myocardial infarction. Here, we determined the role of miR expression in cardiomyocyte apoptosis during hypoxia and reoxygenation. The rat cardiomyocyte cell line H9c2 was incubated for 3 h in normal or hypoxia medium, followed by reoxygenation for 24 h and transfection with a miR-302 mimic or antagomir. The effect of miR-302 on myeloid leukemia cell-differentiation protein-1 (Mcl-1) expression was determined by western blot, real-time polymerase chain reaction, and luciferase reporter assays, with cell viability assays...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28484120/microrna-99a-reduces-lipopolysaccharide-induced-oxidative-injury-by-activating-notch-pathway-in-h9c2-cells
#14
Ran Jing, Zhengming Zhou, Feng Kuang, Lei Huang, Chuanchang Li
microRNA-99a (miR-99a) is recently recognized as a key regulator in various cancers and cardiovascular diseases. In the present study, we sought to investigate the effects of miR-99a in rat cardiomyocyte H9c2 cells against oxidative injury induced by lipopolysaccharide (LPS).MTT assay, reactive oxygen species (ROS) assay, flow cytometry and lactate dehydrogenase (LDH) assay were respectively used to explore viability, ROS levels, apoptosis, and cell death in H9c2 cells. Quantitative PCR (qRT-PCR) was performed to confirm the expression of miR-99a...
May 8, 2017: International Heart Journal
https://www.readbyqxmd.com/read/28478801/involvement-of-trpc1-in-nampt-induced-cardiomyocyte-hypertrophy-through-the-activation-of-er-stress
#15
J Li, W Wu, M Zhao, X Liu
Nicotinamide phosphoribosyltransferase (Nampt) is involved in the development of cardiac hypertrophy. Transient receptor potential canonical channel 1 (TRPC1) and endoplasmic reticulum stress (ER stress) are regarded as critical pathways in cardiac hypertrophy. Therefore, we hypothesizedthat TRPC1 might be associated with ER stress in Nampt-induced cardiac hypertrophy. CulturedH9c2cardiomyocyteswereexposed to Namptfor different timesand the expression of markers of cardiomyocyte hypertrophy and ER stress, as well as TRPC1 were detected...
April 29, 2017: Cellular and Molecular Biology
https://www.readbyqxmd.com/read/28473244/platycodon-grandiflorum-pg-reverses-angiotensin-ii-induced-apoptosis-by-repressing-igf-iir-expression
#16
Yuan-Chuan Lin, Chih-Hsueh Lin, Hsien-Tsung Yao, Wei-Wen Kuo, Chia-Yao Shen, Yu-Lan Yeh, Tsung-Jung Ho, V Vijaya Padma, Yu-Chen Lin, XXXXXXXChih-Yang Huang, Chih-Yang Huang
ETHNOPHARMACOLOGICAL RELEVANCE: Platycodon grandiflorum (PG) is a Chinese medical plant used for decades as a traditional prescription to eliminate phlegm, relieve cough, reduce inflammation and lower blood pressure. PG also has a significant effect on the cardiovascular systems. MATERIALS AND METHODS: The aqueous extract of Platycodon grandiflorum (JACQ.) A. DC. root was screened for inhibiting Ang II-induced IGF-IIR activation and apoptosis pathway in H9c2 cardiomyocytes...
May 1, 2017: Journal of Ethnopharmacology
https://www.readbyqxmd.com/read/28460485/hispidin-induces-autophagic-and-necrotic-death-in-sgc-7901-gastric-cancer-cells-through-lysosomal-membrane-permeabilization-by-inhibiting-tubulin-polymerization
#17
Long-Xian Lv, Zhen-Xing Zhou, Zhan Zhou, Li-Jiang Zhang, Ren Yan, Zhao Zhao, Li-Ya Yang, Xiao-Yuan Bian, Hui-Yong Jiang, Yu-Dong Li, Yi-Sheng Sun, Qin-Qin Xu, Gui-Li Hu, Wen-Jun Guan, Yong-Quan Li
Hispidin and its derivatives are widely distributed in edible mushrooms. Hispidin is more cytotoxic to A549, SCL-1, Bel7402 and Capan-1 cancer cells than to MRC5 normal cells; by contrast, hispidin protects H9c2 cardiomyoblast cells from hydrogen peroxide-induced or doxorubicin-induced apoptosis. Consequently, further research on how hispidin affects normal and cancer cells may help treat cancer and reduce chemotherapy-induced side effects. This study showed that hispidin caused caspase-independent death in SGC-7901 cancer cells but not in GES-1 normal cells...
April 18, 2017: Oncotarget
https://www.readbyqxmd.com/read/28457922/t3-peptide-an-active-fragment-of-tumstatin-inhibits-h2o2-induced-apoptosis-in-h9c2-cardiomyoblasts
#18
Jumpei Yasuda, Muneyoshi Okada, Hideyuki Yamawaki
Tumstatin, a cleaved fragment of α3 chain of type IV collagen, is an endogenous anti-angiogenetic peptide. Although the expression level of tumstatin changes in the heart tissues of certain experimental cardiac disease models, its effect on cardiomyocytes has not been clarified. In this study, we examined the effects of T3 peptide, an active subfragment of tumstatin, on hydrogen peroxide (H2O2)-induced cell death in H9c2 cardiomyoblasts. Cell viability was examined by a cell counting assay. Staining using 4', 6-diamidino-2-phenylindole was performed to observe nuclear morphology...
April 27, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28449869/caffeic-acid-phenethyl-ester-attenuates-pathological-cardiac-hypertrophy-by-regulation-of-mek-erk-signaling-pathway-in-vivo-and-vitro
#19
Jie Ren, Nan Zhang, Haihan Liao, Si Chen, Ling Xu, Jing Li, Zheng Yang, Wei Deng, Qizhu Tang
AIM: To explore the effects of caffeic acid phenethyl ester (CAPE) on cardiac hypertrophy induced by pressure overload. MAIN METHODS: Male wild-type C57 mice, aged 8-10weeks, were used for aortic banding (AB) to induce cardiac hypertrophy. CAPE or (resveratrol) RS was administered from the 3rd day after AB surgery for 6weeks. Echocardiography and hemodynamic analysis were performed to estimate cardiac function. Mice hearts were collected for H&E and PSR staining...
April 24, 2017: Life Sciences
https://www.readbyqxmd.com/read/28447579/glucan-phosphate-inhibits-hmgb-1-release-from-rat-myocardial-h9c2-cells-in-sepsis-via-tlr4-nf-%C3%B0%C2%BAb-signal-pathway
#20
Haizhu Wang, Zhifei Cui, Fei Sun, Huayong Ding
PURPOSE: The effect of glucan phosphate (GP) on the release of HMGB-1 from rat myocardial cells (H9C2) during lipopolysaccharide-induced sepsis, and the underlying mechanisms, were investigated. METHODS: H9C2 cells were divided into three groups: normal; lipopolysaccharide (LPS) (1 mg/ml LPS); and, LPS+GP (2 mg/ml GP). Western blot was used to determine toll-like receptor 4 (TLR4) levels, and electrophoretic mobility-shift assays (EMSA) was used to determine nuclear factor-кB (NF-кB) activity 3, 6 and 9 h after treatment...
April 26, 2017: Clinical and Investigative Medicine. Médecine Clinique et Experimentale
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