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Hyperglycemia and H9C2

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https://www.readbyqxmd.com/read/30280191/overexpression-of-small-ubiquitin%C3%A2-like-modifier-2-ameliorates-high-glucose%C3%A2-induced-reductions-in-cardiomyocyte-proliferation-via-the-transforming-growth-factor%C3%A2-%C3%AE-smad-pathway
#1
Chen Zhao, Qile Shen
Hyperglycemia may induce diabetic cardiomyopathy (DC). In the current study, the mechanism underlying the alleviation of high glucose (HG)‑induced impairments in the proliferation of H9c2 embryo cardiomyocyte proliferation by small ubiquitin‑like modifier 2 (SUMO2) overexpression was investigated. H9c2 cell morphology was identified as classical long shuttle type by optical microscopy. The viability of HG‑injured H9c2 cells was evaluated by a Cell Counting Kit‑8 assay and the results indicated that viability was inhibited in a dose‑dependent (5...
October 1, 2018: Molecular Medicine Reports
https://www.readbyqxmd.com/read/30144576/glucotoxicity-results-in-apoptosis-in-h9c2-cells-via-alteration-in-redox-homeostasis-linked-mitochondrial-dynamics-and-polyol-pathway-and-possible-reversal-with-cinnamic-acid
#2
Nair Anupama, M R Preetha Rani, G L Shyni, K G Raghu
Several mechanisms have been proposed for the heart dysfunction during hyperglycemia. The aim of the present in vitro study is to elucidate the role of alterations in redox homeostasis in the induction of apoptosis during hyperglycemia in H9c2 cells via dysfunction in mitochondria and polyol pathway and evaluation of the beneficial effect of cinnamic acid against the same. The H9c2 cells were incubated with 33 mM glucose for 48 h to simulate the diabetic condition. Cell injury was confirmed with a significant increase of atrial natriuretic peptide and lactate dehydrogenase release...
August 23, 2018: Toxicology in Vitro: An International Journal Published in Association with BIBRA
https://www.readbyqxmd.com/read/30129179/gw0742-activates-peroxisome-proliferator-activated-receptor-%C3%AE-to-reduce-free-radicals-and-alleviate-cardiac-hypertrophy-induced-by-hyperglycemia-in-cultured-h9c2-cells
#3
Kai-Chun Cheng, Wei-Ting Chang, Yingxiao Li, Yung-Ze Cheng, Juei-Tang Cheng, Zhih-Cherng Chen
Peroxisome proliferator-activated receptor δ (PPARδ), the predominant PPAR subtype in the heart, is known to regulate cardiac function. PPARδ activation may inhibit cardiac hypertrophy in H9c2 cells while the potential mechanism has not been elucidated. Then, H9c2 cells incubated with high glucose to induce hypertrophy were used to investigate using GW0742 to activate PPARδ. The fluorescence assays were applied to determine the changes in cell size, cellular calcium levels, and free radicals. Western blot analyses for hypertrophic signals and assays of messenger RNA (mRNA) levels for hypertrophic biomarkers were performed...
August 20, 2018: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/29707106/inhibition-of-aldose-reductase-2-by-a-benzofuroxane-derivative-bf-5m-increases-the-expression-of-kcne1-kcnq1-in-high-glucose-cultured-h9c2-cardiac-cells-and-sudden-cardiac-death
#4
Maria Consiglia Trotta, Monica Salerno, Anna Lisa Brigida, Vincenzo Monda, Antonietta Messina, Carmela Fiore, Roberto Avola, Renato Bernardini, Francesco Sessa, Gabriella Marsala, Guido N Zanghì, Giovanni Messina, Michele D'Amico, Clara Di Filippo
Long QT syndrome (LQTS) is characterized by prolonged QT interval, leading to sudden cardiac death. Hyperglycemia is an important risk factor for LQTS, inhibiting the cardiac rapid component delayed rectifier K+ current (Iks), responsible for QT interval. We previously showed that the new ALR2 inhibitor BF-5m supplies cardioprotection from QT prolongation induced by high glucose concentration in the medium, reducing QT interval prolongation and preserving morphology. Here we investigated the effects of BF-5m on cell cytotoxicity and viability in H9c2 cells, and on cellular potassium ion channels expression...
April 3, 2018: Oncotarget
https://www.readbyqxmd.com/read/29477910/chlorogenic-acid-attenuates-glucotoxicity-in-h9c2-cells-via-inhibition-of-glycation-and-pkc-%C3%AE-upregulation-and-safeguarding-innate-antioxidant-status
#5
M R Preetha Rani, Nair Anupama, Mohan Sreelekshmi, K G Raghu
A series of cardiovascular complications associated with hyperglycemia is a critical threat to the diabetic population. Here we elucidate the link between hyperglycemia and cardiovascular diseases onset, focusing on oxidative stress and associated cardiac dysfunctions. The contribution of advanced glycation end products (AGE) and protein kinase C (PKC) signaling is extensively studied. For induction of hyperglycemia, H9c2 cells were incubated with 33 mM glucose for 48 h to simulate the diabetic condition in in vitro system...
April 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/29392616/kaempferol-attenuates-hyperglycemia-induced-cardiac-injuries-by-inhibiting-inflammatory-responses-and-oxidative-stress
#6
Xuemei Chen, Jianchang Qian, Lintao Wang, Jieli Li, Yunjie Zhao, Jibo Han, Zia Khan, Xiaojun Chen, Jingying Wang, Guang Liang
PURPOSE: Suppression of inflammation and oxidative stress is an attractive strategy to against diabetic cardiomyopathy (DCM). Kaempferol (KPF) exerts both anti-inflammatory and antioxidant pharmacological properties. However, little is known about the effect of KPF on protecting myocardial injury in diabetes. The present study aimed to investigate the effect of KPF on DCM and underlying mechanism. METHODS: Anti-inflammation and anti-oxidative stress activities of KPF were evaluated in H9c2 cells or primary cardiomyocytes by real-time quantitate PCR, immunoblotting, immunofluorescence, ELISA, and FACS...
April 2018: Endocrine
https://www.readbyqxmd.com/read/29130958/propofol-through-upregulating-caveolin-3-attenuates-post-hypoxic-mitochondrial-damage-and-cell-death-in-h9c2-cardiomyocytes-during-hyperglycemia
#7
Fan Deng, Shuang Wang, Liangqing Zhang, Xiang Xie, Shuyun Cai, Haobo Li, Gui-Ling Xie, Hui-Lai Miao, Changmin Yang, Xin Liu, Zhengyuan Xia
BACKGROUND/AIMS: Hearts from diabetic subjects are susceptible to myocardial ischemia reperfusion (I/R) injury. Propofol has been shown to protect against myocardial I/R injury due to its antioxidant properties while the underlying mechanism remained incompletely understood. Thus, this study aimed to determine whether or not propofol could attenuate myocardial I/R injury by attenuating mitochondrial dysfunction/damage through upregulating Caveolin (Cav)-3 under hyperglycemia. METHODS: Cultured rat cardiomyocyte H9C2 cells were subjected to hypoxia/reoxygenation (H/R) in the absence or presence of propofol under high glucose (HG), and cell viability, lactate dehydrogenase (LDH) and mitochondrial viability as well as creatine kinase-MB (CK-MB), cardiac troponin I (cTnI) and intracellular adenosine triphosphate (ATP) content were measured with colorimetric Enzyme-Linked Immunosorbent Assays...
2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29128638/ulk1-regulated-autophagy-a-mechanism-in-cellular-protection-for-aldh2-against-hyperglycemia
#8
Min Liu, Songhe Lu, Wei He, Le Zhang, Ying Ma, Ping Lv, Meijuan Ma, Wenjun Yu, Jiaxing Wang, Mingming Zhang, Yingmei Zhang, Yan Li
Mitochondrial aldehyde dehydrogenase 2 (ALDH2), an important enzyme in the elimination of toxic aldehydes, is involved in cardioprotection against diabetes mellitus. This study was designed to examine the mechanism behind ALDH2-offered protection against high glucose exposure with a focus on autophagy. H9C2 cells were cultured with normal or high glucose medium in the presence or absence of the ALDH2 agonist Alda-1. GFP-LC3 puncta and immunofluorescence were employed to assess autophagosome formation. Western blotting was applied to evaluate autophagy protein markers Atg5, LC3, p62, ULK1 phosphorylation and ALDH2...
February 2018: Toxicology Letters
https://www.readbyqxmd.com/read/29115516/phosphorylation-of-signal-transducer-and-activator-of-transcription-3-induced-by-hyperglycemia-is-different-with-that-induced-by-lipopolysaccharide-or-erythropoietin-via-receptor%C3%A2-coupled-signaling-in-cardiac-cells
#9
Yu-Hsin Chiu, Po-Ming Ku, Yung-Ze Cheng, Yingxiao Li, Juei-Tang Cheng, Ho-Shan Niu
The signal transducer and activator of transcription 3 (STAT3) is known to be involved in hypertrophy and fibrosis in cardiac dysfunction. The activation of STAT3 via the phosphorylation of STAT3 is required for the production of functional activity. It has been established that lipopolysaccharide (LPS)‑induced phosphorylation of STAT3 in cardiomyocytes primarily occurs through a direct receptor‑mediated action. This effect is demonstrated to be produced rapidly. STAT3 in cardiac fibrosis of diabetes is induced by high glucose through promotion of the STAT3‑associated signaling pathway...
January 2018: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28982613/klotho-protects-the-heart-from-hyperglycemia-induced-injury-by-inactivating-ros-and-nf-%C3%AE%C2%BAb-mediated-inflammation-both-in-vitro-and-in-vivo
#10
Yue Guo, Xiaodong Zhuang, Zena Huang, Jing Zou, Daya Yang, Xun Hu, Zhimin Du, Lichun Wang, Xinxue Liao
Cardiac inflammation and oxidative stress play a key role in the pathogenesis of diabetic cardiomyopathy (DCM). The anti-aging protein Klotho has been found to protect cells from inflammation and oxidative stress. The current study aimed to explore the cardioprotective effects of Klotho on DCM and the underlying mechanisms. H9c2 cells and neonatal cardiomyocytes were incubated with 33mM glucose in the presence or absence of Klotho. Klotho pretreatment effectively inhibited high glucose-induced inflammation, ROS generation, apoptosis, mitochondrial dysfunction, fibrosis and hypertrophy in both H9c2 cells and neonatal cardiomyocytes...
January 2018: Biochimica et biophysica acta. Molecular basis of disease
https://www.readbyqxmd.com/read/28914755/thioredoxin-2-offers-protection-against-mitochondrial-oxidative-stress-in-h9c2-cells-and-against-myocardial-hypertrophy-induced-by-hyperglycemia
#11
Hong Li, Changqing Xu, Quanfeng Li, Xiuxiang Gao, Erkio Sugano, Hiroshi Tomita, Liming Yang, Sa Shi
Mitochondrial oxidative stress is thought to be a key contributor towards the development of diabetic cardiomyopathy. Thioredoxin 2 (Trx2) is a mitochondrial antioxidant that, along with Trx reductase 2 (TrxR2) and peroxiredoxin 3 (Prx3), scavenges H₂O₂ and offers protection against oxidative stress. Our previous study showed that TrxR inhibitors resulted in Trx2 oxidation and increased ROS emission from mitochondria. In the present study, we observed that TrxR inhibition also impaired the contractile function of isolated heart...
September 15, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28824303/autophagy-was-involved-in-the-protective-effect-of-metformin-on-hyperglycemia-induced-cardiomyocyte-apoptosis-and-connexin43-downregulation-in-h9c2-cells
#12
Guang-Yu Wang, Ya-Guang Bi, Xiang-Dong Liu, Yu Zhao, Jun-Feng Han, Meng Wei, Qing-Yong Zhang
Background: Increased cardiomyocyte apoptosis under high glucose condition contributes to diabetic cardiomyopathy. Degradation of cardiac Connexin43 (Cx43) has been associated with cardiac dysfunction in diabetic heart. Clinical and experimental studies suggested that metformin (Met) exhibits cardioprotective properties against diabetes. Aim: The aim of this study was to investigate the effect and underlying signaling mechanisms of metformin on apoptosis and Cx43 expression in H9c2 cells presenting with hyperglycemia conditions...
2017: International Journal of Medical Sciences
https://www.readbyqxmd.com/read/28765969/ampk-activation-restores-ischemic-post%C3%A2-conditioning-cardioprotection-in-stz%C3%A2-induced-type-1-diabetic-rats-role-of-autophagy
#13
Bin Zhou, Yan Leng, Shao-Qing Lei, Zhong-Yuan Xia
Although the mechanism remains unclear, ischemic post‑conditioning (IPO) is a promising approach to combat myocardial ischemia reperfusion (IR) injury; however, it has been proven ineffective in diabetes. The present study aimed to identify whether hyperglycemia‑induced AMP‑activated protein kinase (AMPK) inhibition contributes to the ineffectiveness of IPO via autophagy attenuation in diabetic hearts. Diabetic and non‑diabetic rats were subjected to myocardial IR and/or IPO with/without treatment with the AMPK activator A‑769662 and/or autophagy inhibitor 3‑methyladenine (3‑MA)...
September 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28713934/upregulation-of-connexin-43-and-apoptosis%C3%A2-associated-protein-expression-by-high-glucose-in-h9c2-cells-was-improved-by-resveratrol-via-the-autophagy-signaling-pathway
#14
Guang-Yu Wang, Ya-Guang Bi, Xiang-Dong Liu, Jun-Feng Han, Meng Wei, Qing-Yong Zhang
The expression of connexin43 (Cx43) protein and the apoptotic rate of cardiomyocytes may be regulated by autophagy and associated with diabetic cardiomyopathy. It is possible that the beneficial effect of resveratrol on diabetic cardiomyocytes occurs via the autophagy pathway. However, it remains to be elucidated whether resveratrol treatment may attenuate the hyperglycemia‑induced remodeling of Cx43 and apoptosis through the regulation of autophagy. H9c2 cardiac cells were incubated with 5.5 and 25 mM glucose, 25 mM glucose with chloroquine (50 µM), and 25 mM glucose with or without resveratrol (10, 25 µM) for 24 h...
September 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28700904/inhibition-of-high-glucose-induced-inflammation-and-fibrosis-by-a-novel-curcumin-derivative-prevents-renal-and-heart-injury-in-diabetic-mice
#15
Hongjin Chen, Xi Yang, Kongqin Lu, Chun Lu, Yunjie Zhao, Suqing Zheng, Jieli Li, Zhangjian Huang, Yi Huang, Yali Zhang, Guang Liang
Hyperglycemia-induced inflammation and fibrosis have important roles in the pathogenesis of diabetic nephropathy and cardiomyopathy. With inflammatory cytokines and signaling pathways as important mediators, targeting inflammation may be an effective approach to new avenue for treating diabetic complications. J17, a molecule with structural similarities to curcumin, exhibited good anti-inflammatory activities by inhibiting LPS-induced inflammatory response in macrophages. However, its ability to alleviate hyperglycemia-induced injury via its anti-inflammatory actions remained unclear...
August 15, 2017: Toxicology Letters
https://www.readbyqxmd.com/read/28368536/transcription-factor-crem-mediates-high-glucose-response-in-cardiomyocytes-and-in-a-male-mouse-model-of-prolonged-hyperglycemia
#16
Saviana A Barbati, Claudia Colussi, Lorenza Bacci, Aurora Aiello, Agnese Re, Egidio Stigliano, Andrea M Isidori, Claudio Grassi, Alfredo Pontecorvi, Antonella Farsetti, Carlo Gaetano, Simona Nanni
This study aims at investigating the epigenetic landscape of cardiomyocytes exposed to elevated glucose levels. High glucose (30 mM) for 72 hours determined some epigenetic changes in mouse HL-1 and rat differentiated H9C2 cardiomyocytes including upregulation of class I and III histone deacetylase protein levels and activity, inhibition of histone acetylase p300 activity, increase in histone H3 lysine 27 trimethylation, and reduction in H3 lysine 9 acetylation. Gene expression analysis focused on cardiotoxicity revealed that high glucose induced markers associated with tissue damage, fibrosis, and cardiac remodeling such as Nexilin (NEXN), versican, cyclic adenosine 5'-monophosphate-responsive element modulator (CREM), and adrenoceptor α2A (ADRA2)...
July 1, 2017: Endocrinology
https://www.readbyqxmd.com/read/28291959/the-opening-of-atp-sensitive-k-channels-protects-h9c2-cardiac-cells-against-the-high-glucose-induced-injury-and-inflammation-by-inhibiting-the-ros-tlr4-necroptosis-pathway
#17
Weijie Liang, Meiji Chen, Dongdan Zheng, Jianhao Li, Mingcai Song, Wenzhu Zhang, Jianqiang Feng, Jun Lan
BACKGROUND/AIMS: Hyperglycemia activates multiple signaling molecules, including reactive oxygen species (ROS), toll-like receptor 4 (TLR4), receptor-interacting protein 3 (RIP3, a kinase promoting necroptosis), which mediate hyperglycemia-induced cardiac injury. This study explored whether inhibition of ROS-TLR4-necroptosis pathway contributed to the protection of ATP-sensitive K+ (KATP) channel opening against high glucose-induced cardiac injury and inflammation. METHODS: H9c2 cardiac cells were treated with 35 mM glucose (HG) to establish a model of HG-induced insults...
2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/28232492/hyperglycemia-induced-changes-in-zip7-and-znt7-expression-cause-zn-2-release-from-the-sarco-endo-plasmic-reticulum-and-mediate-er-stress-in-the-heart
#18
Erkan Tuncay, Verda C Bitirim, Aysegul Durak, Gaelle R J Carrat, Kathryn M Taylor, Guy A Rutter, Belma Turan
Changes in cellular free Zn2+ concentration, including those in the sarco(endo)plasmic reticulum [S(E)R], are primarily coordinated by Zn2+ transporters (ZnTs) whose identity and role in the heart are not well established. We hypothesized that ZIP7 and ZnT7 transport Zn2+ in opposing directions across the S(E)R membrane in cardiomyocytes and that changes in their activity play an important role in the development of ER stress during hyperglycemia. The subcellular S(E)R localization of ZIP7 and ZnT7 was determined in cardiomyocytes and in isolated S(E)R preparations...
May 2017: Diabetes
https://www.readbyqxmd.com/read/28202395/sulfiredoxin-involved-in-the-protection-of-peroxiredoxins-against-hyperoxidation-in-the-early-hyperglycaemia
#19
Sa Shi, Yunqiu Guo, Yanping Lou, Quanfeng Li, Xiaona Cai, Xin Zhong, Hong Li
As a direct consequence of hyperglycaemia, the excessive generation of ROS is central to the pathogenesis of diabetic cardiomyopathy. We hypothesize that stimulation of high glucose (HG) results in an increased sulfiredoxin (Srx) expression, which regulates ROS signaling through reducing the hyperoxidized peroxiredoxins (Prxs). We show that hyperoxidized Prxs were initially reduced in the preliminary stage but then dramatically increased in advanced stage and these changes corresponded to a significant increase of Srx expression in the heart of diabetic rats...
March 15, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28146135/the-transcription-profile-unveils-the-cardioprotective-effect-of-aspalathin-against-lipid-toxicity-in-an-in-vitro-h9c2-model
#20
Rabia Johnson, Phiwayinkosi V Dludla, Christo J F Muller, Barbara Huisamen, M Faadiel Essop, Johan Louw
Aspalathin, a C-glucosyl dihydrochalcone, has previously been shown to protect cardiomyocytes against hyperglycemia-induced shifts in substrate preference and subsequent apoptosis. However, the precise gene regulatory network remains to be elucidated. To unravel the mechanism and provide insight into this supposition, the direct effect of aspalathin in an isolated cell-based system, without the influence of any variables, was tested using an H9c2 cardiomyocyte model. Cardiomyocytes were exposed to high glucose (33 mM) for 48 h before post-treatment with or without aspalathin...
January 31, 2017: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
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