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heart and endoplasmic reticulum

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https://www.readbyqxmd.com/read/28096195/the-multifunctional-mitochondrial-epac1-controls-myocardial-cell-death
#1
Loubina Fazal, Marion Laudette, Sílvia Paula-Gomes, Sandrine Pons, Caroline Conte, Florence Tortosa, Pierre Sicard, Yannis Sainte-Marie, Malik Bisserier, Olivier Lairez, Alexandre Lucas, Jérôme Roy, Bijan Ghaleh, Jeremy Fauconnier, Jeanne Mialet-Perez, Frank Lezoualc'h
RATIONALE: Although the second messenger cyclic AMP (cAMP) is physiologically beneficial in the heart, it largely contributes to cardiac disease progression when dysregulated. Current evidence suggests that cAMP is produced within mitochondria. However, mitochondrial cAMP signaling and its involvement in cardiac pathophysiology are far from being understood. OBJECTIVE: To investigate the role of mitochondrial exchange protein directly activated by cAMP 1 (MitEpac1) in ischemia/reperfusion (I/R) injury...
January 17, 2017: Circulation Research
https://www.readbyqxmd.com/read/28036323/chemical-chaperone-4-phenylbutyric-acid-reduces-cardiac-ischemia-reperfusion-injury-by-alleviating-endoplasmic-reticulum-stress-and-oxidative-stress
#2
Lian Jian, Yuan Lu, Shan Lu, Chengzhi Lu
BACKGROUND Cardiovascular diseases are the leading cause of death in many countries and myocardial ischemia-reperfusion (I/R) injury is the cause of many serious heart diseases. Recent reports suggested that endoplasmic reticulum (ER) stress is associated with the progress of ischemia/reperfusion (I/R) injury. In a previous study, we illustrated that 4-phenylbutyric acid (4-PBA) reduces I/R-induced cell death in vitro through inhibiting the ER stress-initiated cell apoptosis. In the present study we investigated whether 4-PBA improves heart function in isolated rat hearts subjected to I/R and elucidated the potential mechanisms involved in 4-PBA-induced cardioprotective effects...
December 30, 2016: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
https://www.readbyqxmd.com/read/27997746/autophagy-an-adaptive-physiological-countermeasure-to-cellular-senescence-and-ischaemia-reperfusion-associated-cardiac-arrhythmias
#3
REVIEW
Istvan Lekli, David Donald Haines, Gyorgy Balla, Arpad Tosaki
Oxidative stress placed on tissues that involved in pathogenesis of a disease activates compensatory metabolic changes, such as DNA damage repair that in turn causes intracellular accumulation of detritus and 'proteotoxic stress', leading to emergence of 'senescent' cellular phenotypes, which express high levels of inflammatory mediators, resulting in degradation of tissue function. Proteotoxic stress resulting from hyperactive inflammation following reperfusion of ischaemic tissue causes accumulation of proteinaceous debris in cells of the heart in ways that cause potentially fatal arrhythmias, in particular ventricular fibrillation (VF)...
December 20, 2016: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/27993557/inhibition-of-endoplasmic-reticulum-stress-by-neuregulin-1-protects-against-myocardial-ischemia-reperfusion-injury
#4
Shan-Juan Fang, Peng-Yang Li, Chun-Mei Wang, Yi Xin, Wei-Wei Lu, Xiao-Xia Zhang, Song Zuo, Chang-Sheng Ma, Chao-Shu Tang, Shao-Ping Nie, Yong-Fen Qi
Neuregulin-1 (NRG-1), an endogenously produced polypeptide, is the ligand of cardiomyocyte ErbB receptors, with cardiovascular protective effects. In the present study, we explored whether the cardioprotective effect of NRG-1 against I/R injury is mediated by inhibiting myocardial endoplasmic reticulum (ER) stress. In vitro, NRG-1 directly inhibited the upregulation of ER stress markers such as glucose-regulated protein 78, CCAAT/enhancer binding protein homologous protein and cleaved caspase-12 induced by the ER stress inducers tunicamycin or dithiothreitol in both neonatal and adult ventricular myocytes...
December 16, 2016: Peptides
https://www.readbyqxmd.com/read/27981457/bariatric-surgery-ameliorates-diabetic-cardiac-dysfunction-by-inhibiting-er-stress-in-a-diabetic-rat-model
#5
Xiaoqian Zhang, Shaozhuang Liu, Guangyong Zhang, Mingwei Zhong, Teng Liu, Meng Wei, Dong Wu, Xin Huang, Yugang Cheng, Qunzheng Wu, Sanyuan Hu
BACKGROUND: Cardiac dysfunction is a severe complication of diabetes, with no effective treatment. Currently, bariatric surgery is more and more widely used to attenuate diabetes-associated diseases. The mechanism is not clear. Endoplasmic reticulum (ER) stress-dependent apoptosis has been observed in the progression of diabetic myocardium damage. Therefore, this research was designed to investigate the effects of different bariatric procedures on cardiac dysfunction via ER stress-induced cardiomyocyte apoptosis pathway in a diabetic rat model...
December 15, 2016: Obesity Surgery
https://www.readbyqxmd.com/read/27957794/brd7-mediates-hyperglycaemia-induced-myocardial-apoptosis-via-endoplasmic-reticulum-stress-signalling-pathway
#6
Xiao-Meng Wang, Ying-Cui Wang, Xiang-Juan Liu, Qi Wang, Chun-Mei Zhang, Li-Ping Zhang, Hui Liu, Xin-Yu Zhang, Yang Mao, Zhi-Ming Ge
Bromodomain-containing protein 7 (BRD7) is a tumour suppressor that is known to regulate many pathological processes including cell growth, apoptosis and cell cycle. Endoplasmic reticulum (ER) stress-induced apoptosis plays a key role in diabetic cardiomyopathy (DCM). However, the molecular mechanism of hyperglycaemia-induced myocardial apoptosis is still unclear. We intended to determine the role of BRD7 in high glucose (HG)-induced apoptosis of cardiomyocytes. In vivo, we established a type 1 diabetic rat model by injecting a high-dose streptozotocin (STZ), and lentivirus-mediated short hairpin RNA (shRNA) was used to inhibit BRD7 expression...
December 13, 2016: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/27931779/complement-and-sepsis-induced-heart-dysfunction
#7
Fatemeh Fattahi, Peter A Ward
It is well known that cardiac dysfunction develops during sepsis in both humans and in rodents (rats, mice). These defects appear to be reversible, since after "recovery" from sepsis, cardiac dysfunction disappears and the heart returns to its function that was present before the onset of sepsis. Our studies, using in vivo and in vitro models, have demonstrated that C5a and its receptors (C5aR1 and C5aR2) play key roles in cardiac dysfunction developing during sepsis. Use of a neutralizing antibody to C5a largely attenuates cardiac dysfunction and other adverse events developing during sepsis...
December 5, 2016: Molecular Immunology
https://www.readbyqxmd.com/read/27929749/critical-role-of-x-box-binding-protein-1-in-nadph-oxidase-4-triggered-cardiac-hypertrophy-is-mediated-by-receptor-interacting-protein-kinase-1
#8
Li Chen, Mingyue Zhao, Junli Li, Yu Wang, Qinxue Bao, Siyuan Wu, Xueqin Deng, Xiaoju Tang, Wenchao Wu, Xiaojing Liu
NADPH oxidase 4 (NOX4) and the NOX4-related redox signaling are implicated in cardiac hypertrophy. NOX4 is interrelated with endoplasmic reticulum stress (ERS). Spliced X-box binding protein 1 (Xbp1s) is a key mediator of ERS while its role in cardiac hypertrophy is still poorly understood. Recently, receptor interacting protein kinase 1(RIPK1) has been increasingly reported to be associated with ERS. Therefore, we aimed to test the hypothesis that Xbp1s mediates NOX4-triggered cardiac hypertrophy via RIPK1 signaling...
December 8, 2016: Cell Cycle
https://www.readbyqxmd.com/read/27911441/sirt1-protects-the-heart-from-er-stress-induced-cell-death-through-eif2%C3%AE-deacetylation
#9
Alexandre Prola, Julie Pires Da Silva, Arnaud Guilbert, Lola Lecru, Jérôme Piquereau, Maxance Ribeiro, Philippe Mateo, Mélanie Gressette, Dominique Fortin, Céline Boursier, Cindy Gallerne, Anaïs Caillard, Jane-Lise Samuel, Hélène François, David A Sinclair, Pierre Eid, Renée Ventura-Clapier, Anne Garnier, Christophe Lemaire
Over the past decade, endoplasmic reticulum (ER) stress has emerged as an important mechanism involved in the pathogenesis of cardiovascular diseases including heart failure. Cardiac therapy based on ER stress modulation is viewed as a promising avenue toward effective therapies for the diseased heart. Here, we tested whether sirtuin-1 (SIRT1), a NAD(+)-dependent deacetylase, participates in modulating ER stress response in the heart. Using cardiomyocytes and adult-inducible SIRT1 knockout mice, we demonstrate that SIRT1 inhibition or deficiency increases ER stress-induced cardiac injury, whereas activation of SIRT1 by the SIRT1-activating compound STAC-3 is protective...
December 2, 2016: Cell Death and Differentiation
https://www.readbyqxmd.com/read/27903836/sericin-ameliorated-dysmorphic-mitochondria-in-high-cholesterol-diet-streptozotocin-rat-by-antioxidative-property
#10
Sumate Ampawong, Duangnate Isarangkul, Pornanong Aramwit
Sericin has been implicated in lower cholesterolemic effect due to its properties with several mechanisms. Mitochondria are one of the most important targets to be affected in high blood cholesterol and glucose conditions. The protective role of sericin on mitochondria remains doubtful. To examine this role, electron microscopic, histopathologic, immunohistochemical, and biochemical studies were performed in a high-cholesterol diet/streptozotocin rat model. The results demonstrated that sericin reduced blood cholesterol without hypoglycemic effect...
November 29, 2016: Experimental Biology and Medicine
https://www.readbyqxmd.com/read/27882143/expression-of-connexin-43-ion-channels-and-ca-2-handling-proteins-in-rat-pulmonary-vein-cardiomyocytes
#11
Yaqiong Xiao, Xue Cai, Andrew Atkinson, Sunil Jit Logantha, Mark Boyett, Halina Dobrzynski
Atrial fibrillation (AF) is the most common cardiac arrhythmia. AF is thought to be triggered by ectopic beats, originating primarily in the myocardial sleeves surrounding the pulmonary veins (PVs). The mechanisms underlying these cardiac arrhythmias remain unclear. To investigate this, frozen sections of heart and lung tissue from adult rats without arrhythmia were obtained in different planes, stained with Masson's trichrome, and immunolabeled for connexin 43 (Cx43), caveolin-3 (Cav3), hyperpolarization-activated cyclic nucleotide-gated channel 4 (HCN4), Nav1...
November 2016: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/27875732/sirtuin-1-protects-the-aging-heart-from-contractile-dysfunction-mediated-through-the-inhibition-of-endoplasmic-reticulum-stress-mediated-apoptosis-in-cardiac-specific-sirtuin-1-knockout-mouse-model
#12
Yu-Juei Hsu, Shih-Che Hsu, Chiao-Po Hsu, Yen-Hui Chen, Yung-Lung Chang, Junichi Sadoshima, Shih-Ming Huang, Chien-Sung Tsai, Chih-Yuan Lin
BACKGROUND: The longevity regulator Sirtuin 1 is an NAD(+)-dependent histone deacetylase that regulates endoplasmic reticulum stress and influences cardiomyocyte apoptosis during cardiac contractile dysfunction induced by aging. The mechanism underlying Sirtuin 1 function in cardiac contractile dysfunction related to aging has not been completely elucidated. METHODS: We evaluated cardiac contractile function, endoplasmic reticulum stress, apoptosis, and oxidative stress in 6- and 12month-old cardiac-specific Sirtuin 1 knockout (Sirt1(-/-)) and control (Sirt1(f/f)) mice using western blotting and immunohistochemistry...
February 1, 2017: International Journal of Cardiology
https://www.readbyqxmd.com/read/27871808/new-mechanism-of-lipotoxicity-in-diabetic-cardiomyopathy-deficiency-of-endogenous-h2s-production-and-er-stress
#13
Runmin Guo, Zijun Wu, Jiamei Jiang, Chang Liu, Bin Wu, Xingyue Li, Teng Li, Hailiang Mo, Songjian He, Shanghai Li, Hai Yan, Ruina Huang, Qiong You, Keng Wu
OBJECTIVE: To investigate the roles and mechanisms of endogenous hydrogen sulfide (H2S) and endoplasmic reticulum (ER) stress in the development of diabetic cardiomyopathy (DCM). METHODS: Blood of DCM patients included in the study were collected. The model of DCM rats was established using streptozotocin (STZ) injection. Cardiac lipotoxicity in vitro models were established using 500μM palmitic acid (PA) treatment for 24h in AC16 cardiomyocytes. Endogenous H2S production in plasma, culture supernatant and heart was measured by sulphur ion-selective electrode assay...
November 18, 2016: Mechanisms of Ageing and Development
https://www.readbyqxmd.com/read/27854125/apelin-apj-system-a-novel-therapeutic-target-for-myocardial-ischemia-reperfusion-injury
#14
Zhe Chen, Di Wu, Lanfang Li, Linxi Chen
Apelin is the endogenous ligand of the G protein-coupled receptor, APJ. Recently, researches indicate that the apelin/APJ system involves in myocardial ischemia-reperfusion injury (MIRI), which is a common pathophysiological process in patients with heart diseases and therapies. The reperfusion induces the expression of apelin and APJ receptor, which play an important role in cardioprotection of MIRI. The apelin/APJ system alleviates MIRI mainly by decreasing mitochondrial reactive oxygen species and delaying the opening of mitochondrial permeability transition pores, which induce the initiation of mitophagy...
December 2016: DNA and Cell Biology
https://www.readbyqxmd.com/read/27836743/characterization-of-mitochondrial-glycerol-3-phosphate-acyltransferase-in-notothenioid-fishes
#15
Kelly A Keenan, Theresa J Grove, Corey A Oldham, Kristin M O'Brien
Hearts of Antarctic icefishes (suborder Notothenioidei, family Channichthyidae) have higher densities of mitochondria, and mitochondria have higher densities of phospholipids, compared to red-blooded notothenioids. Glycerol-3-phosphate acyltransferase (GPAT) catalyzes the rate-limiting step in glycerolipid biosynthesis. There are four isoforms of GPAT in vertebrates; GPAT1 and GPAT2 are localized to the outer mitochondrial membrane, whereas GPAT3 and GPAT4 are localized to the endoplasmic reticulum membrane...
February 2017: Comparative Biochemistry and Physiology. Part B, Biochemistry & Molecular Biology
https://www.readbyqxmd.com/read/27815070/direct-detection-of-serca-calcium-transport-and-small-molecule-inhibition-in-giant-unilamellar-vesicles
#16
Tengfei Bian, Joseph M Autry, Denise Casemore, Ji Li, David D Thomas, Gaohong He, Chengguo Xing
We have developed a charge-mediated fusion method to reconstitute the sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA) in giant unilamellar vesicles (GUV). Intracellular Ca(2+) transport by SERCA controls key processes in human cells such as proliferation, signaling, and contraction. Small-molecule effectors of SERCA are urgently needed as therapeutics for Ca(2+) dysregulation in human diseases including cancer, diabetes, and heart failure. Here we report the development of a method for efficiently reconstituting SERCA in GUV, and we describe a streamlined protocol based on optimized parameters (e...
December 9, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27795806/c1q-tnf-related-protein-9-protects-diabetic-rat-heart-against-ischemia-reperfusion-injury-role-of-endoplasmic-reticulum-stress
#17
Sanxing Bai, Liang Cheng, Yang Yang, Chongxi Fan, Dajun Zhao, Zhigang Qin, Xiao Feng, Lin Zhao, Jipeng Ma, Xiaowu Wang, Jian Yang, Xuezeng Xu, Dinghua Yi, Wei Yi
As a newly identified adiponectin paralog, C1q/TNF-related protein 9 (CTRP9) reduces myocardial ischemia reperfusion (IR) injury through partially understood mechanisms. In the present study, we sought to identify the role of endoplasmic reticulum stress (ERS) in CTRP9 induced cardioprotection in diabetic heart. Isolated hearts from high-fat-diet (HFD) induced type 2 diabetic Sprague-Dawley rats were subjected to ex vivo IR protocol via a Langendorff apparatus at the presence of globular CTRP9. CTRP9 significantly improved post-IR heart function and reduced cardiac infarction, cardiomyocytes apoptosis, Caspase-3, Caspase-9, Caspase-12, TNF-α expression, and lactate dehydrogenase activity...
2016: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/27763637/nogo-c-regulates-cardiomyocyte-apoptosis-during-mouse-myocardial-infarction
#18
Shi Jia, Xue Qiao, Jingjing Ye, Xuan Fang, Chunling Xu, Yangpo Cao, Ming Zheng
Myocardial infarction is caused by insufficient coronary blood supply, which leads to myocardial damage and eventually the heart failure. Molecular mechanisms associated with the loss of cardiomyocytes during myocardial infarction (MI) and ischemia-related cardiac diseases are not yet fully understood. Nogo-C is an endoplasmic reticulum protein ubiquitously expressed in tissues including in the heart, however, the cardiac function of Nogo-C is still unknown. In the present study, we found that Nogo-C was upregulated in mouse hearts after MI, and hypoxic treatments also increased Nogo-C protein level in cardiomyocytes...
October 20, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27698420/pore-architecture-of-tric-channels-and-insights-into-their-gating-mechanism
#19
Hanting Yang, Miaohui Hu, Jianli Guo, Xiaomin Ou, Tanxi Cai, Zhenfeng Liu
Intracellular Ca(2+) signalling processes are fundamental to muscle contraction, neurotransmitter release, cell growth and apoptosis. Release of Ca(2+) from the intracellular stores is supported by a series of ion channels in sarcoplasmic or endoplasmic reticulum (SR/ER). Among them, two isoforms of the trimeric intracellular cation (TRIC) channel family, named TRIC-A and TRIC-B, modulate the release of Ca(2+) through the ryanodine receptor or inositol triphosphate receptor, and maintain the homeostasis of ions within SR/ER lumen...
October 27, 2016: Nature
https://www.readbyqxmd.com/read/27667666/suppressors-of-superoxide-h2o2-production-at-site-iq-of-mitochondrial-complex-i-protect-against-stem-cell-hyperplasia-and-ischemia-reperfusion-injury
#20
Martin D Brand, Renata L S Goncalves, Adam L Orr, Leonardo Vargas, Akos A Gerencser, Martin Borch Jensen, Yves T Wang, Simon Melov, Carolina N Turk, Jason T Matzen, Victoria J Dardov, H Michael Petrassi, Shelly L Meeusen, Irina V Perevoshchikova, Heinrich Jasper, Paul S Brookes, Edward K Ainscow
Using high-throughput screening we identified small molecules that suppress superoxide and/or H2O2 production during reverse electron transport through mitochondrial respiratory complex I (site IQ) without affecting oxidative phosphorylation (suppressors of site IQ electron leak, "S1QELs"). S1QELs diminished endogenous oxidative damage in primary astrocytes cultured at ambient or low oxygen tension, showing that site IQ is a normal contributor to mitochondrial superoxide-H2O2 production in cells. They diminished stem cell hyperplasia in Drosophila intestine in vivo and caspase activation in a cardiomyocyte cell model driven by endoplasmic reticulum stress, showing that superoxide-H2O2 production by site IQ is involved in cellular stress signaling...
October 11, 2016: Cell Metabolism
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