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heart and endoplasmic reticulum

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https://www.readbyqxmd.com/read/29335338/crth2-promotes-endoplasmic-reticulum-stress-induced-cardiomyocyte-apoptosis-through-m-calpain
#1
Shengkai Zuo, Deping Kong, Chenyao Wang, Jiao Liu, Yuanyang Wang, Qiangyou Wan, Shuai Yan, Jian Zhang, Juan Tang, Qianqian Zhang, Luheng Lyu, Xin Li, Zhixin Shan, Li Qian, Yujun Shen, Ying Yu
Apoptotic death of cardiac myocytes is associated with ischemic heart disease and chemotherapy-induced cardiomyopathy. Chemoattractant receptor-homologous molecule expressed on T helper type 2 cells (CRTH2) is highly expressed in the heart. However, its specific role in ischemic cardiomyopathy is not fully understood. Here, we demonstrated that CRTH2 disruption markedly improved cardiac recovery in mice postmyocardial infarction and doxorubicin challenge by suppressing cardiomyocyte apoptosis. Mechanistically, CRTH2 activation specifically facilitated endoplasmic reticulum (ER) stress-induced cardiomyocyte apoptosis via caspase-12-dependent pathway...
January 15, 2018: EMBO Molecular Medicine
https://www.readbyqxmd.com/read/29331057/manifestations-and-mechanisms-of-myocardial-lipotoxicity-in-obesity
#2
Arthur C Sletten, Linda R Peterson, Jean E Schaffer
Environmental and socioeconomic changes over the past thirty years have contributed to a dramatic rise in the worldwide prevalence of obesity. Heart disease is among the most serious health risks of obesity, with increases in both atherosclerotic coronary heart disease and heart failure among obese individuals. In this review, we focus on primary myocardial alterations in obesity that include hypertrophic remodeling and diastolic dysfunction. Obesity-associated perturbations in myocardial and systemic lipid metabolism are important contributors to cardiovascular complications of obesity...
January 13, 2018: Journal of Internal Medicine
https://www.readbyqxmd.com/read/29314656/mammalian-target-of-rapamycin-inhibition-attenuates-myocardial-ischaemia-reperfusion-injury-in-hypertrophic-heart
#3
Lei-Lei Ma, Xin Ma, Fei-Juan Kong, Jun-Jie Guo, Hong-Tao Shi, Jian-Bing Zhu, Yun-Zeng Zou, Jun-Bo Ge
Pathological cardiac hypertrophy aggravated myocardial infarction and is causally related to autophagy dysfunction and increased oxidative stress. Rapamycin is an inhibitor of serine/threonine kinase mammalian target of rapamycin (mTOR) involved in the regulation of autophagy as well as oxidative/nitrative stress. Here, we demonstrated that rapamycin ameliorates myocardial ischaemia reperfusion injury by rescuing the defective cytoprotective mechanisms in hypertrophic heart. Our results showed that chronic rapamycin treatment markedly reduced the phosphorylated mTOR and ribosomal protein S6 expression, but not Akt in both normal and aortic-banded mice...
January 4, 2018: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/29307086/iron-overload-impact-on-p-atpases
#4
REVIEW
Leilismara Sousa, Marco Tulio C Pessoa, Tamara G F Costa, Vanessa F Cortes, Herica L Santos, Leandro Augusto Barbosa
Iron is a chemical element that is active in the fundamental physiological processes for human life, but its burden can be toxic to the body, mainly because of the stimulation of membrane lipid peroxidation. For this reason, the action of iron on many ATPases has been studied, especially on P-ATPases, such as the Na+,K+-ATPase and the Ca2+-ATPase. On the Fe2+-ATPase activity, the free iron acts as an activator, decreasing the intracellular Fe2+ and playing a protection role for the cell. On the Ca2+-ATPase activity, the iron overload decreases the enzyme activity, raising the cytoplasmic Ca2+ and decreasing the sarco/endoplasmic reticulum and the Golgi apparatus Ca2+ concentrations, which could promote an enzyme oxidation, nitration, and fragmentation...
January 6, 2018: Annals of Hematology
https://www.readbyqxmd.com/read/29288332/essential-role-for-egfr-tyrosine-kinase-and-er-stress-in-myocardial-infarction-in-type-2-diabetes
#5
Vishal Mali, Samuel Haddox, Corey Hornersmith, Khalid Matrougui, Souad Belmadani
We previously reported that EGFR tyrosine kinase (EGFRtk) activity and endoplasmic reticulum (ER) stress are enhanced in type 2 diabetic (T2D) mice and cause vascular dysfunction. In the present study, we determined the in vivo contribution of EGFRtk and ER stress in acute myocardial infarction induced by acute ischemia (40 min)-reperfusion (24 h) (I/R) injury in T2D (db-/db-) mice. We treated db-/db- mice with EGFRtk inhibitor (AG1478, 10 mg/kg/day) for 2 weeks. Mice were then subjected to myocardial I/R injury...
December 29, 2017: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/29238517/exogenous-h2s-restores-ischemic-post-conditioning-induced-cardioprotection-through-inhibiting-endoplasmic-reticulum-stress-in-the-aged-cardiomyocytes
#6
Weiming Sun, Jinxia Yang, Yuanzhou Zhang, Yuxin Xi, Xin Wen, Di Yuan, Yuehong Wang, Can Wei, Rui Wang, Lingyun Wu, Hongzhu Li, Changqing Xu
Background: A gasotransmitter hydrogen sulfide (H2S) plays an important physiological and pathological role in cardiovascular system. Ischemic post-conditioning (PC) provides cardioprotection in the young hearts but not in the aged hearts. Exogenous H2S restores PC-induced cardioprotection by inhibition of mitochondrial permeability transition pore opening and oxidative stress and increase of autophagy in the aged hearts. However, whether H2S contributes to the recovery of PC-induced cardioprotection via down-regulation of endoplasmic reticulum stress (ERS) in the aged hearts is unclear...
2017: Cell & Bioscience
https://www.readbyqxmd.com/read/29229678/epitope-mapping-of-serca2a-identifies-an-antigenic-determinant-that-induces-mainly-atrial-myocarditis-in-a-j-mice
#7
Bharathi Krishnan, Chandirasegaran Massilamany, Rakesh H Basavalingappa, Arunakumar Gangaplara, Rajkumar A Rajasekaran, Muhammad Z Afzal, Vahid Khalilzad-Sharghi, You Zhou, Jean-Jack Riethoven, Shyam S Nandi, Paras K Mishra, Raymond A Sobel, Jennifer L Strande, David Steffen, Jay Reddy
Sarcoplasmic/endoplasmic reticulum Ca2+ adenosine triphosphatase (SERCA)2a, a critical regulator of calcium homeostasis, is known to be decreased in heart failure. Patients with myocarditis or dilated cardiomyopathy develop autoantibodies to SERCA2a suggesting that they may have pathogenetic significance. In this report, we describe epitope mapping analysis of SERCA2a in A/J mice that leads us to make five observations: 1) SERCA2a contains multiple T cell epitopes that induce varying degrees of myocarditis...
December 11, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/29169992/hax-1-regulates-serca2a-oxidation-and-degradation
#8
Philip A Bidwell, Guan-Sheng Liu, Narayani Nagarajan, Chi Keung Lam, Kobra Haghighi, George Gardner, Wen-Feng Cai, Wen Zhao, Luke Mugge, Elizabeth Vafiadaki, Despina Sanoudou, Jack Rubinstein, Djamel Lebeche, Roger Hajjar, Junichi Sadoshima, Evangelia G Kranias
Ischemia/reperfusion injury is associated with contractile dysfunction and increased cardiomyocyte death. Overexpression of the hematopoietic lineage substrate-1-associated protein X-1 (HAX-1) has been shown to protect from cellular injury but the function of endogenous HAX-1 remains obscure due to early lethality of the knockout mouse. Herein we generated a cardiac-specific and inducible HAX-1 deficient model, which uncovered an unexpected role of HAX-1 in regulation of sarco/endoplasmic reticulum Ca-ATPase (SERCA2a) in ischemia/reperfusion injury...
November 21, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29150445/the-antiapoptotic-protein-hax-1-mediates-half-of-phospholamban-s-inhibitory-activity-on-calcium-cycling-and-contractility-in-the-heart
#9
Philip A Bidwell, Kobra Haghighi, Evangelia G Kranias
The antiapoptotic protein HS-associated protein X-1 (HAX-1) localizes to sarcoplasmic reticulum (SR) in the heart and interacts with the small membrane protein phospholamban (PLN), inhibiting the cardiac sarco/endoplasmic reticulum calcium ATPase (SERCA2a) in the regulation of overall calcium handling and heart muscle contractility. However, because global HAX-1 deletion causes early lethality, how much endogenous HAX-1 contributes to PLN's inhibitory activity on calcium cycling is unknown. We therefore generated a cardiac-specific and inducible knockout mouse model...
November 17, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29129702/fkbp8-protects-the-heart-from-hemodynamic-stress-by-preventing-the-accumulation-of-misfolded-proteins-and-endoplasmic-reticulum-associated-apoptosis-in-mice
#10
Tomofumi Misaka, Tomokazu Murakawa, Kazuhiko Nishida, Yosuke Omori, Manabu Taneike, Shigemiki Omiya, Chris Molenaar, Yoshihiro Uno, Osamu Yamaguchi, Junji Takeda, Ajay M Shah, Kinya Otsu
Protein quality control in cardiomyocytes is crucial to maintain cellular homeostasis. The accumulation of damaged organelles, such as mitochondria and misfolded proteins in the heart is associated with heart failure. During the process to identify novel mitochondria-specific autophagy (mitophagy) receptors, we found FK506-binding protein 8 (FKBP8), also known as FKBP38, shares similar structural characteristics with a yeast mitophagy receptor, autophagy-related 32 protein. However, knockdown of FKBP8 had no effect on mitophagy in HEK293 cells or H9c2 myocytes...
November 10, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29115440/aspirin-ameliorates-cerebral-infarction-through-regulation-of-tlr4-nf%C3%A2-%C3%AE%C2%BAb%C3%A2-mediated-endoplasmic-reticulum-stress-in-mouse-model
#11
Xin Wang, Bin Shen, Dezhou Sun, Xiangyu Cui
Cerebral infarction is a cerebrovascular disease caused by local brain ischemic necrosis or softening, which is associated with diabetes, obesity, hypertension and rheumatic heart arrhythmia. Previous studies have indicated that aspirin is a potential oral anticoagulant in the treatment of cerebral ischemic stroke. However, the potential mechanism mediated by aspirin in cerebral infarction therapy is not well understood. The present study analyzed the therapeutic effects of aspirin on cerebral infarction and investigated the underlying molecular mechanism of aspirin‑ameliorated benefits for thrombolysis...
January 2018: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29115422/melatonin-ameliorates-myocardial-apoptosis-by-suppressing-endoplasmic-reticulum-stress-in-rats-with-long%C3%A2-term-diabetic-cardiomyopathy
#12
Fang-Yuan Xiong, Song-Tao Tang, Huan Su, Hai-Qin Tang, Pin Jiang, Qing Zhou, Yuan Wang, Hua-Qing Zhu
The effects of melatonin (MLT), which exerts cardioprotective effects against myocardial apoptosis, in long‑term diabetic cardiomyopathy are not currently well defined. The present study aimed to investigate how MLT protects the heart through modulating myocardial apoptosis in rats with type 2 diabetes mellitus (DM). In total, 36 rats were randomly divided into three groups, including control (n=12), DM (n=12) and DM + MLT (n=12) groups. The results demonstrated that, in DM rats, a significant increase was observed in the serum fasting blood glucose and lipid levels, in addition to insulin resistance and cardiac dysfunction, which were attenuated in DM rats treated with MLT...
October 20, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29104090/two-novel-calreticulin-related-molecules-with-microbial-binding-and-phagocytosis-enhancing-capacity-in-the-half-smooth-tongue-sole-cynoglossus-semilaevis
#13
Guanghua Wang, Zengjie Jiang, Shuwen He, Min Zhang
Calreticulin (CRT) is highly conserved chaperone located in the endoplasmic reticulum. It plays important roles in innate immunity. Although various immune-related functions of CRT have been reported in vertebrates and invertebrates, information on the potential functions of teleost CRT is very limited. In the present study, we characterized two calreticulin-related molecules from tongue sole (Cynoglossus semilaevis), calreticulin-like1 and calreticulin-like2 (CsCRTL1 and CsCRTL2). CsCRTL1and CsCRTL2 contain signature CRT motifs that are highly conserved in different species...
November 6, 2017: Fish & Shellfish Immunology
https://www.readbyqxmd.com/read/29074428/identification-and-function-analysis-of-canine-stimulator-of-interferon-gene-sting
#14
Yuxiang Zhang, Mengyan Zhu, Gairu Li, Jie Liu, Xiaofeng Zhai, Ruyi Wang, Junyan Zhang, Gang Xing, Jinyan Gu, Liping Yan, Jing Lei, Haifeng Sun, Zhiyu Shi, Fei Liu, Boli Hu, Shuo Su, Jiyong Zhou
Stimulator of interferon gene (STING) plays an important role in the cyclic GMP-AMP synthase (cGAS)-mediated activation of type I IFN responses. In this study, we identified and cloned canine STING gene. Full-length STING encodes a 375 amino acid product that shares the highest similarity with feline STING. Highest levels of mRNA of canine STING were detected in the spleen and lungs while the lowest levels in the heart and muscle. Analysis of its cellular localization showed that STING is localizes to the endoplasmic reticulum...
October 24, 2017: Microbial Pathogenesis
https://www.readbyqxmd.com/read/29066441/endoplasmic-reticulum-stress-is-associated-with-autophagy-and-cardiomyocyte-remodeling-in-experimental-and-human-atrial-fibrillation
#15
Marit Wiersma, Roelien A M Meijering, Xiao-Yan Qi, Deli Zhang, Tao Liu, Femke Hoogstra-Berends, Ody C M Sibon, Robert H Henning, Stanley Nattel, Bianca J J M Brundel
BACKGROUND: Derailment of proteostasis, the homeostasis of production, function, and breakdown of proteins, contributes importantly to the self-perpetuating nature of atrial fibrillation (AF), the most common heart rhythm disorder in humans. Autophagy plays an important role in proteostasis by degrading aberrant proteins and organelles. Herein, we investigated the role of autophagy and its activation pathway in experimental and clinical AF. METHODS AND RESULTS: Tachypacing of HL-1 atrial cardiomyocytes causes a gradual and significant activation of autophagy, as evidenced by enhanced LC3B-II expression, autophagic flux and autophagosome formation, and degradation of p62, resulting in reduction of Ca(2+) amplitude...
October 24, 2017: Journal of the American Heart Association
https://www.readbyqxmd.com/read/29050006/recent-insights-into-the-biological-functions-of-sestrins-in-health-and-disease
#16
Menglong Wang, Yao Xu, Jianfang Liu, Jing Ye, Wenhui Yuan, Huimin Jiang, Zhen Wang, Hong Jiang, Jun Wan
Sestrins (Sesns) have been identified as a family of highly conserved stress-inducible proteins that are strongly up-regulated by various stresses, including DNA damage, oxidative stress, and hypoxia. The Sesns play protective roles in most physiological and pathological conditions mainly through the regulation of oxidative stress, inflammation, autophagy, endoplasmic reticulum stress, and metabolic homeostasis. In this review, we discussed the possible regulators of Sesns expression, such as p53, forkhead box O, nuclear factor erythroid 2 like 2 (Nrf2), NH (2)-terminal kinase (JNK)/c-Jun pathway and hypoxia-inducible factor-1α (Hif-1α), and the downstream pathways regulated by the Sesns including AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling, mitogen-activated protein kinases (MAPKs) signaling, Nrf2 signaling, NADPH oxidase signaling and transforming growth factor β (TGF-β) signaling in heart diseases, lung diseases, gastrointestinal tract diseases, liver and metabolism diseases, neurological diseases, kidney diseases and immunological diseases...
October 19, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29045568/loss-of-protein-kinase-novel-1-pkn1-is-associated-with-mild-systolic-and-diastolic-contractile-dysfunction-increased-phospholamban-thr17-phosphorylation-and-exacerbated-ischaemia-reperfusion-injury
#17
Asvi A Francois, Kofo Obasanjo-Blackshire, James E Clark, Andrii Boguslavskyi, Mark R Holt, Peter Parker, Michael S Marber, Richard J Heads
Aims: PKN1 is a stress-responsive protein kinase acting downstream of small GTP-binding proteins of the Rho/Rac family. The aim was to determine its role in endogenous cardioprotection. Methods and Results: Hearts from PKN1 knockout (KO) or wild type (WT) littermate control mice were perfused in Langendorff mode and subjected to global ischemia and reperfusion (I/R). Myocardial infarct size was doubled in PKN1 KO hearts compared to WT hearts. PKN1 was basally phosphorylated on the activation loop Thr778 PDK1 target site which was unchanged during I/R...
October 16, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/29040818/metformin-attenuates-er-stress-induced-mitochondrial-dysfunction
#18
Qun Chen, Jeremy Thompson, Ying Hu, Anindita Das, Edward J Lesnefsky
Endoplasmic reticulum (ER) stress, a disturbance of the ER function, contributes to cardiac injury. ER and mitochondria are closely connected organelles within cells. ER stress contributes to mitochondrial dysfunction, which is a key factor to increase cardiac injury. Metformin, a traditional anti-diabetic drug, decreases cardiac injury during ischemia-reperfusion. Metformin also inhibits ER stress in cultured cells. We hypothesized that metformin can attenuate the ER stress-induced mitochondrial dysfunction and subsequent cardiac injury...
September 28, 2017: Translational Research: the Journal of Laboratory and Clinical Medicine
https://www.readbyqxmd.com/read/29035876/hydrogen-gas-attenuates-myocardial-ischemia-reperfusion-injury-independent-of-postconditioning-in-rats-by-attenuating-endoplasmic-reticulum-stress-induced-autophagy
#19
Yunan Gao, Hongxiao Yang, Jing Chi, Qiannan Xu, Luqi Zhao, Weijia Yang, Weifan Liu, Wei Yang
BACKGROUND/AIMS: To study the effect of inhaling hydrogen gas on myocardial ischemic/reperfusion(I/R) injury in rats. METHODS: Seventy male Wistar albino rats were divided into five groups at random as the sham group (Sham). The I/R group (I/R), The ischemic postconditioning group (IPo), The I/R plus hydrogen group (IH2) and the ischemic postconditioning plus hydrogen group (IPoH2). The Sham group was without coronary occlusion. In I/R group, Ischemic/reperfusion injury was induced by coronary occlusion for 1 hour...
2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29026925/er-protein-quality-control-and-the-unfolded-protein-response-in-the-heart
#20
A Arrieta, E A Blackwood, C C Glembotski
Cardiac myocytes are the cells responsible for the robust ability of the heart to pump blood throughout the circulatory system. Cardiac myocytes grow in response to a variety of physiological and pathological conditions; this growth challenges endoplasmic reticulum-protein quality control (ER-PQC), a major feature of which includes the unfolded protein response (UPR). ER-PQC and the UPR in cardiac myocytes growing under physiological conditions, including normal development, exercise, and pregnancy, are sufficient to support hypertrophic growth of each cardiac myocyte...
October 13, 2017: Current Topics in Microbiology and Immunology
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