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Sarcoplasmic reticulum

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https://www.readbyqxmd.com/read/28716970/prolonged-force-depression-after-mechanically-demanding-contractions-is-largely-independent-of-ca-2-and-reactive-oxygen-species
#1
Sigitas Kamandulis, Felipe de Souza Leite, Andres Hernández, Abram Katz, Marius Brazaitis, Joseph D Bruton, Tomas Venckunas, Nerijus Masiulis, Dalia Mickeviciene, Nerijus Eimantas, Andrejus Subocius, Dilson E Rassier, Albertas Skurvydas, Niklas Ivarsson, Håkan Westerblad
Increased production of reactive oxygen/nitrogen species (ROS) and impaired cellular Ca(2+) handling are implicated in the prolonged low-frequency force depression (PLFFD) observed in skeletal muscle after both metabolically and mechanically demanding exercise. Metabolically demanding high-intensity exercise can induce PLFFD accompanied by ROS-dependent fragmentation of the sarcoplasmic reticulum Ca(2+) release channels, the ryanodine receptor (RyR)-1. We tested whether similar changes occur after mechanically demanding eccentric contractions...
July 17, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28713824/effects-of-hyperglycemia-on-vascular-smooth-muscle-ca-2-signaling
#2
Nahed El-Najjar, Rashmi P Kulkarni, Nancy Nader, Rawad Hodeify, Khaled Machaca
Diabetes is a complex disease that is characterized with hyperglycemia, dyslipidemia, and insulin resistance. These pathologies are associated with significant cardiovascular implications that affect both the macro- and microvasculature. It is therefore important to understand the effects of various pathologies associated with diabetes on the vasculature. Here we directly test the effects of hyperglycemia on vascular smooth muscle (VSM) Ca(2+) signaling in an isolated in vitro system using the A7r5 rat aortic cell line as a model...
2017: BioMed Research International
https://www.readbyqxmd.com/read/28702845/regulation-of-cardiac-ca-2-and-ion-channels-by-shear-mechanotransduction
#3
REVIEW
Joon-Chul Kim, Min-Jeong Son, Jun Wang, Sun-Hee Woo
Cardiac contraction is controlled by a Ca(2+) signaling sequence that includes L-type Ca(2+) current-gated opening of Ca(2+) release channels (ryanodine receptors) in the sarcoplasmic reticulum (SR). Local Ca(2+) signaling in the atrium differs from that in the ventricle because atrial myocytes lack transverse tubules and have more abundant corbular SR. Myocardium is subjected to a variety of forces with each contraction, such as stretch, shear stress, and afterload, and adapts to those mechanical stresses...
July 12, 2017: Archives of Pharmacal Research
https://www.readbyqxmd.com/read/28701305/redox-and-activation-of-protein-kinase-a-dysregulates-calcium-homeostasis-in-pulmonary-vein-cardiomyocytes-of-chronic-kidney-disease
#4
Shih-Yu Huang, Yao-Chang Chen, Yu-Hsun Kao, Ming-Hsiung Hsieh, Yung-Kuo Lin, Shih-Ann Chen, Yi-Jen Chen
BACKGROUND: Chronic kidney disease (CKD) increases the occurrence of atrial fibrillation and pulmonary vein (PV) arrhythmogenesis. Calcium dysregulation and reactive oxygen species (ROS) enhance PV arrhythmogenic activity. The purposes of this study were to investigate whether CKD modulates PV electrical activity through dysregulation of calcium homeostasis and ROS. METHODS AND RESULTS: Biochemical and electrocardiographic studies were conducted in rabbits with and without CKD (induced by 150 mg/kg per day neomycin sulfate and 500 mg/kg per day cefazolin)...
July 12, 2017: Journal of the American Heart Association
https://www.readbyqxmd.com/read/28698617/loss-of-md1-exacerbates-pressure-overload-induced-left-ventricular-structural-and-electrical-remodelling
#5
Jianye Peng, Yu Liu, Xiaoju Xiong, Congxin Huang, Yang Mei, Zhiqiang Wang, Yanhong Tang, Jing Ye, Bin Kong, Wanli Liu, Teng Wang, He Huang
Myeloid differentiation protein 1 (MD1) has been implicated in numerous pathophysiological processes, including immune regulation, obesity, insulin resistance, and inflammation. However, the role of MD1 in cardiac remodelling remains incompletely understood. We used MD1-knockout (KO) mice and their wild-type littermates to determine the functional significance of MD1 in the regulation of aortic banding (AB)-induced left ventricular (LV) structural and electrical remodelling and its underlying mechanisms. After 4 weeks of AB, MD1-KO hearts showed substantial aggravation of LV hypertrophy, fibrosis, LV dilation and dysfunction, and electrical remodelling, which resulted in overt heart failure and increased electrophysiological instability...
July 11, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28697281/transport-of-the-alpha-subunit-of-the-l-type-calcium-channel-through-the-sarcoplasmic-reticulum-occurs-prior-to-localization-to-triads-and-requires-the-beta-subunit-but-not-stac3-in-skeletal-muscles
#6
Jeremy W Linsley, I-Uen Hsu, Wenjai Wang, John Y Kuwada
Contraction of skeletal muscle is initiated by excitation-contraction (EC) coupling during which membrane voltage is transduced to intracellular Ca(2+) release. EC coupling requires dihydropyridine receptors (DHPR) located at triads, which are junctions between the transverse (T) tubule and SR membranes, that sense membrane depolarization in the T tubule membrane. Reduced EC coupling is associated with ageing, and disruptions of EC coupling result in congenital myopathies for which there are few therapies. The precise localization of DHPRs to triads is critical for EC coupling, yet trafficking of the DHPR to triads is not well understood...
July 11, 2017: Traffic
https://www.readbyqxmd.com/read/28684623/calcium-and-excitation-contraction-coupling-in-the-heart
#7
REVIEW
David A Eisner, Jessica L Caldwell, Kornél Kistamás, Andrew W Trafford
Cardiac contractility is regulated by changes in intracellular Ca concentration ([Ca(2+)]i). Normal function requires that [Ca(2+)]i be sufficiently high in systole and low in diastole. Much of the Ca needed for contraction comes from the sarcoplasmic reticulum and is released by the process of calcium-induced calcium release. The factors that regulate and fine-tune the initiation and termination of release are reviewed. The precise control of intracellular Ca cycling depends on the relationships between the various channels and pumps that are involved...
July 7, 2017: Circulation Research
https://www.readbyqxmd.com/read/28683791/in-vivo-administration-of-urolithin-a-and-b-prevents-the-occurrence-of-cardiac-dysfunction-in-streptozotocin-induced-diabetic-rats
#8
Monia Savi, Leonardo Bocchi, Pedro Mena, Margherita Dall'Asta, Alan Crozier, Furio Brighenti, Donatella Stilli, Daniele Del Rio
BACKGROUND: Emerging evidence suggests that specific (poly)phenols may constitute new preventative strategies to counteract cell oxidative stress and myocardial tissue inflammation, which have a key role in the patho-physiology of diabetic cardiomyopathy. In a rat model of early diabetes, we evaluated whether in vivo administration of urolithin A (UA) or urolithin B (UB), the main gut microbiota phenolic metabolites of ellagitannin-rich foods, can reduce diabetes-induced microenvironmental changes in myocardial tissue, preventing cardiac functional impairment...
July 6, 2017: Cardiovascular Diabetology
https://www.readbyqxmd.com/read/28665545/inhibition-of-mevalonate-pathway-prevents-ischemia-induced-cardiac-dysfunction-in-rats-via-rhoa-independent-signaling-pathway
#9
Ying Yang, Xiqing Rong, Xue Lv, Wenbing Jiang, Yuan Yang, Dongwu Lai, Shiming Xu, Guosheng Fu
AIM: We previously demonstrated that anoxia-mediated Ca(2+) handling dysfunction could be ameliorated through inhibition of mevalonate pathway via RhoA- and Ras-related mechanisms in H9c2 cells. In this study, we further explored whether inhibition of mevalonate pathway is associated with cardiac remodeling and dysfunction in ischemic cardiomyopathy, and discuss the possible role of Ras, Rac and RhoA in cardiac dysfunction. METHODS: We investigated the role of mevalonate pathway in cardiac remodeling and cardiomyocyte Ca(2+) handling proteins expression in a rat model of cardiac dysfunction due to myocardial infarction (MI)...
June 30, 2017: Cardiovascular Therapeutics
https://www.readbyqxmd.com/read/28656113/cardiac-dysrhythmias-and-neurological-dysregulation-manifestations-of-profound-hypomagnesemia
#10
Sagger Mawri, Edward Gildeh, Namita Joseph, Bobak Rabbani, Bryan Zweig
Magnesium is the second most common intracellular cation and serves as an important metabolic cofactor to over 300 enzymatic reactions throughout the human body. Among its various roles, magnesium modulates calcium entry and release from sarcoplasmic reticulum and regulates ATP pumps in myocytes and neurons, thereby regulating cardiac and neuronal excitability. Therefore, deficiency of this essential mineral may result in serious cardiovascular and neurologic derangements. In this case, we present the clinical course of a 76-year-old woman who presented with marked cardiac and neurological signs and symptoms which developed as a result of severe hypomagnesemia...
2017: Case Reports in Cardiology
https://www.readbyqxmd.com/read/28653141/physiology-and-pathophysiology-of-excitation-contraction-coupling-the-functional-role-of-ryanodine-receptor
#11
Gaetano Santulli, Daniel R Lewis, Andrew R Marks
Calcium (Ca(2+)) release from intracellular stores plays a key role in the regulation of skeletal muscle contraction. The type 1 ryanodine receptors (RyR1) is the major Ca(2+) release channel on the sarcoplasmic reticulum (SR) of myocytes in skeletal muscle and is required for excitation-contraction (E-C) coupling. This article explores the role of RyR1 in skeletal muscle physiology and pathophysiology.
June 26, 2017: Journal of Muscle Research and Cell Motility
https://www.readbyqxmd.com/read/28648626/mechanosensitivity-of-microdomain-calcium-signalling-in-the-heart
#12
REVIEW
Patrick Schönleitner, Uli Schotten, Gudrun Antoons
In cardiac myocytes, calcium (Ca(2+)) signalling is tightly controlled in dedicated microdomains. At the dyad, i.e. the narrow cleft between t-tubules and junctional sarcoplasmic reticulum (SR), many signalling pathways combine to control Ca(2+)-induced Ca(2+) release during contraction. Local Ca(2+) gradients also exist in regions where SR and mitochondria are in close contact to regulate energetic demands. Loss of microdomain structures, or dysregulation of local Ca(2+) fluxes in cardiac disease, is often associated with oxidative stress, contractile dysfunction and arrhythmias...
June 22, 2017: Progress in Biophysics and Molecular Biology
https://www.readbyqxmd.com/read/28648117/alteration-of-sarcoplasmic-reticulum-ca-2-atpase-expression-in-lower-limb-ischemia-caused-by-atherosclerosis-obliterans
#13
J Fodor, A Gomba-Tóth, T Oláh, E Zádor, Zs Cs Tóth, I Ioannis, B Molnár, I Kovács, L Csernoch
Atherosclerosis is a disease caused by a build-up of fatty plaques and cholesterol in the arteries. The lumen of the vessels is obliterated resulting in restricted blood supply to tissues. In ischemic conditions, the cytosolic Ca(2+) level of skeletal muscle may increase, indicating the alteration of Ca(2+) removal mechanisms. Ca(2+) is transported from cytosol into the sarcoplasmic reticulum by Ca(2+) ATPase (SERCA), with its 1a isoform expressed in adult, while its 1b isoform in neonatal and regenerating fast-twitch skeletal muscle...
June 26, 2017: Physiology International
https://www.readbyqxmd.com/read/28644055/regulation-of-transient-receptor-potential-melastatin-4-channel-by-sarcoplasmic-reticulum-inositol-trisphosphate-receptors-role-in-human-detrusor-smooth-muscle-function
#14
Aaron Provence, Eric S Rovner, Georgi V Petkov
We recently reported key physiologic roles for Ca(2+)-activated transient receptor potential melastatin 4 (TRPM4) channels in detrusor smooth muscle (DSM). However, the Ca(2+)-signaling mechanisms governing TRPM4 channel activity in human DSM cells are unexplored. As the TRPM4 channels are activated by Ca(2+), inositol 1,4,5-trisphosphate receptor (IP3R)-mediated Ca(2+) release from the sarcoplasmic reticulum represents a potential Ca(2+) source for TRPM4 channel activation. We used clinically-characterized human DSM tissues to investigate the molecular and functional interactions of the IP3Rs and TRPM4 channels...
June 23, 2017: Channels
https://www.readbyqxmd.com/read/28640447/role-of-serca-pump-in-muscle-thermogenesis-and-metabolism
#15
Muthu Periasamy, Santosh Kumar Maurya, Sanjaya Kumar Sahoo, Sushant Singh, Sanjaya Kumar Sahoo, Felipe C G Reis, Naresh Chandra Bal
In muscle cells, the sarcoplasmic reticulum (SR) not only acts as a Ca2+ store, but also regulates the contractile characteristics of the muscle. Ca2+ release from the SR is the primary mechanism for activating muscle contraction and reuptake of Ca2+ by the sarcoplasmic reticulum Ca2+ ATPase (SERCA) pump causes muscle relaxation. The SERCA pump isoforms are encoded by three genes, SERCA 1, 2, and 3, which are differentially expressed in muscle and determine SR Ca2+ dynamics by affecting the rate and amount of Ca2+ uptake, thereby affecting SR store and release of Ca2+ in muscle...
June 18, 2017: Comprehensive Physiology
https://www.readbyqxmd.com/read/28638997/follistatin-treatment-suppresses-serca1b-levels-independently-of-other-players-of-calcium-homeostasis-in-c2c12-myotubes
#16
János Fodor, Adrienn Gomba-Tóth, Tamás Oláh, János Almássy, Ernő Zádor, László Csernoch
Follistatin (FS) is a high affinity activin-binding protein, neutralizing the effects of the Transforming Growth Factor-beta (TGF-β) superfamily members, as myostatin (MSTN). Since MSTN emerged as a negative regulator, FS has been considered as a stimulator of skeletal muscle growth and differentiation. Here, we studied the effect of FS administration on the Ca(2+)-homeostasis of differentiating C2C12 skeletal muscle cells. FS-treatment increased the fusion index, the size of terminally differentiated myotubes, and transiently elevated the expression of the calcium-dependent protein phosphatase, calcineurin, at the beginning of differentiation...
June 21, 2017: Journal of Muscle Research and Cell Motility
https://www.readbyqxmd.com/read/28637456/the-modified-yi-qi-decoction-protects-cardiac-ischemia-reperfusion-induced-injury-in-rats
#17
Xiao Yu, Xiao-Dong Zhao, Rong-Qi Bao, Jia-Yu Yu, Guo-Xing Zhang, Jing-Wei Chen
BACKGROUND: To investigate the effects and involved mechanisms of the modified Yi Qi decoction (MYQ) in cardiac ischemia-reperfusion (IR) induced injury. METHODS: Male Sprague-Dawley rats were subjected to a 30-min coronary arterial occlusion followed by reperfusion, low or high dose decoction of MYQ was administrated orally for 1 week or 1 month. RESULTS: Both in 1 week and 1 month IR rat groups, cardiac function indexes were significantly impaired compared with sham group rats, accompanied with higher ratio of infarct size to risk size, decreased expressions of sodium calcium exchanger (NCX1) and sarcoplasmic reticulum Ca(2+)-ATPase (Serca2a), and different expressions of autophagic proteins, Beclin-1 and LC3...
June 21, 2017: BMC Complementary and Alternative Medicine
https://www.readbyqxmd.com/read/28636017/effect-of-cisplatin-on-the-transport-activity-of-pii-type-atpases
#18
Francesco Tadini-Buoninsegni, Giacomo Sordi, Serena Smeazzetto, Giovanni Natile, Fabio Arnesano
Cisplatin (cis-diamminedichlorido-Pt(ii)) is extensively used as a chemotherapeutic agent against various types of tumors. However, cisplatin administration causes serious side effects, including nephrotoxicity, ototoxicity and neurotoxicity. It has been shown that cisplatin can interact with P-type ATPases, e.g., Cu(+)-ATPases (ATP7A and ATP7B) and Na(+),K(+)-ATPase. Cisplatin-induced inhibition of Na(+),K(+)-ATPase has been related to the nephrotoxic effect of the drug. To investigate the inhibitory effects of cisplatin on the pumping activity of PII-type ATPases, electrical measurements were performed on sarcoplasmic reticulum Ca(2+)-ATPase (SERCA) and Na(+),K(+)-ATPase embedded in vesicles/membrane fragments adsorbed on a solid-supported membrane...
July 19, 2017: Metallomics: Integrated Biometal Science
https://www.readbyqxmd.com/read/28630914/deregulated-ca-2-cycling-underlies-the-development-of-arrhythmia-and-heart-disease-due-to-mutant-obscurin
#19
Li-Yen R Hu, Maegen A Ackermann, Peter A Hecker, Benjamin L Prosser, Brendan King, Kelly A O'Connell, Alyssa Grogan, Logan C Meyer, Christopher E Berndsen, Nathan T Wright, W Jonathan Lederer, Aikaterini Kontrogianni-Konstantopoulos
Obscurins are cytoskeletal proteins with structural and regulatory roles encoded by OBSCN. Mutations in OBSCN are associated with the development of hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM). Specifically, the R4344Q mutation present in immunoglobulin domain 58 (Ig58) was the first to be linked with the development of HCM. To assess the effects of R4344Q in vivo, we generated the respective knock-in mouse model. Mutant obscurins are expressed and incorporated normally into sarcomeres...
June 2017: Science Advances
https://www.readbyqxmd.com/read/28630169/patient-specific-drug-screening-using-a-human-induced-pluripotent-stem-cell-model-of-catecholaminergic-polymorphic-ventricular-tachycardia-type-2
#20
Leonid Maizels, Irit Huber, Gil Arbel, Anke J Tijsen, Amira Gepstein, Asaad Khoury, Lior Gepstein
BACKGROUND: Catecholaminergic polymorphic ventricular tachycardia type 2 (CPVT2) results from autosomal recessive CASQ2 mutations, causing abnormal Ca(2+)-handling and malignant ventricular arrhythmias. We aimed to establish a patient-specific human induced pluripotent stem cell (hiPSC) model of CPVT2 and to use the generated hiPSC-derived cardiomyocytes to gain insights into patient-specific disease mechanism and pharmacotherapy. METHODS AND RESULTS: hiPSC cardiomyocytes were derived from a CPVT2 patient (D307H-CASQ2 mutation) and from healthy controls...
June 2017: Circulation. Arrhythmia and Electrophysiology
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