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Cardiomyocyte turn over

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https://www.readbyqxmd.com/read/26386426/cardiomyocyte-specific-overexpression-of-the-ubiquitin-ligase-wwp1-contributes-to-reduction-in-connexin-43-and-arrhythmogenesis
#1
Wassim A Basheer, Brett S Harris, Heather L Mentrup, Measho Abreha, Elizabeth L Thames, Jessica B Lea, Deborah A Swing, Neal G Copeland, Nancy A Jenkins, Robert L Price, Lydia E Matesic
Gap junctions (GJ) are intercellular channels composed of connexin subunits that play a critical role in a diverse number of cellular processes in all tissue types. In the heart, GJs mediate electrical coupling between cardiomyocytes and display mislocalization and/or downregulation in cardiac disease (a process known as GJ remodeling), producing an arrhythmogenic substrate. The main constituent of GJs in the ventricular myocardium is Connexin 43 (Cx43), an integral membrane protein that is rapidly turned over and shows decreased expression or function with age...
November 2015: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/24412254/left-atrial-endocardial-dysfunction-and-platelet-activation-in-patients-with-atrial-fibrillation-and-mitral-stenosis
#2
Zhi-Qiang Luo, Xing-Hai Hao, Jin-Hua Li, Jiang Dai, Ke-Ye Liu, Yong-Qiang Lai
OBJECTIVE: This study demonstrated left atrial endocardial dysfunction and platelet activation in patients with atrial fibrillation and mitral stenosis. METHODS: Study included 80 patients with mitral stenosis and atrial fibrillation (40 each with and without left atrial thrombosis), 15 healthy volunteers, and 10 left atrial appendage (LAA) specimens from donor hearts. Blood samples were collected through peripheral vein and left atrium, with peripheral blood samples of volunteers as controls...
November 2014: Journal of Thoracic and Cardiovascular Surgery
https://www.readbyqxmd.com/read/23834776/antiadrenergic-effect-of-adenosine-involves-connexin-43-turn-over-in-h9c2-cells
#3
Ada Popolo, Silvana Morello, Rosalinda Sorrentino, Aldo Pinto
Connexin 43 (Cx43) is the major protein of cardiac ventricular gap junctions and is crucial to cell-cell communication and cardiac function. Several authors report that adrenergic stimulation affects Cx43 expression via protein kinase A (PKA) and MAPK-regulated pathways. Adenosine has been shown to exert direct antiadrenergic effects on the heart, protecting it from toxic effects of overstimulation. The aim of our study was to understand the involvement of Cx43 in the anti-adrenergic effect of adenosine on cardiomyocytes...
September 5, 2013: European Journal of Pharmacology
https://www.readbyqxmd.com/read/23519595/the-constant-beat-cardiomyocytes-adapt-their-forces-by-equal-contraction-upon-environmental-stiffening
#4
Nils Hersch, Benjamin Wolters, Georg Dreissen, Ronald Springer, Norbert Kirchgeßner, Rudolf Merkel, Bernd Hoffmann
Cardiomyocytes are responsible for the permanent blood flow by coordinated heart contractions. This vital function is accomplished over a long period of time with almost the same performance, although heart properties, as its elasticity, change drastically upon aging or as a result of diseases like myocardial infarction. In this paper we have analyzed late rat embryonic heart muscle cells' morphology, sarcomere/costamere formation and force generation patterns on substrates of various elasticities ranging from ∼1 to 500 kPa, which covers physiological and pathological heart stiffnesses...
March 15, 2013: Biology Open
https://www.readbyqxmd.com/read/23441952/differential-effects-of-retinoids-and-inhibitors-of-erk-and-p38-signaling-on-adipogenic-and-myogenic-differentiation-of-p19-stem-cells
#5
Frédéric Bouchard, Joanne Paquin
All-trans-retinoic acid (atRA) is an essential signaling molecule in embryonic development. It regulates cell differentiation by activating nuclear retinoic acid receptors (RAR) and retinoid-X receptors (RXR), which both control gene expression. In addition, atRA could act in the cytoplasm by modulating the activity of mitogen-activated protein kinases (MAPK) ERK and p38, which also have a role in cell differentiation. AtRA can induce the differentiation of P19 embryonic carcinoma stem cells into adipocytes, cardiomyocytes, and skeletal muscle cells, concurrently, in the same culture...
July 15, 2013: Stem Cells and Development
https://www.readbyqxmd.com/read/23326547/mir-30-regulated-autophagy-mediates-angiotensin-ii-induced-myocardial-hypertrophy
#6
Wei Pan, Yun Zhong, Chuanfang Cheng, Benrong Liu, Li Wang, Aiqun Li, Longgen Xiong, Shiming Liu
Dysregulated autophagy may lead to the development of disease. Role of autophagy and the diagnostic potential of microRNAs that regulate the autophagy in cardiac hypertrophy have not been evaluated. A rat model of cardiac hypertrophy was established using transverse abdominal aortic constriction (operation group). Cardiomyocyte autophagy was enhanced in rats from the operation group, compared with those in the sham operation group. Moreover, the operation group showed up-regulation of beclin-1 (an autophagy-related gene), and down-regulation of miR-30 in cardiac tissue...
2013: PloS One
https://www.readbyqxmd.com/read/22499902/contribution-of-impaired-mitochondrial-autophagy-to-cardiac-aging-mechanisms-and-therapeutic-opportunities
#7
REVIEW
Debapriya Dutta, Riccardo Calvani, Roberto Bernabei, Christiaan Leeuwenburgh, Emanuele Marzetti
The prevalence of cardiovascular disease increases with advancing age. Although long-term exposure to cardiovascular risk factors plays a major role in the etiopathogenesis of cardiovascular disease, intrinsic cardiac aging enhances the susceptibility to developing heart pathologies in late life. The progressive decline of cardiomyocyte mitochondrial function is considered a major mechanism underlying heart senescence. Damaged mitochondria not only produce less ATP but also generate increased amounts of reactive oxygen species and display a greater propensity to trigger apoptosis...
April 13, 2012: Circulation Research
https://www.readbyqxmd.com/read/22394373/ablation-of-mmp9-induces-survival-and-differentiation-of-cardiac-stem-cells-into-cardiomyocytes-in-the-heart-of-diabetics-a-role-of-extracellular-matrix
#8
Paras Kumar Mishra, Vishalakshi Chavali, Naira Metreveli, Suresh C Tyagi
The contribution of extracellular matrix (ECM) to stem cell survival and differentiation is unequivocal, and matrix metalloproteinase-9 (MMP9) induces ECM turn over; however, the role of MMP9 in the survival and differentiation of cardiac stem cells is unclear. We hypothesize that ablation of MMP9 enhances the survival and differentiation of cardiac stem cells into cardiomyocytes in diabetics. To test our hypothesis, Ins2(+/-) Akita, C57 BL/6J, and double knock out (DKO: Ins2(+/-)/MMP9(-/-)) mice were used...
March 2012: Canadian Journal of Physiology and Pharmacology
https://www.readbyqxmd.com/read/21908927/establishment-of-a-confluent-cardiomyocyte-culture-in-a-cylindrical-microchannel
#9
Yo Tanaka, Hiroto Akaike, Yasuhiko Sugii, Takehiko Kitamori
We established a confluent cardiomyocyte culture method using an 800-µm diameter cylindrical microchannel in this report. This was realized by introducing cardiomyocytes 2 times before and after turning over a microchip. The optimum condition was starting the flowing medium 2.0 h after seeding and flowing the medium at 1.0 µL/min. By applying this technology to a cardiomyocyte-based spherical heart pump device, one may develop self-fluid regulated devices that could be applied for implantable or circulation analysis device on a chip...
2011: Analytical Sciences: the International Journal of the Japan Society for Analytical Chemistry
https://www.readbyqxmd.com/read/21856786/prokineticin-receptor-1-pkr1-signalling-in-cardiovascular-and-kidney-functions
#10
REVIEW
Mounia Boulberdaa, Kyoji Urayama, Canan G Nebigil
Prokineticins (PK1 and PK2) are peptide hormones that exert their biological activity via two common G-protein-coupled receptors: prokineticin receptor (PKR) 1 and 2. Their physiology was originally explored mostly in the context of angiogenic actions in the reproductive tract and gut motility. Since autocrine and paracrine loops have been established between PK2 and PKR1 in the heart, in this review we focus on the PK2/PKR1 signalling in the functions of the heart and kidney. PKR1 signalling is required for cardiomyocyte survival and angiogenesis...
November 1, 2011: Cardiovascular Research
https://www.readbyqxmd.com/read/20865352/mitochondrial-fission-and-autophagy-in-the-normal-and-diseased-heart
#11
REVIEW
Myriam Iglewski, Joseph A Hill, Sergio Lavandero, Beverly A Rothermel
Sustained hypertension promotes structural, functional and metabolic remodeling of cardiomyocyte mitochondria. As long-lived, postmitotic cells, cardiomyocytes turn over mitochondria continuously to compensate for changes in energy demands and to remove damaged organelles. This process involves fusion and fission of existing mitochondria to generate new organelles and separate old ones for degradation via autophagy. Autophagy is a lysosome-dependent proteolytic pathway capable of processing cellular components, including organelles and protein aggregates...
December 2010: Current Hypertension Reports
https://www.readbyqxmd.com/read/20353489/mechanisms-of-exercise-induced-improvements-in-the-contractile-apparatus-of-the-mammalian-myocardium
#12
REVIEW
O J Kemi, U Wisløff
One of the main outcomes of aerobic endurance exercise training is the improved maximal oxygen uptake, and this is pivotal to the improved work capacity that follows the exercise training. Improved maximal oxygen uptake in turn is at least partly achieved because exercise training increases the ability of the myocardium to produce a greater cardiac output. In healthy subjects, this has been demonstrated repeatedly over many decades. It has recently emerged that this scenario may also be true under conditions of an initial myocardial dysfunction...
August 2010: Acta Physiologica
https://www.readbyqxmd.com/read/19632578/brain-death-effects-on-catecholamine-levels-and-subsequent-cardiac-damage-assessed-in-organ-donors
#13
Silvia Pérez López, Jesús Otero Hernández, Natalia Vázquez Moreno, Dolores Escudero Augusto, Francisco Alvarez Menéndez, Aurora Astudillo González
BACKGROUND: Brain death (BD) causes hemodynamic and neuroendocrine alterations including a catecholamine surge, which in turn causes histologic lesions in cardiac muscle such as contraction bands, focal mononuclear cell infiltrates and cardiomyocyte necrosis. These changes are likely to compromise heart function and could therefore also affect the graft response after heart transplantation. This study was designed to examine the catecholamine surge, the catecholamine release pattern and the histologic lesions traditionally described as characteristic of BD in hearts procured from BD donors...
August 2009: Journal of Heart and Lung Transplantation
https://www.readbyqxmd.com/read/19358331/the-a-kinase-anchor-protein-akap121-is-a-negative-regulator-of-cardiomyocyte-hypertrophy
#14
Bernard Abrenica, Mohamed AlShaaban, Michael P Czubryt
Pathologic cardiac hypertrophy imposes a significant clinical burden on patients, yet the precise intracellular mechanisms responsible for its induction are only partially understood. We examined a potential role for AKAP121 to regulate cardiomyocyte hypertrophy, since recent reports have implicated other AKAPs in this process. We report here that knockdown of AKAP121 expression in isolated neonatal rat cardiomyocytes results in pronounced cellular hypertrophy. Loss of AKAP121 expression is associated with dephosphorylation and nuclear localization of NFATc3, a downstream effector of the hypertrophic phosphatase calcineurin...
May 2009: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/19342590/evidence-for-cardiomyocyte-renewal-in-humans
#15
Olaf Bergmann, Ratan D Bhardwaj, Samuel Bernard, Sofia Zdunek, Fanie Barnabé-Heider, Stuart Walsh, Joel Zupicich, Kanar Alkass, Bruce A Buchholz, Henrik Druid, Stefan Jovinge, Jonas Frisén
It has been difficult to establish whether we are limited to the heart muscle cells we are born with or if cardiomyocytes are generated also later in life. We have taken advantage of the integration of carbon-14, generated by nuclear bomb tests during the Cold War, into DNA to establish the age of cardiomyocytes in humans. We report that cardiomyocytes renew, with a gradual decrease from 1% turning over annually at the age of 25 to 0.45% at the age of 75. Fewer than 50% of cardiomyocytes are exchanged during a normal life span...
April 3, 2009: Science
https://www.readbyqxmd.com/read/18773197/the-metalloporphyrin-fetpps-but-not-by-cyclosporin-a-antagonizes-the-interaction-of-peroxynitrate-and-hydrogen-peroxide-on-cardiomyocyte-cell-death
#16
Shaun S Klassen, Simon W Rabkin
The objective of this study was to determine whether the metalloporphyrin, 5,10,15,20-tetrakis(4-sulfonatophenyl) porphyrinato iron (III) chloride (FeTPPS), antagonized the effect of peroxynitrite, oxygen-free radicals, and the combination of the two, on cardiomyocyte cell viability. We further sought to compare the effects of FeTPPS to an inhibitor of the mitochondrial transmembrane permeability transition pores (PTP)-cyclosporin A. Cardiomyocytes from embryonic chick heart were treated with 3-morpholinosydnonimine (SIN-1), which decomposes to liberate NO and superoxide anion (O(2) (-)) which in turn generates peroxynitrite...
February 2009: Naunyn-Schmiedeberg's Archives of Pharmacology
https://www.readbyqxmd.com/read/18167217/heat-shock-protein-27-regulates-oxidative-stress-induced-apoptosis-in-cardiomyocytes-mechanisms-via-reactive-oxygen-species-generation-and-akt-activation
#17
Li Liu, Xiao-jin Zhang, Su-rong Jiang, Zheng-nian Ding, Guo-xian Ding, Jun Huang, Yun-lin Cheng
BACKGROUND: Increased reactive oxygen species (ROS) formation, which in turn promotes cardiomyocytes apoptosis, is associated with the pathogenesis and progression of various cardiac diseases such as ischemia and heart failure. Recent studies have shown that over expression of heat shock protein 27 (Hsp27) confers resistance to cardiac ischemia/reperfusion injury. However, not much is known about the regulation of myocyte survival by Hsp27. METHODS: The rat cardiac cell line H9c2, with a stable overexpression of Hsp27, was established, with empty vector transfected H9c2 cells as controls...
December 20, 2007: Chinese Medical Journal
https://www.readbyqxmd.com/read/18165153/modulation-of-cardiac-function-by-a-kinase-anchoring-proteins
#18
REVIEW
Dario Diviani
The cAMP-dependent kinase (PKA) is a broad specificity kinase that controls several fundamental processes in the heart including the strength and the frequency of contraction, the duration of the cardiac action potential as well as the activation of signaling pathways associated with the onset of cardiac hypertrophy and heart failure. It is now appreciated that to perform these functions, PKA must be precisely targeted in proximity to its cellular substrates. Evidence collected over the last years demonstrates that compartmentalization of the kinase is achieved through the association with A-kinase anchoring proteins (AKAPs)...
April 2008: Current Opinion in Pharmacology
https://www.readbyqxmd.com/read/17548171/non-hypoxic-preconditioning-of-myocardium-against-postoperative-atrial-fibrillation-mechanism-based-on-enhancement-of-the-antioxidant-defense-system
#19
Ramón Rodrigo, Rodrigo Castillo, Mauricio Cereceda, René Asenjo, Jaime Zamorano, Julia Araya
Oxidative stress underlies postoperative atrial fibrillation and electrophysiological remodelling associated with rapid atrial pacing. An increasing body of evidence indicates that the formation of reactive oxygen species (ROS) released following extracorporeal circulation are involved in the structural and functional myocardial impairment derived from the ischemia-reperfusion cycle. ROS behave as intracellular messengers mediating pathological processes, such as inflammation, apoptosis and necrosis, thereby participating in the pathophysiology of atrial fibrillation...
2007: Medical Hypotheses
https://www.readbyqxmd.com/read/17224877/glucose-insulin-and-potassium-for-metabolic-support-in-acute-myocardial-infarction-is-the-jury-still-out
#20
REVIEW
Howard J Broder, Richard W Nesto
During ischemic and cardiomyopathic conditions, carbohydrate (glucose) metabolism in cardiomyocytes predominates over use of free fatty acids. The shift to glucose metabolism is a physiologic response to ischemia, which in many patients, particularly diabetics or those who are insulin-resistant, is blunted. Free fatty acid metabolism during ischemia produces higher levels of lactate and hydrogen ions within the ischemic cells. This in turn degrades myocardial contractility, induces diastolic dysfunction, and reduces the arrhythmogenic threshold of the cardiomyocyte...
2006: Reviews in Cardiovascular Medicine
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