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myocyte turnover

Shweta R Motiwala, Hanna K Gaggin
Left ventricular remodeling appears to be a critical link between cardiac injury and the development and progression of heart failure with reduced ejection fraction (HFrEF). Several drug and device therapies that modify and reverse the remodeling process in patients with HFrEF are closely associated with improvement in clinical outcomes. Reverse remodeling, including partial or complete recovery of systolic function and structure, is possible but its determinants are incompletely understood. Methods to predict reverse remodeling in response to therapy are not well defined...
October 10, 2016: Current Heart Failure Reports
Merry L Lindsey, Michael E Hall, Romain Harmancey, Yonggang Ma
Following myocardial infarction (MI), the left ventricle (LV) undergoes a series of cardiac wound healing responses that involve stimulation of robust inflammation to clear necrotic myocytes and tissue debris and induction of extracellular matrix (ECM) protein synthesis to generate a scar. Proteomic strategies provide us with a means to index the ECM proteins expressed in the LV, quantify amounts, determine functions, and explore interactions. This review will focus on the efforts taken in the proteomics research field that have expanded our understanding of post-MI LV remodeling, concentrating on the strengths and limitations of different proteomic approaches to glean information that is specific to ECM turnover in the post-MI setting...
2016: Clinical Proteomics
Sebastian Kötter, Malgorzata Kazmierowska, Christian Andresen, Katharina Bottermann, Maria Grandoch, Simone Gorressen, Andre Heinen, Jens M Moll, Jürgen Scheller, Axel Gödecke, Jens W Fischer, Joachim P Schmitt, Martina Krüger
RATIONALE: Myocardial infarction (MI) increases the wall stress in the viable myocardium and initiates early adaptive remodeling in the left ventricle to maintain cardiac output. Later remodeling processes include fibrotic reorganization that eventually leads to cardiac failure. Understanding the mechanisms that support cardiac function in the early phase post MI and identifying the processes that initiate transition to maladaptive remodeling are of major clinical interest. OBJECTIVE: To characterize MI-induced changes in titin-based cardiac myocyte stiffness and to elucidate the role of titin in ventricular remodeling of remote myocardium in the early phase after MI...
October 14, 2016: Circulation Research
T Lam, R Harmancey, H Vasquez, B Gilbert, N Patel, V Hariharan, A Lee, M Covey, H Taegtmeyer
We have previously observed the reversal of lipid droplet deposition in skeletal muscle of morbidly obese patients following bariatric surgery. We now investigated whether activation of autophagy is the mechanism underlying this observation. For this purpose, we incubated rat L6 myocytes over a period of 6 days with long-chain fatty acids (an equimolar, 1.0 mM, mixture of oleate and palmitate in the incubation medium). At day 6, the autophagic inhibitor (bafilomycin A1, 200 nM) and the autophagic activator (rapamycin, 1 μM) were added separately or in combination for 48 h...
2016: Cell Death Discovery
Udi Sarig, Hadar Sarig, Elio de-Berardinis, Su-Yin Chaw, Evelyne B V Nguyen, Vaibavi S Ramanujam, Vu D Thang, Muthafar Al-Haddawi, Susan Liao, Dror Seliktar, Theodoros Kofidis, Freddy Y C Boey, Subbu S Venkatraman, Marcelle Machluf
OBJECTIVE: To evaluate the regenerative capacity of non-supplemented and bioactive patches made of decellularized porcine cardiac extracellular matrix (pcECM) and characterize the biological key factors involved in possible cardiac function (CF) restoration following acute and 8weeks chronic MI. BACKGROUND: pcECM is a key natural biomaterial that can affect cardiac regeneration following myocardial infarction (MI), through mechanisms, which are still not clearly understood...
October 15, 2016: Acta Biomaterialia
Konstantinos Malliaras, Styliani Vakrou, Chris J Kapelios, John N Nanas
INTRODUCTION: The -once viewed as heretical- concept of the adult mammalian heart as a dynamic organ capable of endogenous regeneration has recently gained traction. However, estimated rates of myocyte turnover vary wildly and the underlying mechanisms of cardiac plasticity remain controversial. It is still unclear whether the adult mammalian heart gives birth to new myocytes through proliferation of resident myocytes, through cardiomyogenic differentiation of endogenous progenitors or through both mechanisms...
November 2016: Expert Opinion on Biological Therapy
Brian B Hasinoff, Daywin Patel, Xing Wu
Bortezomib and carfilzomib are anticancer drugs that target the proteasome. However, these agents have been shown to exhibit some specific cardiac toxicities by as yet unknown mechanisms. Bortezomib and carfilzomib are also being used clinically in combination with doxorubicin, which is also cardiotoxic. A primary neonatal rat myocyte model was used to study these cardiotoxic mechanisms. Exposure to submicromolar concentrations of bortezomib and carfilzomib resulted in significant myocyte damage and induced apoptosis...
July 7, 2016: Cardiovascular Toxicology
Rugmani Padmanabhan Iyer, Mira Jung, Merry L Lindsey
Following myocardial infarction (MI), the left ventricle (LV) undergoes a series of cardiac wound healing responses that involve both the stimulation of robust inflammation to clear necrotic myocytes and tissue debris and the induction of extracellular matrix (ECM) protein synthesis to generate an infarct scar. The collective changes in myocardial structure and function are termed LV remodeling, and matrix metalloproteinase-9 (MMP-9) is a key instigator of post-MI LV remodeling. Through direct molecular effects on ECM and inflammatory protein turnover as well as indirect effects on major cell types that coordinate cardiac wound healing, namely the infiltrating leukocytes and the cardiac fibroblasts, MMP-9 coordinates multiple aspects of LV remodeling...
July 1, 2016: American Journal of Physiology. Heart and Circulatory Physiology
Michael J Goldenthal
As the heart is an energy-demanding organ, impaired cardiac energy metabolism and mitochondrial function have been inexorably linked to cardiac dysfunction. There is a growing recognition that mitochondrial dysfunction contributes to impaired myocardial energetics and increased oxidative stress in cardiomyopathies, cardiac ischemic damage and heart failure (HF), and mitochondrial permeability transition pore opening has been reported a critical trigger of myocyte death and myocardial remodeling. It is well established that mitochondria play pivotal roles in intracellular signaling in both cell death as well as in cardioprotective pathways...
March 2016: Heart Failure Reviews
Ritin Bomb, Mark R Heckle, Yao Sun, Salvatore Mancarella, Ramareddy V Guntaka, Ivan C Gerling, Karl T Weber
Myofibroblasts (myoFb) are phenotypically transformed, contractile fibroblast-like cells expressing α-smooth muscle actin microfilaments. They are integral to collagen fibrillogenesis with scar tissue formation at sites of repair irrespective of the etiologic origins of injury or tissue involved. MyoFb can persist long after healing is complete, where their ongoing turnover of collagen accounts for a progressive structural remodeling of an organ (a.k.a. fibrosis, sclerosis or cirrhosis). Such persistent metabolic activity is derived from a secretome consisting of requisite components in the de novo generation of angiotensin (Ang) II...
2016: Expert Review of Cardiovascular Therapy
Stephanie L C Scofield, Parthiv Amin, Mahipal Singh, Krishna Singh
Ubiquitin (UB) is a highly conserved low molecular weight (8.5 kDa) protein. It consists of 76 amino acid residues and is found in all eukaryotic cells. The covalent linkage of UB to a variety of cellular proteins (ubiquitination) is one of the most common posttranslational modifications in eukaryotic cells. This modification generally regulates protein turnover and protects the cells from damaged or misfolded proteins. The polyubiquitination of proteins serves as a signal for degradation via the 26S proteasome pathway...
January 2015: Comprehensive Physiology
J Fernández-Solà, R Estruch, A Urbano-Marquez
Ethanol consumption may induce acute and chronic effects on the myocardium. High-dose acute ethanol intake may induce a decrease in myocardial contraction and produce a variety of rhythm disturbances. These effects are more relevant in patients with underlying cardiomyopathy. Chronic ethanol intake may induce the development of a dilated cardiomyopathy, which is clinically and functionally similar to idiopathic dilated cardiomyopathy. Alcoholic cardiomyopathy is potentially reversible with abstinence. The prognosis depends on the persistence or abstinence of ethanol intake...
January 1997: Addiction Biology
Ailian Du, Shiqian Huang, Xiaonan Zhao, Yun Zhang, Lixun Zhu, Ji Ding, Congfeng Xu
After binding by acetylcholine released from a motor neuron, a nicotinic acetylcholine receptor at the neuromuscular junction produces a localized end-plate potential, which leads to muscle contraction. Improper turnover and renewal of acetylcholine receptors contributes to the pathogenesis of myasthenia gravis. In the present study, we demonstrate that endoplasmic reticulum (ER) stress contributes to acetylcholine receptor degradation in C2C12 myocytes. We further show that ER stress promotes acetylcholine receptor endocytosis and lysosomal degradation, which was dampened by blocking endocytosis or treating with lysosome inhibitor...
January 15, 2016: Journal of Neuroimmunology
David E Lee, Jacob L Brown, Megan E Rosa, Lemuel A Brown, Richard A Perry, Michael P Wiggs, Mats I Nilsson, Stephen F Crouse, James D Fluckey, Tyrone A Washington, Nicholas P Greene
Insulin resistant diabetes, currently at epidemic levels in developed countries, begins in the skeletal muscle and is linked to altered protein turnover. microRNAs downregulate targeted mRNA translation decreasing the amount of translated protein, thereby regulating many cellular processes. Regulation of miRNAs and their function in skeletal muscle insulin resistance is largely unexplored. The purpose of this study was to identify the effects of insulin resistance on contents of skeletal muscle miRNAs with potential functions in protein turnover...
August 2016: Journal of Cellular Biochemistry
Kristine Y DeLeon-Pennell, Yuan Tian, Bai Zhang, Courtney A Cates, Rugmani Padmanabhan Iyer, Presley Cannon, Punit Shah, Paul Aiyetan, Ganesh V Halade, Yonggang Ma, Elizabeth Flynn, Zhen Zhang, Yu-Fang Jin, Hui Zhang, Merry L Lindsey
BACKGROUND: After myocardial infarction, the left ventricle undergoes a wound healing response that includes the robust infiltration of neutrophils and macrophages to facilitate removal of dead myocytes as well as turnover of the extracellular matrix. Matrix metalloproteinase (MMP)-9 is a key enzyme that regulates post-myocardial infarction left ventricular remodeling. METHODS AND RESULTS: Infarct regions from wild-type and MMP-9 null mice (n=8 per group) analyzed by glycoproteomics showed that of 541 N-glycosylated proteins quantified, 45 proteins were at least 2-fold upregulated or downregulated with MMP-9 deletion (all P<0...
February 2016: Circulation. Cardiovascular Genetics
Amanda Finan, Sylvain Richard
The healthy adult heart has a low turnover of cardiac myocytes. The renewal capacity, however, is augmented after cardiac injury. Participants in cardiac regeneration include cardiac myocytes themselves, cardiac progenitor cells, and peripheral stem cells, particularly from the bone marrow compartment. Cardiac progenitor cells and bone marrow stem cells are augmented after cardiac injury, migrate to the myocardium, and support regeneration. Depletion studies of these populations have demonstrated their necessary role in cardiac repair...
2015: Frontiers in Cell and Developmental Biology
Mari E Strand, Jan Magnus Aronsen, Bjørn Braathen, Ivar Sjaastad, Heidi Kvaløy, Theis Tønnessen, Geir Christensen, Ida G Lunde
Inflammation is central to heart failure progression. Innate immune signaling increases expression of the transmembrane proteoglycan syndecan-4 in cardiac myocytes and fibroblasts, followed by shedding of its ectodomain. Circulating shed syndecan-4 is increased in heart failure patients, however the pathophysiological and molecular consequences associated with syndecan-4 shedding remain poorly understood. Here we used lipopolysaccharide (LPS) challenge to investigate the effects of syndecan-4 shedding in the heart...
November 2015: Journal of Molecular and Cellular Cardiology
Arun Sharma, Sean M Wu
A low level of cardiomyocyte turnover occurs in the adult mammalian heart, but the source of these new cells remains unknown. Kimura et al., 2015 utilized a novel hypoxia-induced fate mapping system to identify a rare population of adult cardiomyocytes undergoing cell-cycle entry and expansion in healthy adult hearts and following ischemic injury.
September 1, 2015: Cell Metabolism
Marie-Claude Drolet, Vincent Desbiens-Brassard, Elise Roussel, Veronique Tu, Jacques Couet, Marie Arsenault
BACKGROUND: Hypertrophy (H) is an adaptive response of the heart to a hemodynamic overload. Severe left ventricular (LV) volume overload (VO) from valve regurgitations (aortic (AR) or mitral regurgitation) leads to eccentric LVH. Increased protein turnover is a major event during development of LVH and the mechanistic target of rapamycin (mTOR) is a key molecule for its control. The role of mTOR inhibition in the development of LVH using rapamycin for relatively short periods of time (days to a few weeks) has been studied in the past in pressure overload models but not in VO models...
2015: SpringerPlus
Rafael Salto, Jose D Vílchez, María D Girón, Elena Cabrera, Nefertiti Campos, Manuel Manzano, Ricardo Rueda, Jose M López-Pedrosa
β-Hydroxy-β-methylbutyrate (HMB) has been shown to enhance cell survival, differentiation and protein turnover in muscle, mainly activating phosphoinositide-3-kinase/protein kinase B (PI3K/Akt) and mitogen-activated protein kinases/ extracellular-signal-regulated kinases (MAPK/ERK) signaling pathways. Since these two pathways are related to neuronal survival and differentiation, in this study, we have investigated the neurotrophic effects of HMB in mouse neuroblastoma Neuro2a cells. In Neuro2a cells, HMB promotes differentiation to neurites independent from any effects on proliferation...
2015: PloS One
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