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https://www.readbyqxmd.com/read/28606910/na-k-pump-inactivation-subsarcolemmal-na-measurements-and-cytoplasmic-ion-turnover-kinetics-contradict-restricted-na-spaces-in-murine-cardiac-myocytes
#1
Fang-Min Lu, Donald W Hilgemann
Decades ago, it was proposed that Na transport in cardiac myocytes is modulated by large changes in cytoplasmic Na concentration within restricted subsarcolemmal spaces. Here, we probe this hypothesis for Na/K pumps by generating constitutive transsarcolemmal Na flux with the Na channel opener veratridine in whole-cell patch-clamp recordings. Using 25 mM Na in the patch pipette, pump currents decay strongly during continuous activation by extracellular K (τ, ∼2 s). In contradiction to depletion hypotheses, the decay becomes stronger when pump currents are decreased by hyperpolarization...
July 3, 2017: Journal of General Physiology
https://www.readbyqxmd.com/read/28572498/edward-f-adolph-distinguished-lecture-exercise-teaching-myocytes-new-tricks
#2
Scott K Powers
Endurance exercise training promotes numerous cellular adaptations in both cardiac myocytes and skeletal muscle fibers. For example, exercise training fosters changes in mitochondrial dynamics including increased mitochondrial biogenesis and accelerated mitochondrial turnover. Additionally, endurance exercise training alters the abundance of numerous cytosolic and mitochondrial proteins in both cardiac and skeletal muscle myocytes, resulting in a protective phenotype in the active fibers; this exercise-induced protection of cardiac and skeletal muscle fibers is often referred to as "exercise preconditioning...
June 1, 2017: Journal of Applied Physiology
https://www.readbyqxmd.com/read/28321411/different-densities-of-na-ca-exchange-current-in-t-tubular-and-surface-membranes-and-their-impact-on-cellular-activity-in-a-model-of-rat-ventricular-cardiomyocyte
#3
M Pásek, J Šimurda, G Christé
The ratio of densities of Na-Ca exchanger current (INaCa) in the t-tubular and surface membranes (INaCa-ratio) computed from the values of INaCa and membrane capacitances (Cm) measured in adult rat ventricular cardiomyocytes before and after detubulation ranges between 1.7 and 25 (potentially even 40). Variations of action potential waveform and of calcium turnover within this span of the INaCa-ratio were simulated employing previously developed model of rat ventricular cell incorporating separate description of ion transport systems in the t-tubular and surface membranes...
2017: BioMed Research International
https://www.readbyqxmd.com/read/28087623/a-p53-based-genetic-tracing-system-to-follow-postnatal-cardiomyocyte-expansion-in-heart-regeneration
#4
Qi Xiao, Guoxin Zhang, Huijuan Wang, Lai Chen, Shuangshuang Lu, Dejing Pan, Geng Liu, Zhongzhou Yang
For heart regeneration, the proliferative potential of cardiomyocytes in postnatal mice is under intense investigations. However, solely relying on immunostaining of proliferation markers, the long term proliferation dynamics and potential of the cardiomyocytes cannot be readily addressed. Previously, we found that a p53 promoter driving reporter predominantly marked the proliferating lineages in mice. Here, we established a p53 based genetic tracing system to investigate postnatal cardiomyocyte proliferation and heart regeneration...
January 13, 2017: Development
https://www.readbyqxmd.com/read/28018900/redox-regulation-of-heart-regeneration-an-evolutionary-tradeoff
#5
Waleed M Elhelaly, Nicholas T Lam, Mohamed Hamza, Shuda Xia, Hesham A Sadek
Heart failure is a costly and deadly disease, affecting over 23 million patients worldwide, half of which die within 5 years of diagnosis. The pathophysiological basis of heart failure is the inability of the adult heart to regenerate lost or damaged myocardium. Although limited myocyte turnover does occur in the adult heart, it is insufficient for restoration of contractile function (Nadal-Ginard, 2001; Laflamme et al., 2002; Quaini et al., 2002; Hsieh et al., 2007; Bergmann et al., 2009, 2012). In contrast to lower vertebrates (Poss et al...
2016: Frontiers in Cell and Developmental Biology
https://www.readbyqxmd.com/read/27881552/cardiac-t-tubule-microanatomy-and-function
#6
REVIEW
TingTing Hong, Robin M Shaw
Unique to striated muscle cells, transverse tubules (t-tubules) are membrane organelles that consist of sarcolemma penetrating into the myocyte interior, forming a highly branched and interconnected network. Mature t-tubule networks are found in mammalian ventricular cardiomyocytes, with the transverse components of t-tubules occurring near sarcomeric z-discs. Cardiac t-tubules contain membrane microdomains enriched with ion channels and signaling molecules. The microdomains serve as key signaling hubs in regulation of cardiomyocyte function...
2017: Physiological Reviews
https://www.readbyqxmd.com/read/27826738/transcription-factor-pex1-modulates-extracellular-matrix-turnover-through-regulation-of-mmp-9-expression
#7
Alicia Jurado Acosta, Jaana Rysä, Zoltan Szabo, Anne-Mari Moilanen, Hiba Komati, Mona Nemer, Heikki Ruskoaho
The phenylephrine-induced complex-1 (PEX1) transcription factor, also known as zinc-finger protein 260 (Zfp260), is an effector of endothelin-1 and α1-adrenergic signaling in cardiac hypertrophy. However, the role of PEX1 in transcriptional regulation of myocardial remodeling remains largely unknown. In the present study, we used PEX1 gain- and loss-of-function to examine the effects of PEX1 on left ventricular remodeling. Adenoviral constructs expressing PEX1, antisense PEX1, or LacZ were delivered by local injection into the anterior wall of the left ventricle in Sprague-Dawley rats...
February 2017: Cell and Tissue Research
https://www.readbyqxmd.com/read/27806245/aerobic-exercise-training-as-a-potential-cardioprotective-strategy-to-attenuate-doxorubicin-induced-cardiotoxicity
#8
Samir A Kouzi, Mohammad Nasir Uddin
Doxorubicin is one of the most commonly used cytotoxic anticancer drugs against several cancers.  Although a highly effective anticancer drug, the clinical use of doxorubicin is severely limited by its cardiotoxicity which results in morbidity, poor quality of life, and premature mortality.  Only very few clinically accepted methods to minimize doxorubicin-induced cardiac injury are available today, but none of them have proven to be completely successful.  Due to limited alternative strategies, a number of potential cardioprotective therapies are currently being investigated for treating and/or preventing doxorubicin-induced cardiotoxicity...
July 2016: Journal of Pharmacy & Pharmaceutical Sciences: a Publication of the Canadian Society for Pharmaceutical Sciences
https://www.readbyqxmd.com/read/27726056/biomarkers-to-predict-reverse-remodeling-and-myocardial-recovery-in-heart-failure
#9
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 2016: Current Heart Failure Reports
https://www.readbyqxmd.com/read/27651752/adapting-extracellular-matrix-proteomics-for-clinical-studies-on-cardiac-remodeling-post-myocardial-infarction
#10
REVIEW
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
https://www.readbyqxmd.com/read/27650557/titin-based-cardiac-myocyte-stiffening-contributes-to-early-adaptive-ventricular-remodeling-after-myocardial-infarction
#11
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
https://www.readbyqxmd.com/read/27625792/reversal-of-intramyocellular-lipid-accumulation-by-lipophagy-and-a-p62-mediated-pathway
#12
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
https://www.readbyqxmd.com/read/27545814/natural-myocardial-ecm-patch-drives-cardiac-progenitor-based-restoration-even-after-scarring
#13
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
https://www.readbyqxmd.com/read/27484198/innate-heart-regeneration-endogenous-cellular-sources-and-exogenous-therapeutic-amplification
#14
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
https://www.readbyqxmd.com/read/27388042/molecular-mechanisms-of-the-cardiotoxicity-of-the-proteasomal-targeted-drugs-bortezomib-and-carfilzomib
#15
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 2017: Cardiovascular Toxicology
https://www.readbyqxmd.com/read/27208160/mmp-9-signaling-in-the-left-ventricle-following-myocardial-infarction
#16
REVIEW
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
https://www.readbyqxmd.com/read/26886225/mitochondrial-involvement-in-myocyte-death-and-heart-failure
#17
REVIEW
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
https://www.readbyqxmd.com/read/26818589/myofibroblast-secretome-and-its-auto-paracrine-signaling
#18
REVIEW
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
https://www.readbyqxmd.com/read/26756642/extracellular-ubiquitin-role-in-myocyte-apoptosis-and-myocardial-remodeling
#19
REVIEW
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...
December 15, 2015: Comprehensive Physiology
https://www.readbyqxmd.com/read/26735437/alcohol-and-heart-muscle-disease
#20
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
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