Interaction Between Cardiac Myocytes and the Extracellular Matrix in Failing Human Myocardium

1995 ◽  
pp. 275-285 ◽  
Author(s):  
Jutta Schaper ◽  
Hanke Mollnau ◽  
Stefan Hein ◽  
Brigitte Münkel
Keyword(s):  
Extracellular Matrix ◽  
Cardiac Myocytes ◽  
Human Myocardium

Cardiac myocytes cultured on a basement membrane extract of the ehs tumor

1986 ◽  
Vol 44 ◽  
pp. 270-271
Author(s):  
L. Terracio ◽  
A. Dewey ◽  
K. Rubin ◽  
T.K. Borg
Keyword(s):  
Extracellular Matrix ◽  
Basement Membrane ◽  
Cardiac Myocytes ◽  
Normal Tissue ◽  
Cell Spreading ◽  
Collagen Iv ◽  
Basement Membrane Extract ◽  
Membrane Extract ◽  
Growth Development ◽  
Multicellular Organisms

The recognition and interaction of cells with the extracellular matrix (ECM) effects the normal physiology as well as the pathology of all multicellular organisms. These interactions have been shown to influence the growth, development, and maintenance of normal tissue function. In previous studies, we have shown that neonatal cardiac myocytes specifically interacts with a variety of ECM components including fibronectin, laminin, and collagens I, III and IV. Culturing neonatal myocytes on laminin and collagen IV induces an increased rate of both cell spreading and sarcomerogenesis.

scholarly journals Quantifying the Release of Biomarkers of Myocardial Necrosis from Cardiac Myocytes and Intact Myocardium

2017 ◽  
Vol 63 (5) ◽  
pp. 990-996 ◽  
Author(s):  
Jack Marjot ◽  
Thomas E Kaier ◽  
Eva D Martin ◽  
Shiney S Reji ◽  
O'Neal Copeland ◽  
...  
Keyword(s):  
Human Serum ◽  
Cardiac Myocytes ◽  
Cardiac Myocyte ◽  
Troponin T ◽  
Myocardial Necrosis ◽  
High Sensitivity ◽  
Volume Of Distribution ◽  
Human Myocardium ◽  
Myosin Binding Protein ◽  
Rule Out

AbstractBACKGROUNDMyocardial infarction is diagnosed when biomarkers of cardiac necrosis exceed the 99th centile, although guidelines advocate even lower concentrations for early rule-out. We examined how many myocytes and how much myocardium these concentrations represent. We also examined if dietary troponin can confound the rule-out algorithm.METHODSIndividual rat cardiac myocytes, rat myocardium, ovine myocardium, or human myocardium were spiked into 400-μL aliquots of human serum. Blood was drawn from a volunteer after ingestion of ovine myocardium. High-sensitivity assays were used to measure cardiac troponin T (cTnT; Roche, Elecsys), cTnI (Abbott, Architect), and cardiac myosin-binding protein C (cMyC; EMD Millipore, Erenna®).RESULTSThe cMyC assay could only detect the human protein. For each rat cardiac myocyte added to 400 μL of human serum, cTnT and cTnI increased by 19.0 ng/L (95% CI, 16.8–21.2) and 18.9 ng/L (95% CI, 14.7–23.1), respectively. Under identical conditions cTnT, cTnI, and cMyC increased by 3.9 ng/L (95% CI, 3.6–4.3), 4.3 ng/L (95% CI, 3.8–4.7), and 41.0 ng/L (95% CI, 38.0–44.0) per μg of human myocardium. There was no detectable change in cTnI or cTnT concentration after ingestion of sufficient ovine myocardium to increase cTnT and cTnI to approximately 1 × 108 times their lower limits of quantification.CONCLUSIONSBased on pragmatic assumptions regarding cTn and cMyC release efficiency, circulating species, and volume of distribution, 99th centile concentrations may be exceeded by necrosis of 40 mg of myocardium. This volume is much too small to detect by noninvasive imaging.

scholarly journals Bioengineering Human Myocardium on Native Extracellular Matrix

2016 ◽  
Vol 118 (1) ◽  
pp. 56-72 ◽  
Author(s):  
Jacques P. Guyette ◽  
Jonathan M. Charest ◽  
Robert W. Mills ◽  
Bernhard J. Jank ◽  
Philipp T. Moser ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Human Myocardium

scholarly journals Lipoprotein lipase is produced by cardiac myocytes rather than interstitial cells in human myocardium.

1994 ◽  
Vol 14 (9) ◽  
pp. 1445-1451 ◽  
Author(s):  
K D O'Brien ◽  
M Ferguson ◽  
D Gordon ◽  
S S Deeb ◽  
A Chait
Keyword(s):  
Lipoprotein Lipase ◽  
Cardiac Myocytes ◽  
Interstitial Cells ◽  
Human Myocardium

Preparation of cardiac extracellular matrix scaffolds by decellularization of human myocardium

2013 ◽  
Vol 102 (9) ◽  
pp. 3263-3272 ◽  
Author(s):  
Barbara Oberwallner ◽  
Andreja Brodarac ◽  
Yeong-Hoon Choi ◽  
Tomo Saric ◽  
Petra Anić ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Human Myocardium ◽  
Extracellular Matrix Scaffolds

The Expression and Role of Protein Kinase C in Neonatal Cardiac Myocyte Attachment, Cell Volume, and Myofibril Formation Is Dependent on the Composition of the Extracellular Matrix

2005 ◽  
Vol 11 (3) ◽  
pp. 224-234 ◽  
Author(s):  
Tara A. Bullard ◽  
Thomas K. Borg ◽  
Robert L. Price
Keyword(s):  
Extracellular Matrix ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Cell Volume ◽  
Cardiac Myocytes ◽  
Cardiac Myocyte ◽  
Dynamic Component ◽  
Laminin 5 ◽  
Kinase C

The extracellular matrix (ECM) is a dynamic component of tissues that influences cellular phenotype and behavior. We sought to determine the role of specific ECM substrates in the regulation of protein kinase C (PKC) isozyme expression and function in cardiac myocyte attachment, cell volume, and myofibril formation. PKC isozyme expression was ECM substrate specific. Increasing concentrations of the PKC δ inhibitor rottlerin attenuated myocyte attachment to randomly organized collagen (1, 5, and 10 μM), laminin (5 and 10 μM), aligned collagen (5 and 10 μM), and fibronectin (10 μM). Rottlerin significantly decreased cell volume on laminin and randomly organized collagen, and inhibited myofibril formation on laminin. The PKC α inhibitor Gö 6976 inhibited attachment to randomly organized collagen at 6 nM but did not affect cell volume. The general PKC inhibitor Bisindolylmalemide I (10 and 30 μM) did not affect myocyte attachment; however, it significantly decreased cell volume on randomly organized collagen. Our data indicate that PKC isozymes are expressed and utilized by neonatal cardiac myocytes during attachment, cell growth, and myofibril formation. Specifically, it appears that PKC δ and/or its downstream effectors play an important role in the interaction between cardiac myocytes and laminin, providing further evidence that the ECM influences cardiac myocyte behavior.

scholarly journals Mitochondrial function in engineered cardiac tissues is regulated by extracellular matrix elasticity and tissue alignment

2017 ◽  
Vol 313 (4) ◽  
pp. H757-H767 ◽  
Author(s):  
Davi M. Lyra-Leite ◽  
Allen M. Andres ◽  
Andrew P. Petersen ◽  
Nethika R. Ariyasinghe ◽  
Nathan Cho ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Oxygen Consumption ◽  
Cardiac Myocytes ◽  
Mitochondrial Function ◽  
Stress Responses ◽  
Ventricular Myocytes ◽  
Neonatal Rat ◽  
Sprague Dawley ◽  
Cardiac Tissues ◽  
Matrix Elasticity

Mitochondria in cardiac myocytes are critical for generating ATP to meet the high metabolic demands associated with sarcomere shortening. Distinct remodeling of mitochondrial structure and function occur in cardiac myocytes in both developmental and pathological settings. However, the factors that underlie these changes are poorly understood. Because remodeling of tissue architecture and extracellular matrix (ECM) elasticity are also hallmarks of ventricular development and disease, we hypothesize that these environmental factors regulate mitochondrial function in cardiac myocytes. To test this, we developed a new procedure to transfer tunable polydimethylsiloxane disks microcontact-printed with fibronectin into cell culture microplates. We cultured Sprague-Dawley neonatal rat ventricular myocytes within the wells, which consistently formed tissues following the printed fibronectin, and measured oxygen consumption rate using a Seahorse extracellular flux analyzer. Our data indicate that parameters associated with baseline metabolism are predominantly regulated by ECM elasticity, whereas the ability of tissues to adapt to metabolic stress is regulated by both ECM elasticity and tissue alignment. Furthermore, bioenergetic health index, which reflects both the positive and negative aspects of oxygen consumption, was highest in aligned tissues on the most rigid substrate, suggesting that overall mitochondrial function is regulated by both ECM elasticity and tissue alignment. Our results demonstrate that mitochondrial function is regulated by both ECM elasticity and myofibril architecture in cardiac myocytes. This provides novel insight into how extracellular cues impact mitochondrial function in the context of cardiac development and disease. NEW & NOTEWORTHY A new methodology has been developed to measure O2 consumption rates in engineered cardiac tissues with independent control over tissue alignment and matrix elasticity. This led to the findings that matrix elasticity regulates basal mitochondrial function, whereas both matrix elasticity and tissue alignment regulate mitochondrial stress responses.

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