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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
MeSH Review

Muscle Cells

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Disease relevance of Muscle Cells


Psychiatry related information on Muscle Cells

  • We suggest that CHOP-10 is a negative modulator of the activity of C/EBP-like proteins in certain terminally differentiated cells, similar to the regulatory function of Id on the activity of MyoD and MyoD-related proteins important in the development of muscle cells [6].
  • The recently reported finding that a moderate alcohol consumption may lower the risk of cardiovascular disease prompted a study of the effects of ethanol and acetaldehyde on proliferation, viability and collagen secretion of rabbit aortic myocytes in culture and on the spontaneous efflux reaction of human platelets in vitro [7].
  • The data provided here demonstrated that IGFBP-5 has the potential to affect proliferation of PEMCs during critical periods of in vitro muscle cell development and therefore may impact the capacity for ultimate postnatal muscle mass development in vivo [8].

High impact information on Muscle Cells

  • In developing skeletal muscle, an important interplay between muscle cells and the ECM is present, and some evidence from adult human muscle suggests common signaling pathways to stimulate contractile and ECM components [9].
  • (There is an obvious trade-off between transducer sensitivity, which affects noise and drift and compliance.) Some success has been reported with the use of intact rat myocytes supported by suction micropipettes and in guinea pig ventricular myocytes adhering to poly-L-lysine-coated glass beams [10].
  • Accordingly, loss of ventricular muscle cell lineage specification into trabecular and conduction system myocytes is a new mechanistic pathway for progressive cardiomyopathy and conduction defects in congenital heart disease [11].
  • Muscle cells lacking IL-4 or the IL-4alpha receptor subunit form normally but are reduced in size and myonuclear number [12].
  • This interdependence of thin-filament protein expression led us to postulate that some mutations in tnnt2 may trigger misregulation of thin-filament protein expression, resulting in sarcomere loss and myocyte disarray, the life-threatening hallmarks of TNNT2 mutations in mice and humans [13].

Chemical compound and disease context of Muscle Cells

  • Here, we show that blocking the intrinsic catabolism of cGMP with an oral phosphodiesterase-5A (PDE5A) inhibitor (sildenafil) suppresses chamber and myocyte hypertrophy, and improves in vivo heart function in mice exposed to chronic pressure overload induced by transverse aortic constriction [14].
  • In contrast, NE-stimulated cAMP content in glucose-deprived hypoxic myocytes fell by 31% (n = 5, P less than 0.05) and did not return to control levels with reoxygenation. beta AR-agonist affinity assessed by (-)-isoproterenol displacement curves was unaltered after 2 h of hypoxia irrespective of glucose content [15].
  • Hypoxia also induced a 100-fold reduction in the concentration of norepinephrine required to elicit a threshold increase in inositol trisphosphate (10(-9) M), compared with control normoxic myocytes (10(-7) M) [16].
  • Cultured myocytes expressing AT1-i2m exhibited a left and upward shift of the Ang II dose-response curve of hypertrophy compared with those expressing AT1-WT [17].
  • Muscle carnitine levels remained low in all cystinosis patients, even though cystinotic muscle cells in culture took up L-[3H]carnitine normally [18].

Biological context of Muscle Cells


Anatomical context of Muscle Cells


Associations of Muscle Cells with chemical compounds

  • We suggest that similar changes occur in working muscle cells and contribute to the improved glucose tolerance induced by exercise [29].
  • Degradation of the acetylcholine receptor in cultured muscle cells: selective inhibitors and the fate of undegraded receptors [30].
  • Our finding that the major uterine protein induced by estrogen is also synthesized in liver and muscle cells is significant in that it points to a more general cellular function for the protein, rather than a unique role within uterine cells [31].
  • Plasminogen activator in chick embryo muscle cells: induction of enzyme by RSV, PMA and retinoic acid [32].
  • Oncogenically transformed C3H/10T1/2CL8 cells also developed muscle cells after exposure to 5-azacytidine, but at a reduced rate when compared to the parent line [33].

Gene context of Muscle Cells

  • These mutations may interfere with caveolin-3 oligomerization and disrupt caveolae formation at the muscle cell plasma membrane [34].
  • CONCLUSIONS: Programmed death of myocytes occurs in the decompensated human heart in spite of the enhanced expression of BCL2; this phenomenon may contribute to the progression of cardiac dysfunction [35].
  • In skn-1 mutant embryos, EMS instead produces hypodermal cells and body wall muscle cells, much like its sister blastomere [36].
  • Comparative analysis of primary sequences highlights regions of functional importance, including those that may mediate the localization of DRP and dystrophin in the muscle cell [37].
  • Here we identify PKC-alpha as a fundamental regulator of cardiac contractility and Ca(2+) handling in myocytes [38].

Analytical, diagnostic and therapeutic context of Muscle Cells


  1. Duchenne muscular dystrophy: deficiency of dystrophin at the muscle cell surface. Bonilla, E., Samitt, C.E., Miranda, A.F., Hays, A.P., Salviati, G., DiMauro, S., Kunkel, L.M., Hoffman, E.P., Rowland, L.P. Cell (1988) [Pubmed]
  2. Late cardiac effects of doxorubicin therapy for acute lymphoblastic leukemia in childhood. Lipshultz, S.E., Colan, S.D., Gelber, R.D., Perez-Atayde, A.R., Sallan, S.E., Sanders, S.P. N. Engl. J. Med. (1991) [Pubmed]
  3. IGF-1 induces skeletal myocyte hypertrophy through calcineurin in association with GATA-2 and NF-ATc1. Musarò, A., McCullagh, K.J., Naya, F.J., Olson, E.N., Rosenthal, N. Nature (1999) [Pubmed]
  4. Adiponectin and adiponectin receptors. Kadowaki, T., Yamauchi, T. Endocr. Rev. (2005) [Pubmed]
  5. Thymic muscle cells bear acetylcholine receptors: possible relation to myasthenia gravis. Kao, I., Drachman, D.B. Science (1977) [Pubmed]
  6. CHOP, a novel developmentally regulated nuclear protein that dimerizes with transcription factors C/EBP and LAP and functions as a dominant-negative inhibitor of gene transcription. Ron, D., Habener, J.F. Genes Dev. (1992) [Pubmed]
  7. Effects of ethanol and acetaldehyde on cultured rabbit aortic myocytes and human platelets in vitro. Stavenow, L., Jerntorp, P., Ohlin, H. Eur. J. Clin. Invest. (1984) [Pubmed]
  8. Production of recombinant porcine IGF-binding protein-5 and its effect on proliferation of porcine embryonic myoblast cultures in the presence and absence of IGF-I and Long-R3-IGF-I. Pampusch, M.S., Xi, G., Kamanga-Sollo, E., Loseth, K.J., Hathaway, M.R., Dayton, W.R., White, M.E. J. Endocrinol. (2005) [Pubmed]
  9. Role of extracellular matrix in adaptation of tendon and skeletal muscle to mechanical loading. Kjaer, M. Physiol. Rev. (2004) [Pubmed]
  10. Mechanical properties of isolated cardiac myocytes. Brady, A.J. Physiol. Rev. (1991) [Pubmed]
  11. Nkx2-5 pathways and congenital heart disease; loss of ventricular myocyte lineage specification leads to progressive cardiomyopathy and complete heart block. Pashmforoush, M., Lu, J.T., Chen, H., Amand, T.S., Kondo, R., Pradervand, S., Evans, S.M., Clark, B., Feramisco, J.R., Giles, W., Ho, S.Y., Benson, D.W., Silberbach, M., Shou, W., Chien, K.R. Cell (2004) [Pubmed]
  12. IL-4 acts as a myoblast recruitment factor during mammalian muscle growth. Horsley, V., Jansen, K.M., Mills, S.T., Pavlath, G.K. Cell (2003) [Pubmed]
  13. Cardiac troponin T is essential in sarcomere assembly and cardiac contractility. Sehnert, A.J., Huq, A., Weinstein, B.M., Walker, C., Fishman, M., Stainier, D.Y. Nat. Genet. (2002) [Pubmed]
  14. Chronic inhibition of cyclic GMP phosphodiesterase 5A prevents and reverses cardiac hypertrophy. Takimoto, E., Champion, H.C., Li, M., Belardi, D., Ren, S., Rodriguez, E.R., Bedja, D., Gabrielson, K.L., Wang, Y., Kass, D.A. Nat. Med. (2005) [Pubmed]
  15. Hypoxia and glucose independently regulate the beta-adrenergic receptor-adenylate cyclase system in cardiac myocytes. Rocha-Singh, K.J., Honbo, N.Y., Karliner, J.S. J. Clin. Invest. (1991) [Pubmed]
  16. Enhanced inositol trisphosphate response to alpha 1-adrenergic stimulation in cardiac myocytes exposed to hypoxia. Heathers, G.P., Evers, A.S., Corr, P.B. J. Clin. Invest. (1989) [Pubmed]
  17. Cardiac-specific overexpression of AT1 receptor mutant lacking G alpha q/G alpha i coupling causes hypertrophy and bradycardia in transgenic mice. Zhai, P., Yamamoto, M., Galeotti, J., Liu, J., Masurekar, M., Thaisz, J., Irie, K., Holle, E., Yu, X., Kupershmidt, S., Roden, D.M., Wagner, T., Yatani, A., Vatner, D.E., Vatner, S.F., Sadoshima, J. J. Clin. Invest. (2005) [Pubmed]
  18. Oral carnitine therapy in children with cystinosis and renal Fanconi syndrome. Gahl, W.A., Bernardini, I., Dalakas, M., Rizzo, W.B., Harper, G.S., Hoeg, J.M., Hurko, O., Bernar, J. J. Clin. Invest. (1988) [Pubmed]
  19. Apoptosis in myocytes in end-stage heart failure. Narula, J., Haider, N., Virmani, R., DiSalvo, T.G., Kolodgie, F.D., Hajjar, R.J., Schmidt, U., Semigran, M.J., Dec, G.W., Khaw, B.A. N. Engl. J. Med. (1996) [Pubmed]
  20. Developmental progression of myosin gene expression in cultured muscle cells. Silberstein, L., Webster, S.G., Travis, M., Blau, H.M. Cell (1986) [Pubmed]
  21. Adult-onset acid maltase deficiency. Morphologic and biochemical abnormalities reproduced in in cultured muscle. Askanas, V., Engel, W.K., DiMauro, S., Brooks, B.R., Mehler, M. N. Engl. J. Med. (1976) [Pubmed]
  22. Mechanisms controlling mitochondrial biogenesis and respiration through the thermogenic coactivator PGC-1. Wu, Z., Puigserver, P., Andersson, U., Zhang, C., Adelmant, G., Mootha, V., Troy, A., Cinti, S., Lowell, B., Scarpulla, R.C., Spiegelman, B.M. Cell (1999) [Pubmed]
  23. The gamete fusion process is defective in eggs of Cd9-deficient mice. Kaji, K., Oda, S., Shikano, T., Ohnuki, T., Uematsu, Y., Sakagami, J., Tada, N., Miyazaki, S., Kudo, A. Nat. Genet. (2000) [Pubmed]
  24. Reprogramming cell differentiation in the absence of DNA synthesis. Chiu, C.P., Blau, H.M. Cell (1984) [Pubmed]
  25. Early expression of angiogenesis factors in acute myocardial ischemia and infarction. Lee, S.H., Wolf, P.L., Escudero, R., Deutsch, R., Jamieson, S.W., Thistlethwaite, P.A. N. Engl. J. Med. (2000) [Pubmed]
  26. Synthesis, transport and fate of acetylcholinesterase in cultured chick embryos muscle cells. Rotundo, R.L., Fambrough, D.M. Cell (1980) [Pubmed]
  27. Association of the synaptic form of acetylcholinesterase with extracellular matrix in cultured mouse muscle cells. Inestrosa, N.C., Silberstein, L., Hall, Z.W. Cell (1982) [Pubmed]
  28. Metabolism of acetylcholine receptor in chick embryo muscle cells: effects of RSV and PMA. Miskin, R., Easton, T.G., Maelicke, A., Reich, E. Cell (1978) [Pubmed]
  29. Increased insulin receptors after exercise in patients with insulin-dependent diabetes mellitus. Pedersen, O., Beck-Nielsen, H., Heding, L. N. Engl. J. Med. (1980) [Pubmed]
  30. Degradation of the acetylcholine receptor in cultured muscle cells: selective inhibitors and the fate of undegraded receptors. Libby, P., Bursztajn, S., Goldberg, A.L. Cell (1980) [Pubmed]
  31. Modulation by estrogen of synthesis of specific uterine proteins. Skipper, J.K., Eakle, S.D., Hamilton, T.H. Cell (1980) [Pubmed]
  32. Plasminogen activator in chick embryo muscle cells: induction of enzyme by RSV, PMA and retinoic acid. Miskin, R., Easton, T.G., Reich, E. Cell (1978) [Pubmed]
  33. Multiple new phenotypes induced in 10T1/2 and 3T3 cells treated with 5-azacytidine. Taylor, S.M., Jones, P.A. Cell (1979) [Pubmed]
  34. Mutations in the caveolin-3 gene cause autosomal dominant limb-girdle muscular dystrophy. Minetti, C., Sotgia, F., Bruno, C., Scartezzini, P., Broda, P., Bado, M., Masetti, E., Mazzocco, M., Egeo, A., Donati, M.A., Volonte, D., Galbiati, F., Cordone, G., Bricarelli, F.D., Lisanti, M.P., Zara, F. Nat. Genet. (1998) [Pubmed]
  35. Apoptosis in the failing human heart. Olivetti, G., Abbi, R., Quaini, F., Kajstura, J., Cheng, W., Nitahara, J.A., Quaini, E., Di Loreto, C., Beltrami, C.A., Krajewski, S., Reed, J.C., Anversa, P. N. Engl. J. Med. (1997) [Pubmed]
  36. skn-1, a maternally expressed gene required to specify the fate of ventral blastomeres in the early C. elegans embryo. Bowerman, B., Eaton, B.A., Priess, J.R. Cell (1992) [Pubmed]
  37. Primary structure of dystrophin-related protein. Tinsley, J.M., Blake, D.J., Roche, A., Fairbrother, U., Riss, J., Byth, B.C., Knight, A.E., Kendrick-Jones, J., Suthers, G.K., Love, D.R. Nature (1992) [Pubmed]
  38. PKC-alpha regulates cardiac contractility and propensity toward heart failure. Braz, J.C., Gregory, K., Pathak, A., Zhao, W., Sahin, B., Klevitsky, R., Kimball, T.F., Lorenz, J.N., Nairn, A.C., Liggett, S.B., Bodi, I., Wang, S., Schwartz, A., Lakatta, E.G., DePaoli-Roach, A.A., Robbins, J., Hewett, T.E., Bibb, J.A., Westfall, M.V., Kranias, E.G., Molkentin, J.D. Nat. Med. (2004) [Pubmed]
  39. Activation of muscarinic potassium currents by ATP gamma S in atrial cells. Otero, A.S., Breitwieser, G.E., Szabo, G. Science (1988) [Pubmed]
  40. Slow ventricular conduction in mice heterozygous for a connexin43 null mutation. Guerrero, P.A., Schuessler, R.B., Davis, L.M., Beyer, E.C., Johnson, C.M., Yamada, K.A., Saffitz, J.E. J. Clin. Invest. (1997) [Pubmed]
  41. Temporal correlation between maximum tetanic force and cell death in postischemic rat skeletal muscle. Suzuki, H., Poole, D.C., Zweifach, B.W., Schmid-Schönbein, G.W. J. Clin. Invest. (1995) [Pubmed]
  42. Tumor necrosis factor-alpha gene and protein expression in adult feline myocardium after endotoxin administration. Kapadia, S., Lee, J., Torre-Amione, G., Birdsall, H.H., Ma, T.S., Mann, D.L. J. Clin. Invest. (1995) [Pubmed]
  43. The lethal effects of cytokine-induced nitric oxide on cardiac myocytes are blocked by nitric oxide synthase antagonism or transforming growth factor beta. Pinsky, D.J., Cai, B., Yang, X., Rodriguez, C., Sciacca, R.R., Cannon, P.J. J. Clin. Invest. (1995) [Pubmed]
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