A novel mechanism of myocyte degeneration involving the Ca2+-permeable growth factor-regulated channel

Journal of Cell Biology

Volumn 161, Issue 5, 2003, Pages 957-967

  Iwata, Yuko ^a   Katanosaka, Yuki ^a   Arai, Yuji ^a   Komamura, Kazuo ^a   Miyatake, Kunio ^a   Shigekawa, Munekazu ^a  

^a NATIONAL CEREBRAL AND CARDIOVASCULAR CENTER   (Japan)

Author keywords

Calcium entry; Cardiomyopathy; Dystrophin glycoprotein complex; Muscular dystrophy; Nonselective cation channel

Indexed keywords

CALCIUM CHANNEL; CREATINE KINASE; DELTA SARCOGLYCAN; DYSTROPHIN; GLYCOPROTEIN; MEMBRANE PROTEIN; SARCOGLYCAN; UNCLASSIFIED DRUG;

ANIMAL CELL; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CALCIUM TRANSPORT; CARDIOMYOPATHY; CELL DAMAGE; DYSTROPHY; GROWTH FACTOR REGULATED CHANNEL; HUMAN; MALE; MOUSE; MUSCLE ATROPHY; MUSCLE STRETCHING; MYOTUBE; NONHUMAN; PATHOGENESIS; PRIORITY JOURNAL; PROTEIN DEFECT; SARCOLEMMA;

ANIMALS; CALCIUM; CALCIUM CHANNELS; CALCIUM SIGNALING; CARDIOMYOPATHIES; CELL DEATH; CHO CELLS; CREATINE KINASE; CRICETINAE; CYTOSKELETAL PROTEINS; DISEASE MODELS, ANIMAL; DYSTROPHIN; GENE EXPRESSION REGULATION; MALE; MEMBRANE GLYCOPROTEINS; MICE; MICE, INBRED MDX; MICROSCOPY, ELECTRON; MUSCLE CELLS; MUSCLE FIBERS; MUSCULAR DYSTROPHIES; SARCOGLYCANS; SARCOLEMMA; TRPV CATION CHANNELS;

ANIMALIA; CRICETINAE; MUS MUSCULUS;

EID: 0038457838     PISSN: 00219525     EISSN: None     Source Type: Journal    
DOI: 10.1083/jcb.200301101     Document Type: Article

References (47)

1. Alderton, J.M., and R.A. Steinhardt. 2000a. Calcium influx through calcium leak channels is responsible for the elevated levels of calcium-dependent proteolysis in dystrophic myotubes. J. Biol. Chem. 275:9452-9460.
2. Alderton, J.M., and R.A. Steinhardt. 2000b. How calcium influx through calcium leak channels is responsible for the elevated levels of calcium-dependent proteolysis in dystrophic myotubes. Trends Cardiovasc Med. 10:268-272.
3. Bajusz, E., F. Homburger, J.R. Baker, and P. Bogdonoff. 1969. Dissociation of factors influencing myocardial degeneration and generalized cardiocirculatory failure. Ann. NY Acad. Sci. 156:396-420.
4. Barton, E.R., L. Morris, A. Musarao, N. Rosenthal, and H.L. Sweeney. 2002. Muscle-specific expression of insulin-like growth factor 1 counters muscle decline in mdx mice. J. Cell Biol. 157:137-147.
5. + exchanger isoform 1 (NHE1) is a novel member of the calmodulin-binding proteins. Identification and characterization of calmodulin-binding sites. J. Biol. Chem. 269:13703-13709.
6. 2+-permeable channel GRC. J. Cell Sci. 114:3599-3606.
7. Brown, S.C., and J.A. Lucy. 1997. Functions of dystrophin. In Dystrophin. Gene, Protein and Cell Biology. S.C. Brown and J.A. Lucy, editors. Cambridge University Press, Cambridge. 163-200.
8. Caterina, M.J., T.A. Rosen, M. Tominaga, A.J. Brake, and D. Julius. 1997. The capsaicin receptor: a heat-activated ion channel in the pain pathway. Nature. 389:816-824.
9. Caterina, M.J., T.A. Rosen, M. Tominaga, A.J. Brake, and D. Julius. 1999. A capsaicin-receptor homologue with a high threshold for noxious heat. Nature. 398:436-441.
10. Cullen, M.J., and J.J. Fulthorpe. 1975. Stages in fiber breakdown in Duchenne muscular dystrophy. An electron-microscopic study. J. Neurol. Sci. 24:179-200.
11. Cullen, M.J., and E. Jaros. 1988. Ultrastructure of the skeletal muscle in the X chromosome-linked dystrophic (mdx) mouse. Comparison with Duchenne muscular dystrophy. Acta Neuropathol. (Berl). 77:69-81.
12. Delaughter, M.C., G.E. Taffet, M.L. Fiorotto, M.L. Entman, and R.J. Schwartz. 1999. Local insulin-like growth factor I expression induces physiologic, then pathologic, cardiac hypertrophy in transgenic mice. FASEB J. 13:1923-1929.
13. Duerr, R.L., S. Huang, H.R. Miraliakbar, R. Clark, K.R. Chien, and J. Ross, Jr. 1995. Insulin-like growth factor-1 enhances ventricular hypertrophy and function during the onset of experimental cardiac failure. J. Clin. Invest. 95:619-627.
14. Fong, P.Y., P.R. Turner, W.F. Denetclaw, and R.A. Steinhardt. 1990. Increased activity of calcium leak channels in myotubes of Duchenne human and mdx mouse origin. Science. 250:673-676.
15. Franco-Obregon, A., Jr., and J.B. Lansman. 1994. Mechanosensitive ion channels in skeletal muscle from normal and dystrophic mice. J. Physiol. 481:299-309.
16. Grynkiewicz, G., M. Poenie, and R.Y. Tsien. 1985. A new generation of calcium indicators with greatly improved fluorescence properties. J. Biol. Chem. 260:3440-3450.
17. Iwata, Y., H. Nakamura, Y. Mizuno, M. Yoshida, E. Ozawa, and M. Shigekawa. 1993. Defective association of dystrophin with sarcolemmal glycoproteins in the cardiomyopathic hamster heart. FEBS Lett. 329:227-231.
18. Iwata, Y., Y. Pan, H. Hanada, T. Yoshida, and M. Shigekawa. 1996. Dystrophinglycoprotein complex purified from hamster cardiac muscle. Comparison of the complexes from cardiac and skeletal muscles of hamster and rabbit. J. Mol. Cell. Cardiol. 28:2501-2509.
19. Kanzaki, M., Y.Q. Zhang, H. Mashima, H. Shibata, and I. Kojima. 1999. Translocation of a calcium-permeable cation channel induced by insulin-like growth factor-1. Nat. Cell Biol. 1:165-170.
20. MacLennan, P.A., A. McArdle, and R.H.T. Edwards. 1991. Effects of calcium on protein turnover of incubated muscles from mdx mice. Am. J. Physiol. 260:E594-E598.
21. + channels. Proc. Natl. Acad. Sci. USA. 97:4950-4955.
22. Menke, A., and H. Jockusch. 1991. Decreased osmotic stability of dystrophin-less muscle cells from the mdx mouse. Nature. 349:69-71.
23. Mokri, B., and A.G. Engel. 1975. Duchenne dystrophy: electronic microscopic findings pointing to a basic or early abnormality in the plasma membrane of muscle fiber. Neurology. 25:1111-1120.
24. Montell, C., and L. Birnbaumer. 2002. The TRP channels, a remarkably functional family. Cell. 108:595-598.
25. Nakamura, T.Y., Y. Iwata, M. Sampaolesi, H. Hanada, N. Saito, M. Artman, W.A. Coetzee, and M. Shigekawa. 2001. Stretch-activated cation channels in skeletal muscle myotubes from sarcoglycan-deficient hamsters. Am. J. Physiol. Cell Physiol. 281:C690-C699.
26. Naruse, K., T. Yamada, and M. Sokabe. 1998. Involvement of SA channels in orienting response of cultured endothelial cells to cyclic stretch. Am. J. Physiol. 274:H1532-H1538.
27. Nigro, V., Y. Okazaki, A. Belsito, G. Piluso, Y. Matsuda, L. Politano, G. Nigro, C. Ventura, C. Abbondanza, A.M. Molinari, et al. 1997. Identification of the Syrian hamster cardiomyopathy gene. Hum. Mol. Genet. 6:601-607.
28. Ozawa, E., S. Noguchi, Y. Mizuno, Y. Hagiwara, and M. Yoshida. 1998. From dystrophinopathy to sarcoglycanopathy: evolution of a concept of muscular dystrophy. Muscle Nerve. 21:421-438.
29. Petrof, B.J., J.B. Shrager, H.H. Stedman, A.M. Kelly, and H.L. Sweeney. 1993. Dystrophin protects the sarcolemma from stresses developed during muscle contraction. Proc. Natl. Acad. Sci. USA. 90:3710-3714.
30. Rando, T.A., and H.M. Blau. 1994. Primary mouse myoblast purification, characterization, and transplantation for cell-mediated gene therapy. J. Cell Biol. 125:1275-1287.
31. Reimer, K.A., and R.B. Jenning. 1986. Myocardial ischemia, hypoxia, and infarction. In The Heart and Cardiovascular System. H.A. Fozzard, E.H. Habor, R. B. Jennings, A.M. Katz, and H.E. Morgan, editors. Raven Press, New York. 1133-1202.
32. Robert, V., M.L. Massimino, V. Tosello, R. Marsault, M. Cantini, V. Sorrentino, and T. Pozzan. 2001. Alteration in calcium handling at the subcellular level in mdx myotubes. J. Biol. Chem. 276:4647-4651.
33. Saito, S., Y. Hiroi, Y. Zou, R. Aikawa, H. Toko, F. Shibasaki, Y. Yazaki, R. Nagai, and I. Komuro. 2000. β-Adrenergic pathway induces apoptosis through calcineurin activation in cardiac myocytes. J. Biol. Chem. 275:34528-34533.
34. Sampaolesi, M., Y. Yoshida, Y. Iwata, H. Hanada, and M. Shigekawa. 2001. Stretch-induced cell damage in sarcoglycan-deficient myotubes. Pflugers Arch. 442:161-170.
35. Shirinsky, V.P., A.S. Antonov, K.G. Birukov, A.V. Sobolevsky, Y.A. Romanov, N.V. Kabaeva, G.N. Antonova, and V.N. Smirnov. 1989. Mechano-chemical control of human endothelium orientation and size. J. Cell Biol. 109:331-339.
36. Spencer, M.J., D.E. Croall, and J.G. Tidball. 1995. Calpains are activated in necrotic fibers from mdx dystrophic mice. J. Biol. Chem. 270:10909-10914.
37. Stewart, C., and P. Rotwein. 1996. Growth, differentiation, and survival: multiple physiological functions for insulin-like growth factors. Physiol. Rev. 76:1005-1026.
38. Straub, V., and K.P. Campbell. 1997. Muscular dystrophies and the dystrophinglycoprotein complex. Curr. Opin. Neurol. 10:168-175.
39. Suzuki, M., J. Sato, K. Kutsuwada, G. Ooki, and M. Imai. 1999. Cloning of a stretch-inhibitable nonselective cation channel. J. Biol. Chem. 274:6330-6335.
40. Torres, L.F., and L.W. Duchen. 1987. The mutant mdx: inherited myopathy in the mouse. Morphological studies of nerves, muscles and end-plates. Brain. 110:269-299.
41. Towbin, J.A., and N.E. Bawles. 2002. The failing heart. Nature. 415:227-233.
42. Turner, P.R., T. Westwood, C.M. Regen, and R.A. Steinhardt. 1988. Increased protein degradation results from elevated free calcium levels found in muscle from mdx mice. Nature. 335:735-738.
43. Tutdibi, O., H. Brinkmeier, R. Rudel, and K.J. Föhr. 1999. Increased calcium entry into dystrophin-deficient muscle fibers of MDX and ADR-MDX mice is reduced by ion channel blockers. J. Physiol. 515:859-868.
44. Vandebrouck, C., G. Dupont, C. Cognard, and G. Raymond. 2001. Cationic channels in normal and dystrophic myotubes. Neuromuscul. Disord. 11:72-79.
45. Vandebrouck, C., D. Martin, M. Colson-Van Schoor, H. Debaix, and P. Gailly. 2002. Involvement of TRPC in the abnormal calcium influx observed in dystrophic (mdx) mouse skeletal muscle fibers. J. Cell Biol. 158:1089-1096.
46. + exchanger isoform 1. J. Biol. Chem. 275:7942-7949.
47. Yoshida, T., Y. Pan, H. Hanada, Y. Iwata, and M. Shigekawa. 1998. Bidirectional signaling between sarcoglycans and the integrin adhesion system in cultured L6 myocytes. J. Biol. Chem. 273:1583-1590.