La partecipazione della glicogeno sintasi chinasi 3 alla modulazione delle vie ipertrofiche muscolari e le influenze esercitate dall'esercizio delle forze in questi segnali

  • Bruno Gil Aldenucci Programa de Pós Graduação Lato Sensu da Universidade Gama Filho em Fisiologia do Exercí­cio: Prescrição de Exercí­cio. Fisioterapeuta e Mestrando do Programa de Biologia Celular e Molecular, na área de concentração de Fisiologia Humana, da Universidade Federal do Paraná
  • Luis Fernando Hoinaski Programa de Pós Graduação Lato Sensu da Universidade Gama Filho em Fisiologia do Exercí­cio: Prescrição de Exercí­cio. Bacharel em Educação Fí­sica pela Pontifí­cia Universidade Católica do Paraná
  • Everson Araújo Nunes Programa de Pós Graduação Lato Sensu da Universidade Gama Filho em Fisiologia do Exercí­cio: Prescrição de Exercí­cio. Doutor pelo Programa de Biologia Celular e Molecular pela Universidade Federal do Paraná
Parole chiave: Esercizio di forza, Ipertrofia, Glicogeno sintase chinasi 3, Proteina chinasi B (Akt)

Abstract

Obiettivo: L'obiettivo di questo lavoro è rivedere le influenze della glicogeno sintasi chinasi 3 nella modulazione delle vie ipertrofiche muscolari esercitate dall'esercizio di forza. Revisione della letteratura: la glicogeno sintasi chinasi 3 (GSK-3) è una serina/treonina presente in tutti gli eucarioti. Regola varie funzioni cellulari, tra cui lo sviluppo, il metabolismo, l'espressione genica, la traduzione delle proteine, l'organizzazione del citoscheletro, la regolazione del ciclo cellulare e l'apoptosi. Inoltre, è un regolatore negativo della crescita sia patologica che normale. È inibito da percorsi come la fosfatidilinositolo-3-chinasi/proteina chinasi B (chiamata anche Akt). Durante l'esercizio fisico, l'attività di Akt aumenta significativamente, inibendo GSK-3. GSK-3 esercita un'influenza negativa su fattori trascrizionali quali: fattore nucleare delle cellule T attivate (NFAT), β-catenina e fattore di iniziazione eucariotica 2B (eIF2B), che stimolano la sintesi proteica e la conseguente ipertrofia muscolare. Conclusione: la comprensione dei meccanismi di segnalazione che controllano lo sviluppo del muscolo scheletrico aiuta nella formazione di trattamenti per malattie cataboliche, disturbi neuromuscolari e può anche ridurre il tempo di riabilitazione dopo un trauma muscoloscheletrico.

Riferimenti bibliografici

-Abbott, K.L.; Friday, B.B.; Thaloor, D.; Murphy, T.J.; Pavlath, G.K. Activation and Cellular Localization of the Cyclosporine A-sensitive Transcription Factor NF-AT in Skeletal Muscle Cells. Molecular Biology of the Cell. Atlanta. Vol.9. 1998. p. 2905-2916.

-Aberle, H.; Bauer, A.; Stappert, J.; Kispert, A.; Kemler, R. β-catenin is a target for the ubiquitin–proteasome pathway. The EMBO Journal. Thomson. Vol. 16. Num. 13. 1997. p. 3797-3804.

-Aguila, L.F.D.; Krishnan, R.K.; Ulbrecht, J.S.; Farrell, P.A.; Correll, P.H.; Lang, C.H.; Zierath, J.R.; Kirwan, J.P. Muscle damage impairs insulin stimulation of IRS-1, PI 3-kinase, and Akt-kinase in human skeletal muscle. American Journal of Physiology –Endocrinology and Metabolism. Stanford. Vol. 279. 2000. p. E206-E212.

-Anderson, K.E.; Coadwell, J.; Stephens, L.R.; Hawkins, P.T. Translocation of PDK-1 to the plasma membrane is important in allowing PDK-1 to activate protein kinase B. Current Biology. Cambridge. Vol. 8. 1998. p. 684-691.

-Andjelkovic, M.; Alessi, D.R.; Meier, R.; Fernandez, A.; Lamb, N.J.C.; Frech, M.; Cron, P.; Cohen, P.; Lucocq, J.M.; Hemmings, B.A. Role of Translocation in the Activation and Function of Protein Kinase B. The Journal of Biological Chemistry. Stanford. Vol. 272. Num. 50. 1997. p. 31515-31524.

-Antos, C.L; McKinsey, T.A.; Frey, N.; Kutschke, W.; McAnally, J.; Shelton, J.M.; Richardson, J.A.; Joseph,A.;Hill, J.A.; Olson, E.N. Activated glycogen synthase-3βsuppresses cardiac hypertrophy in vivo. Proceedings of the National Academy of Sciences of the United States of America. Stanford. Vol. 99. 2002. p. 907-912.

-Aschenbach, W.G.; Ho, R.C.; Sakamoto, K.; Fujii, N.; Li, Y.; Kim, Y.; Hirshman, M.F.; Goodyear, L.J. Regulation of Dishevelled and β-catenin in rat skeletal muscle: an alternative exercise-induced GSK-3βsignaling pathway. American Journal of Physiology -Endocrinology and Metabolism. Stanford. Vol. 291. 2006. p. E152–E158.

-Beals, C.R.; Sheridan, C.M.; Turck, C.W.; Gardner, P.; Crabtree, G.R.; Nuclear Export of NFATc enhanced by glycogen synthase kinase 3. Sciences. Stanford. Vol. 275. 1997. p. 1930-1933.

-Bedair, H.S.; Ho, A.M.; Fu, F.H.; Huard, J. Skeletal Muscle Regeneration: an updateon recent findings. Current Opinion in Orthopaedics. Philadelphia. Vol. 15. 2004. p. 360-363.

-Behrens, J.; Jerchow, B.A.; Wurtele, M.; Grimm, J.; Asbrand, C.; Wirtz, R.; Kuhl, M.; Wedlich, D.; Birchmeier, W. Functional Interaction of an Axin Homolog,Conductin, with β-Catenin, APC, and GSK3β. Science. Stanford. Vol. 280. 1998. p. 596-599.

-Bodine, S.C.; Stitt, T.N.; Gonzalez, M.; Kline, W.O.; Stover, G.L.; Bauerlein, R.; Zlotchenko, E.; Scrimgeour, A.; Lawrence, J.C.; Glass, D.J.; Yancopoulos, G.D. Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo. Nature Cell Biology. Houston. Vol. 3. 2001. p. 1014-1019.

-Cadigan, K.M.; Liu, Y.I. Wnt signaling: complexity at the surface. Journal of Cell Science. Cambridge. Vol. 119. 2005. p. 395-402.

-Coffey, V.G.; Zhong, Z.; Shield, A.; Canny, B.J.; Chibalin, A.V.; Zierath, J.R.; Hawley, J.A. Early signaling responses to divergent exercise stimuli in skeletal muscle from well-trained humans. The FASEB Journal. Stanford. Vol. 20. 2006. p. 190-192.

-Coolican, S.A.; Samuel, D.S.; Ewton, D.Z.; McWade, F.J.; Florini, J.R. The Mitogenic and Myogenic Actions of Insulin-like Growth Factors Utilize Distinct Signaling Pathways. The Journal of BiologicalChemistry. Stanford. Vol. 272. Num. 10. 1997. p. 6653-6662.

-Crabtree, G.R.; Olson, E.N. NFAT Signaling: Choreographing the Social Lives of Cells. Cell. Cambridge. Vol. 109. 2002. p. S67-S79.

-Christ-Roberts, C.Y.; Pratipanawatr, T.; Pratipanawatr, W.; Berria, R.; Belfort, R.; Mandarino, L.J. Increased insulin receptor signaling and glycogen synthase activity contribute to the synergistic effect of exercise on insulin action. Journal Of Applied Physiology. Stanford. Vol. 95. 2003. p. 2519-2529.

-Deshmukh, A.; Coffey, V.G.; Zhong, Z.; Chibalin, A.V.; Hawley, J.A.; Zierath, J.R. Exercise-Induced Phosphorylation of the Novel Akt Substrates AS160 and Filamin A in Humans Skeletal Muscle. Diabetes. Stanford. Vol. 55. 2006. p. 1776-1782.

-DeVol, D.L.; Rotwein, P.; Sadow, J.L.; Novakofski, J.; Bechtel, P.J. Activation of insulin-like growth factor gene expression during work-induced skeletal muscle growth. American Journal of Physiology-Endocrinology and Metabolism. Stanford. Vol. 259. 1990. p. E89-E95.

-Ding, V.W.; Chen, R.H.; McCormick, F. Differential Regulation of Glycogen Synthae Kinase 3βby Insulin and Wnt Signaling. The Journal of BIological Chemistry. Stanford. Vol. 275. Num. 42. 2000. p. 32475-32481.

-Doble, B.W.; Woodgett, J.R. GSK-3: tricks of the trade for a multi-tasking kinase. Journal of Cell Science. Cambridge. Vol. 116. 2003. p. 1175-1186.

-Farrell, P.A.; Hernandez, J.M.; Fedele, M.J.; Vary, T.C.; Kimball, S.R.; Jefferson, L.S. Eukaryotic initiation factors and protein synthesis after resistance exercise in rats. Journal of Applied Physiology. Stanford. Vol. 88. 2000. p. 1036-1042.

-Farrell, P.A.; Fedele, M.J.; Vary, T.C.; Kimball, S.R.; Lang, C.H.; Jefferson, L.S. Regulation of protein synthesis after acute resistance exercise in diabetic rats. American Journal of Physiology-Endocrinology and Metabolism. Stanford. Vol. 39. 1999. p. E721-E727.

-Frech, M.; Andjelkovic, M.; Ingley, E.; Reddy, K.K.; Falck, J.R.; Hemmings, B.A. High Affinity Binding of Inositol Phosphates and Phosphoinositides to the Pleckstrin Homology Domain of RAC/Protein Kinase B and Their Influence on Kinase Activity. The Journal of Biological Chemistry. Stanford. Vol. 272. Num. 13. 1997. p. 8474-8481.

-Frost, R.A.; Lang, C.H. Protein Kinase B/Akt: a nexus of growth factor and cytokine signaling in determining muscle mass. Journal Of Applied Physiology. Stanford. Vol. 103. 2007. p. 378-387.

-Gerald,W.;Dorn,L.L.;Force, T. Protein Kinase Cascades In The Regulation of Cardiac hypertrophy. The Journal of Clinical Investigation. Michigan. Vol. 115. Num. 3. 2005. p. 527-537.

-Goichberg, P.; Shtutman, M.; Ben-Ze’ev, A.; Geiger, B. Recruitment of β-catenin to cadherin-mediated intercellular adhesions is involved in myogenic induction. Journal of Cell Science. Cambridge. Vol. 114. 2001. p. 1309-1319.

-Gold, M.R.; Scheid, M.P.; Santos, L.; Dang-Lawson, M.; Roth, R.A.; Matsuuchi, L.; Duronio, V.; Krebs, D.L. The B Cell Antigen Receptor Activates the Akt (Protein Kinase B)/Glycogen Synthase Kinase-3 Signaling Pathway Via Phosphatidylinositol 3-Kinase. The Journal of Immunology. Maryland. Vol. 163. 1999. p. 1894-1905.

-Haddad, F.; Adams, G.R. Inhibition of MAP/ERK kinase prevents IGF-I-induced hypertrophy in rat muscles. Journal Of Applied Physiology. Stanford. Vol. 96. 2004. p. 203-210.

-Hardt, S.E.; Sadoshima, J. Glycogen Synthase Kinase-3 A Novel Regulator of Cardiac Hypertrophy and Development. Journal of the American Heat Association. Dallas. Vol. 90. 2002. p. 1055-1063.

-Hilioti, Z.; Gallagher, D.A.; Low-Nam, S.T.; Ramaswamy, P.; Gajer, P.; Kingsbury, T.J.; Birchwood, C.J.; Levchenko, A.; Cunningham, K.W. GSK-3 kinases enhance calcineurin signaling by phosphorylation of RCNs. Genes & Development. New York. Vol. 18. 2004. p. 35-47.

-Hinoi, T.; Yamamoto, H.; Kishida, M.; Takada, S.; Kishida, S.; Kikuchi, A. Complex formation of adenomatous polyposis coli gene product and axin facilitates glycogen synthase kinase-3 β-dependent phosphorylation of β-catenin and down-regulates β-catenin. Journal of Biological Chemistry. Stanford. Vol. 275. 2000. p. 34399–34406.

-Hoppler, S.; Kavanagh, C.L. Wnt signaling: variety at the core. Journal of Cell Science. Cambridge. Vol. 120. 2006. p. 385-393.

-Horsley, V.; Jansen, K.M.; Mills, S.T.; Pavlath, G.K. IL-4 Acts as a Myoblast Recruitment Factor during Mammalian Muscle Growth. Cell. Cambridge. Vol. 113. 2003. p. 483-494.

-Horsley, V.; Friday, B.F.; Matteson, S.; Kegley, K.M.; Gephart, J.; Grace K. Pavlath, G.K. Regulation of the Growth of Multinucleated Muscle Cells by an NFATC2-dependent Pathway. The Journal of Cell Biology. Stanford. Vol 153. Num. 2. 2001. p. 329-338.

-Hunter, T. Oncoprotein Networks. Cell. Cambridge. Vol. 88. 1997. p. 333-346.

-Hurlstone, A.;Clevers, H. T-cell factors: turn-ons and turn-offs. The EMBO Journal. Thomson. Vol. 21. Num. 10. 2002. p. 2303-2311.

-Jacquemin, V.; Butler-Browne, G.S.; Furling, D.; Mouly, V. IL-13 mediates the recruitment of reserve cells for fusion during IGF-1-induced hypertrophy of human myotubes. Journal of Cell Science. Cambridge. Vol. 120. 2007. p. 670-681.

-Kirwan, J.P.; Aguila, L.F.D. Insulin Signalling, Exercise and Cellular Integrity. Biochemical Society Transactions. London. Vol. 31. 2003. p. 1281-1285.

-Kraemer, W.J.; Adams, K.; Cafarelli, E.; Dudley, G.A.; Dooly, C.; Feigenbaum, M.S.; Fleck, S.J.; Franklin, B.; Fry, A.C.; Hoffman, J.R.; Newton, R.U.; Potteiger, J.; Stone, M.H.; Ratamess, N.A.; McBride, T.T. Progression models in resistance training for healthy adults. Medicine & Science In Sports & Exercise. Indianapolis. Vol. 34. Num. 2. 2002. p. 364-380.

-Kraemer, J.W.; Hakkinen, K.; Newton, R.U.; Nindl, B.C.;Volek, J.S.; Mccormick, M.; Gotshalk, L.A.; Gordon, S.E.; Fleck, S.J.; Campbell, W.W.; Putukian, M.; Evans, W.J. Effects of heavy-resistance training on hormonal response patterns in younger vs. older men. Journal of Applied Physiology. Stanford. Vol. 87. Num. 3. 1999. p. 982-992.

-Kubica, N.; Kimball, S.R.; Jefferson, L.S.; Farrell, P. A. Alterations in the expression of mRNAs and proteins that code for species relevant to eIF2B activity after an acute bout of resistance exercise. Journal Of Applied Physiology. Stanford. Vol. 96. 2004. p. 679-687.

-Lai, K.M.V.; Gonzalez, M.; Poueymirou, W.T.; Kline, W.O.; Na, E.; Zlotchenko, E.; Stitt, T.N.; Economides, A.N.; Yancopoulos, G.D.; Glass, D.J. Conditional Activation of Akt in Adult Skeletal Muscle Induces Rapid Hypertrophy. Molecular and Cellular Biology. Washigton. Vol. 24. Num. 21. 2004. p. 9295-9304.

-Lajoie, C.; Calderone, A.; Trudeau, F.; Lavoie, N.; Massicotte, G.; Gagnon, S.; Béliveau, L. Exercise Training attenuated the PKB and GSK-3 dephosphorylation in the myocardium of ZDF rats. Journal of Applied Physiology. Stanford. Vol. 96. 2004. p. 1606-1612.

-Molenaar, M.; Roose, J.; Peterson, J.; Venanzi, S.; Clevers, H.; Destre ́e, O. Differential expression of the HMG box transcription factorsXTcf-3 and XLef-1 during early Xenopus development. Mechanisms of Development. Amsterdam. Vol. 75. 1998. p. 151-154.

-Nader, G.A.; Esser, K.A. Intracellular signaling specificity in skeletal muscle in response to different modes of exercise. Journal Of Applied Physiology. Stanford. Vol. 90. 2001. p. 1936-1942.

-Nakamura, T.; Hamada, F.; Ishidate, T.; Anai, K.; Kawahara, K.; Toyoshima, K.; Akiyama, T. Axin, an inhibitor of the Wnt signalling pathway, interacts with β-catenin, GSK-3βand APC and reduces the β-catenin level. Genes to Cells. Stanford. Vol.3. 1998. p. 395-403.

-Nikoulina, S.E.; Ciaraldi, T.P.; Mudaliar, S.; Carter, L.; Johnson, K.; Henry, R.R. Inhibition of Glycogen Synthase Kinase 3 Improves Insulin Action and Glucose Metabolism in Human Skeletal Muscle. Diabetes. Stanford. Vol. 51. 2002. p. 2190-2198.

-Olmeda, D.; Castel, S.; Vilaró, S.; Cano, A. β-Catenin Regulation during the Cell Cycle: Implications in G2/M and Apoptosis. Molecular Biology Of The Cell. Stanford. Vol. 14. 2003. p. 2844-2860.

-Ougolkov, A.V.; Fernandez-Zapico, M.E.; Savoy, D.N.; Urrutia, R.A.; Billadeau, D.D. Glycogen Synthase Kinase-3B Participates in Nuclear Factor KB–Mediated Gene Transcription and Cell Survival in Pancreatic Cancer Cells. Cancer Research. Stanford. Vol. 65. 2005. p. 2076-2081.

-Pan, W.; Jia, Y.; Wang, J.; Tao, D.; Gan, X.; Tsiokas, L.; Jing, N.; Wu, D.; Li, L. β-Catenin regulates myogenesis by relieving I-mfa-mediated suppression of myogenic regulatory factors in P19 cells. Proceedings of the National Academy of Scincies of the Unted States of America. Stanford. Proceedings of the National Academy of Scincies ofthe Unted States of America. Stanford. Vol. 102. Num. 48. 2005. p. 17378–17383.

-Pap, M.; Cooper, G.M. Role of Translation Initiation Factor 2B in Control of Cell Survival by the Phosphatidylinositol 3-Kinase/Akt/Glycogen Synthase Kinase 3βSignaling Pathway. Molecular and Cellular Biology. Washington. Vol. 22. Num. 2. 2002. p. 578-586.

-Peifer,M.; Sweeton D.; Casey M.; Wieschaus E. Wingless signal and Zeste-white 3 kinase trigger opposing changes in the intracellular distribution of Armadillo. Development. Cambridge. Vol. 120. 1994. p. 369–380.

-Rosas, M.; Dijkers, P.F.; Lindemans, C.L.; Lammers, J.J.; Koenderman, L.; Coffer, P.J. IL-5-mediated eosinophil survival requires inhibition of GSK-3 and correlates with β-catenin relocalization. Journal of Leukocyte Biology. Stanford. Vol. 80. 2006. p. 186-195.

-Rommel, C.; Bodine, S.C.; Clarke, B.A.; Rossman, R.; Nunez, L.; Stitt, T. N.; Yancopoulos, G.D.; Glass, D.J. Mediation of IGF-1-induced skeletal myotube hypertrophy by PI(3)K/Akt/mTOR and PI(3)K/Akt/GSK3 pathways. Nature Cell Biology, Houston. Vol. 3. 2001. p. 1009–1013.

-Sadowski, C.L.; Wheeler, T.T.; Wang, L.; Sadowski, H.B. GH Regulation of IGF-I and Suppressor of Cytokine Signaling Gene Expression in C2C12 Skeletal Muscle Cells. Endocrinology. Stanford. Vol. 142Num. 9. 2001. p. 3890-3900.

-Sakamoto, K.; Arnolds, D.E.; Ekberg, I.; Thorell, A.; Goodyear, L.J. Exercise regulates Akt and glycogen synthase kinase-3 activities in human skeletal muscle. Biochemical and Biophysical Research Communications. Amsterdam. Vol. 319. Num. 2. 2004. p. 419-425.

-Sakamoto, K.; Aschenbach, W.G.; Hirshman, M.F.; Goodyear, L.J. Akt Signaling in Skeletal Muscle: regulation by exercise and passive stretch. American Journal of Physiology-Endocrinology and Metabolism. Stanford. Vol. 285. 2003. p. E1081-E1088.

-Sakamoto, K.; Goodyear, L.J. Exercise Effects on Muscle Insulin Signaling and Action Invited Review: Intracellular signaling in contracting skeletal muscle. Journal of Applied Physiology. Stanford. Vol. 93. 2002. p. 369-383.

-Shen, T.; Liu, Y.; Cseresnye ́s, Z.; Hawkins, A.; Randall, W.R.; Schneider, M.F. Activity-and Calcineurin-independent Nuclear Shuttling of NFATc1, but Not NFATc3, in Adult Skeletal Muscle Fibers. Molecular Biology of the Cell. Stanford. Vol. 17. 2006. p. 1570-1582.

-Smilios, I.; Pilianidis, T.; Karamouzis, M.; Tokmakidis, S.P. Hormonal Responses after Various Resistance Exercise Protocols. Medicine & Science in Sports & Exercise. Indianapolis Vol. 35. Num. 4. 2003. p. 644-654.

-Vanhaesebroeck, B.; Alessi, D.R. The PI3K–PDK1 connection : more than just a road to PKB. Biochemical Journal. Portland. Vol. 346. 2000. p. 561-576.

-Velden, J.L.J.V.D.; Langen, R.C.J.; Kelders, M.C.J.M.; Wouters, E.F.M.; Heininger, Y.M.W.J.; Schols, A.M.W.J. Inhibiton of glycogen synthase kinase 3B activity is sufficient to stimulate myogenic differentiation. American Journal Physiology-Cell Physiology. Stanford. Vol. 290. 2006. p. C453-C462.

-Vyas, D.R.; Spangenburg, E.E.; Abraha, T.W.; Childs, T.E.; Booth, F.W. GSK-3βnegatively regulates skeletal myotube hypertrophy. Journal of Applied Physiology. Stanford. Vol. 283. 2002. p. C545-C551.

-Weeren, P.C.V.; Bruyn, K.M.T.; Smits, A.M.M. V.; Lint, J.V.; Burgering, B.M.T. Essential Role for Protein Kinase B (PKB) in Insulin-induced Glycogen Synthase Kinase 3 Inactivation. The Journal of Biological Chemestry. Stanford. Vol. 273. Num. 21. 1998. p. 13150-13156.

-Welsh, G.I.; Miller, C.M.; Loughlin, A.J.; Price, N.T.; Proud, C.G. Regulation of eukaryotic initiation factor eIF2B: glycogen synthase kinase-3 phosphorylates a conserved serine which undergoes dephosphorylation in response to insulin. Federation of European Biochemical Societies. Cambridge. Vol. 421. 1998. p. 125-130.

-Williams, D.D.; Pavitt, G.D.; Proud, C.G. Characterization of the Initiation Factor eIF2B and Its Regulation in Drosophila melanogaster. The Journal of Biological Chemistry. Stanford. Vol. 276. Num. 6. 2001. p. 3733-3742.

-Wojtazsewski, J.F.P.; Nielsen, P.; Kiens, B.; Richter, E.A. Regulation of Glycogen Synthase Kinase-3 in Human Skeletal Muscle Effects of Food Intake and Bicycle Exercise. Diabetes. Stanford. Vol. 50. 2001. p. 265-269.

Pubblicato
2011-12-31
Come citare
Aldenucci, B. G., Hoinaski, L. F., & Nunes, E. A. (2011). La partecipazione della glicogeno sintasi chinasi 3 alla modulazione delle vie ipertrofiche muscolari e le influenze esercitate dall’esercizio delle forze in questi segnali. Giornale Brasiliano Di Prescrizione E Fisiologia dell’esercizio, 4(19). Recuperato da https://www.rbpfex.com.br/index.php/rbpfex/article/view/227
Sezione
Articoli scientifici - Originali