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Original Articles

Cross-talk between TRPC-1, mTOR, PGC-1α and PPARδ in the dystrophic muscle cells treated with tempol

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Pages 245-257 | Received 23 Jul 2021, Accepted 03 May 2022, Published online: 12 May 2022

References

  • Mendell JR, Shilling C, Leslie ND, et al. Evidence-based path to newborn screening for duchenne muscular dystrophy. Ann Neurol. 2012;71(3):304–313.
  • Whitehead NP, Yeung EW, Allen DG. Muscle damage in mdx (dystrophic) mice: role of calcium and reactive oxygen species. Clin Exp Pharmacol Physiol. 2006;33(7):657–662.
  • Vandebrouck C, Martin D, Colson-Van Schoor M, et al. Involvement of TRPC in the abnormal calcium influx observed in dystrophic (mdx) mouse skeletal muscle fibers. J Cell Biol. 2002;158(6):1089–1096.
  • Gervásio OL, Whitehead NP, Yeung EW, et al. TRPC1 binds to caveolin-3 and is regulated by src kinase - role in duchenne muscular dystrophy. J Cell Sci. 2008;121(13):2246–2255.
  • Chung HS, Kim GE, Holewinski RJ, et al. Transient receptor potential channel 6 regulates abnormal cardiac S-nitrosylation in duchenne muscular dystrophy. Proc Natl Acad Sci USA. 2017;114:10763–10771.
  • Franco A, Jr, Lansman JB. Calcium entry through stretch-inactivated ion channels in mdx myotubes. Nature. 1990;344(6267):670–673.
  • Vandebrouck C, Duport G, Cognard C, et al. Cationic channels in normal and dystrophic human myotubes. Neuromuscul Disord. 2001;11(1):72–79.
  • Nishida M, Kuwahara K, Kozai D, et al. TRP channels: their function and potentiality as drug targets. In: Nakao K, Minato N, Uemoto S, editors. Innovative medicine: basic research and development. Tokyo: Springer; 2015.
  • Burns DP, Ali I, Rieux C, et al. Tempol supplementation restores diaphragm force and metabolic enzyme activities in mdx mice. Antioxidants. 2017;6(4):101.
  • Hermes TA, Mâncio RD, Macedo AB, et al. Tempol treatment shows phenotype improvement in mdx mice. PLoS One. 2019;14(4):e0215590.
  • Hermes TA, Mizobuti DS, Rocha GL, et al. Tempol improves redox status in mdx dystrophic diaphragm muscle. Int J Exp Pathol. 2020;101(6):289–297.
  • da Silva HNM, Covatti C, Rocha GL, et al. Elaine minatel E. Oxidative stress, inflammation, and activators of mitochondrial biogenesis: tempol targets in the diaphragm muscle of exercise trained-mdx mice. Front Physiol. 2021;12:649793.
  • Godin R, Daussin F, Matecki S, et al. Peroxisome proliferator-activated receptor γ coactivator1- gene α transfer restores mitochondrial biomass and improves mitochondrial calcium handling in post-necrotic mdx mouse skeletal muscle. J Physiol. 2012;590(21):5487–5502.
  • Choi JH, Jeong SY, Oh MR, et al. TRPCs: influential mediators in skeletal muscle. Cells. 2020;9(4):850.
  • Rando TA, Blau HM. Primary mouse myoblast purification, characterization, and transplantation for cell-mediated gene therapy. J Cell Biol. 1994;125(6):1275–1287.
  • Lai EY, Luo Z, Onozato ML, et al. Effects of the antioxidant drug tempol on renal oxygenation in mice with reduced renal mass. Am J Physiol Renal Physiol. 2012;303:64–74.
  • Neil S, Huh J, Baronas V, et al. Oral administration of the nitroxide radical TEMPOL exhibits immunomodulatory and therapeutic properties in multiple sclerosis models. Brain Behav Immun. 2017;62:332–343.
  • Whitehead NP, Yeung EW, Froehner SC, et al. Skeletal muscle NADPH oxidase is increased and triggers stretch-induced damage in the mdx mouse. PLoS ONE. 2010;5(12):e15354.
  • Matsumura CY, Taniguti APT, Pertille A, et al. Stretch-activated calcium channel protein TRPC1 is correlated with the different degrees of the dystrophic phenotype in mdx mice. Am J Physiol Cell Physiol. 2011;301(6):C1344–50.
  • Rando TA. Oxidative stress and the pathogenesis of muscular dystrophies. J Phys Med Rehabil. 2002;81:175–186.
  • Disatnik MH, Dhawan J, Yu Y, et al. Evidence of oxidative stress in mdx mouse muscle: studies of the pre-necrotic state. J Neurol Sci. 1998;161(1):77–84.
  • Hool LC. Evidence for the regulation of L-type Ca2+ channels in the heart by reactive oxygen species: mechanism for mediating pathology. Clin Exp Pharmacol Physiol. 2008;35(2):229–234.
  • Gupte SA, Wolin MS. Oxidant and redox signaling in vascular oxygen sensing: implications for systemic and pulmonary hypertension. Antioxid Redox Signal. 2008;10(6):1137–1152.
  • Suresh K, Servinsky L, Jiang H, et al. Reactive oxygen species induced Ca(2+) influx via TRPV4 and microvascular endothelial dysfunction in the SU5416/hypoxia model of pulmonary arterial hypertension. Am J Physiol Lung Cell Mol Physiol. 2018;314:893–907.
  • Vogel PA, Yang X, Moss NG, et al. Superoxide enhances Ca2+ entry through L-type channels in the renal afferent arteriole. Hypertension. 2015;66(2):374–381.
  • Olah T, Fodor J, Ruzsnavszky O, et al. Overexpression of transient receptor potential canonical type 1 (TRPC1) alters both store operated calcium entry and depolarization-evoked calcium signals in C2C12 cells. Cell Calcium. 2011;49(6):415–425.
  • Brand-Saberi B, Christ B. Genetic and epigenetic control of muscle development in vertebrates. Cell Tissue Res. 1999;296(1):199–212.
  • Trendelenburg AU, Meyer A, Rohner D, et al. Myostatin reduces akt/TORC1/p70S6K signaling, inhibiting myoblast differentiation and myotube size. Am J Physiol Cell Physiol. 2009;296:1258–1270.
  • Laplante M, Sabatini DM. mTOR signaling in growth control and disease. Cell. 2012;149(2):274–293.
  • Bentzinger CF, Romanino K, Cloëtta D, et al. Skeletal muscle-specific ablation of raptor, but not of rictor, causes metabolic changes and results in muscle dystrophy. Cell Metab. 2008;8(5):411–424.
  • Vernier M, Vincent Giguère V. Aging, senescence and mitochondria: the PGC-1/ERR axis. J Mol Endocrinol. 2021;66:1–14.
  • Cunningham JT, Rodgers JT, Arlow DH, et al. mTOR controls mitochondrial oxidative function through a YY1-PGC-1alpha transcriptional complex. Nature. 2007;450(7170):736–740.
  • Yoon MS. mTOR as a key regulator in maintaining skeletal muscle mass. Front Physiol. 2017;8:788.
  • Mastropasqua F, Giulia Girolimetti G, Shoshan M. PGC1α: friend or foe in cancer? Genes (Basel. 2018;9(1):48.
  • Phua WWT, Wong MXY, Liao Z, et al. An aPPARent functional consequence in skeletal muscle physiology via peroxisome Proliferator-Activated receptors. IJMS. 2018;19(5):1425.
  • Bell EL, Shine RW, Dwyer P, et al. PPARδ modulation rescues mitochondrial fatty acid oxidation defects in the mdx model of muscular dystrophy. Mitochondrion. 2019;46:51–58.,
  • Liu J, Liang X, Zhou D, et al. Coupling of mitochondrial function and skeletal muscle fiber type by a miR-499/Fnip1/AMPK circuit. EMBO Mol Med. 2016;8(10):1212–1228.
  • Selsby JT, Morine KJ, Pendrak K, et al. Rescue of dystrophic skeletal muscle by PGC-1α involves a fast to slow fiber type shift in the mdx mouse. PLoS One. 2012;7(1):e30063.
  • Lin Y, Zhao Y, Li R, et al. PGC-1α is associated with C2C12 myoblast differentiation. Cent Eur J Biol. 2014;9(11):1030–1036.
  • Eisele PS, Handschin C. Functional crosstalk of PGC-1 coactivators and inflammation in skeletal muscle pathophysiology. Semin Immunopathol. 2014;36(1):27–53.
  • Wenz T, Rossi SG, Rotundo RL, et al. Increased muscle PGC-1α expression protects from sarcopenia and metabolic disease during aging. Proc Natl Acad Sci USA. 2009;106(48):20405–20410.
  • Wilcox CS. Effects of tempol and redox-cycling nitroxides in models of oxidative stress. Pharmacol Ther. 2010;126(2):119–145.
  • Batinic-Haberle I, Reboucas JS, Spasojevic I. Superoxide dismutase mimics: chemistry, pharmacology, and therapeutic potential. Antioxid Redox Signal. 2010;13:877–918.
  • Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) method. Methods. 2001;25(4):402–408.
  • Patel K, Chen Y, Dennehy K, et al. Acute antihypertensive action of nitroxides in the spontaneously hypertensive rat. Am J Physiol Regul Integr Comp Physiol. 2006;290:37–43.
  • Soule BP, Hyodo F, Matsumoto K, et al. The chemistry and biology of nitroxide compounds. Free Radic Biol Med. 2007;42(11):1632–1650.
  • Wilcox CS, Pearlman A. Chemistry and antihypertensive effects of tempol and other nitroxides. Pharmacol Rev. 2008;60(4):418–469.
  • Lima TI, Guimarães DSPSF, Oliveira AG, et al. Opposing action of NCoR1 and PGC-1α in mitochondrial redox homeostasis. Free Radic Biol Med. 2019;143:203–208.
  • Pinar N, Kaplan M, Ozgur T, et al. Ameliorating effects of tempol on methotrexate-induced liver injury in rats. Biomed Pharmacother. 2018;102:758–764.
  • Ranjbar A, Kheiripour N, Ghasemi H, et al. Antioxidative effects of tempol on mitochondrial dysfunction in diabetic nephropathy. Iran J Kidney Dis. 2018;12:84–90.
  • Lü JM, Lin PH, Yao Q, et al. Chemical and molecular mechanisms of antioxidants: experimental approaches and model systems. J Cell Mol Med. 2010;14(4):840–860.
  • Gygi SP, Rochon Y, Franza BR, et al. Correlation between protein and mRNA abundance in yeast. Mol Cell Biol. 1999;19(3):1720–1730.
  • Bustin SA, Benes V, Garson JA, et al. The MIQE guidelines: minimum information for publication of quantitative real-time PCR experiments. Clin Chem. 2009;55(4):611–622.
  • Sarangarajan R, Meera S, Rukkumani R, et al. Antioxidants: friend or foe? Asian Pac J Trop Med. 2017;10(12):1111–1116.
  • Dröge W. Free radicals in the physiological control of cell function. Physiol Rev. 2002;82(1):47–95.
  • Mailloux RJ. Mitochondrial antioxidants and the maintenance of cellular hydrogen peroxide levels. Oxid Med Cell Longev. 2018;2018:7857251.

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