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2010 | 70 | 4 |
Tytuł artykułu

Hypoxia and high glucose activate tetrodotoxin-resistant Na plus currents through PKA and PKC

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Warianty tytułu
Języki publikacji
EN
Abstrakty
EN
Voltage-gated sodium channels are critical for the initiation and propagation of action potentials and for the regulation of neuronal excitability. Hyperglycemia and hypoxia are two main changes in diabetes frequently associated with several complications. Although many studies on streptozotocin-induced diabetic rats indicate that early diabetic neuropathy is associated with increased amplitude and faster kinetics of sodium channels, the distinctive roles of high glucose and hypoxia have not been completely clarified. Here we show that hypoxic and high glucose conditions (overnight exposure) increase activation and inactivation of TTX-R INa in DRG neurons without affecting the level of expression. Hypoxia and high glucose alone were potent enough to induce similar or even greater sensitization than when both conditions were present, without any of them having a predominant effect. PKA is mainly responsible of the one condition effect, while under both hypoxia and high glucose PKC was also contributing to alter the kinetics, although not in a cumulative manner. These data indicate that TTX-R INa is significantly modulated under short-time exposure to hypoxia and high glucose, a mechanism which might be relevant for diabetes-related complications or other diseases associated with acute hypoxia.
Słowa kluczowe
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-
Rocznik
Tom
70
Numer
4
Opis fizyczny
p.351-361,fig.,ref.
Twórcy
  • Department of Anatomy, Physiology and Biophysics, Faculty of Biology, University of Bucharest, Bucharest, Romania
autor
  • Department of Anatomy, Physiology and Biophysics, Faculty of Biology, University of Bucharest, Bucharest, Romania
autor
  • Department of Anatomy, Physiology and Biophysics, Faculty of Biology, University of Bucharest, Bucharest, Romania
autor
  • Department of Anatomy, Physiology and Biophysics, Faculty of Biology, University of Bucharest, Bucharest, Romania
autor
  • Department of Anatomy, Physiology and Biophysics, Faculty of Biology, University of Bucharest, Bucharest, Romania
autor
  • Department of Anatomy, Physiology and Biophysics, Faculty of Biology, University of Bucharest, Bucharest, Romania
Bibliografia
  • Cang CL, Zhang H, Zhang YQ, Zhao ZQ (2009) PKCepsilon- dependent potentiation of TTX-resistant Nav1.8 current by neurokinin-1 receptor activation in rat dorsal root gan­glion neurons. Mol Pain 5: 33.
  • Cantrell AR, Tibbs VC, Yu FH, Murphy BJ, Sharp EM, Qu Y, Catterall WA, Scheuer T (2002) Molecular mechanism of convergent regulation of brain Na(+) channels by pro­tein kinase C and protein kinase A anchored to AKAP-15. Mol Cell Neurosci 21: 63-80.
  • Catrina SB, Okamoto K, Pereira T, Brismar K, Poellinger L (2004) Hyperglycemia regulates hypoxia-inducible fac- tor-1alpha protein stability and function. Diabetes 53: 3226-3232.
  • Chahine M, Ziane R, Vijayaragavan K, Okamura Y (2005) Regulation of Nav channels in sensory neurons. Trends Pharmacol Sci 26: 496-502.
  • Chao D, Xia Y (2010) Ionic storm in hypoxic/ischemic stress: can opioid receptors subside it? Prog Neurobiol 90: 439-470.
  • Cheng JK, Ji RR (2008) Intracellular signaling in primary sensory neurons and persistent pain. Neurochem Res 33: 1970-1978.
  • Craner MJ, Klein JP, Renganathan M, Black JA, Waxman SG (2002) Changes of sodium channel expression in experimental painful diabetic neuropathy. Ann Neurol 52: 786-792.
  • Cummins TR, Sheets PL, Waxman SG (2007) The roles of sodium channels in nociception: Implications for mecha­nisms of pain. Pain 131: 243-257.
  • Denac H, Mevissen M, Scholtysik G (2000) Structure, func­tion and pharmacology of voltage-gated sodium chan­nels. Naunyn Schmiedebergs Arch Pharmacol 362: 453­479.
  • Dib-Hajj S, Black JA, Cummins TR, Waxman SG (2002) NaN/Nav1.9: a sodium channel with unique properties. Trends Neurosci 25: 253-259.
  • Dobretsov M, Hastings SL, Stimers JR, Zhang JM (2001) Mechanical hyperalgesia in rats with chronic perfusion of lumbar dorsal root ganglion with hyperglycemic solution. J Neurosci Methods 110: 9-15.
  • Ekberg J, Adams DJ (2006) Neuronal voltage-gated sodium channel subtypes: key roles in inflammatory and neuro­pathic pain. Int J Biochem Cell Biol 38: 2005-2010.
  • Flake NM, Lancaster E, Weinreich D, Gold MS (2004) Absence of an association between axotomy-induced changes in sodium currents and excitability in DRG neu­rons from the adult rat. Pain 109: 471-480.
  • Gold MS, Levine JD, Correa AM (1998) Modulation of TTX-R INa by PKC and PKA and their role in PGE2- induced sensitization of rat sensory neurons in vitro. J Neurosci 18: 10345-10355.
  • Gold MS, Reichling DB, Shuster MJ, Levine JD (1996) Hyperalgesic agents increase a tetrodotoxin-resistant Na+ current in nociceptors. Proc Natl Acad Sci U S A 93: 1108-1112.
  • Hayase F, Matsuura H, Sanada M, Kitada-Hamada K, Omatsu- Kanbe M, Maeda K, Kashiwagi A, Yasuda H (2007) Inhibitory action of protein kinase Cbeta inhibitor on tetro- dotoxin-resistant Na+ current in small dorsal root ganglion neurons in diabetic rats. Neurosci Lett 417: 90-94.
  • Hirade M, Yasuda H, Omatsu-Kanbe M, Kikkawa R, Kitasato H (1999) Tetrodotoxin-resistant sodium chan­nels of dorsal root ganglion neurons are readily activated in diabetic rats. Neuroscience 90: 933-939.
  • Hong S, Morrow TJ, Paulson PE, Isom LL, Wiley JW (2004) Early painful diabetic neuropathy is associated with dif­ferential changes in tetrodotoxin-sensitive and-resistant sodium channels in dorsal root ganglion neurons in the rat. J Biol Chem 279: 29341-29350.
  • Hong S, Wiley JW (2006) Altered expression and function of sodium channels in large DRG neurons and myelinated A-fibers in early diabetic neuropathy in the rat. Biochem Biophys Res Commun 339: 652-660.
  • Huang ZJ, Song XJ (2008) Differing alterations of sodium currents in small dorsal root ganglion neurons after gan­glion compression and peripheral nerve injury. Mol Pain 4: 20.
  • Hudmon A, Choi JS, Tyrrell L, Black JA, Rush AM, Waxman SG, Dib-Hajj SD (2008) Phosphorylation of sodium channel Na(v)1.8 by p38 mitogen-activated pro­tein kinase increases current density in dorsal root gan­glion neurons. J Neurosci 28: 3190-3201.
  • Ikeda M, Yoshida S, Kadoi J, Nakano Y, Mastumoto S (2005) The effect of PKC activity on the TTX-R sodium currents from rat nodose ganglion neurons. Life Sci 78: 47-53.
  • Inoguchi T, Battan R, Handler E, Sportsman JR, Heath W, King GL (1992) Preferential elevation of protein kinase C isoform beta II and diacylglycerol levels in the aorta and heart of diabetic rats: differential reversibility to glycemic control by islet cell transplantation. Proc Natl Acad Sci USA 89: 11059-11063.
  • Iwase M, Imoto H, Murata A, Nakamura U, Nohara S, Uchizono Y, Iino K, Iida M (2007) Altered postural regu­lation of foot skin oxygenation and blood flow in patients with type 2 diabetes mellitus. Exp Clin Endocrinol Diabetes 115: 444-447.
  • Liu C, Li Q, Su Y, Bao L (2009) Prostaglandin E2 promotes Na1.8 trafficking via its intracellular RRR motif through the protein kinase A pathway. Traffic 11: 405-417.
  • Livak KJ, Schmittgen TD (2001) Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. Methods 25: 402-408.
  • Lopez-Santiago LF, Pertin M, Morisod X, Chen C, Hong S, Wiley J, Decosterd I, Isom LL (2006) Sodium channel beta2 subunits regulate tetrodotoxin-sensitive sodium channels in small dorsal root ganglion neurons and modu­late the response to pain. J Neurosci 26: 7984-7994.
  • Maulik D, Ashraf QM, Mishra OP, Delivoria-Papadopoulos M (2008) Activation of p38 mitogen-activated protein kinase (p38 MAPK), extracellular signal-regulated kinase (ERK) and c-jun N-terminal kinase (JNK) during hypox- ia in cerebral cortical nuclei of guinea pig fetus at term: role of nitric oxide. Neurosci Lett 439: 94-99.
  • Nyengaard JR, Ido Y, Kilo C, Williamson JR (2004) Interactions between hyperglycemia and hypoxia: impli­cations for diabetic retinopathy. Diabetes 53: 2931-2938.
  • O'Reilly JP, Cummins TR, Haddad GG (1997) Oxygen deprivation inhibits Na+ current in rat hippocampal neu­rones via protein kinase C. J Physiol 503: 479-488.
  • Obrosova IG (2009) Diabetes and the peripheral nerve. Biochim Biophys Acta 1792: 931-940.
  • Patrick Harty T, Waxman SG (2007) Inactivation properties of sodium channel Nav1.8 maintain action potential amplitude in small DRG neurons in the context of depo­larization. Mol Pain 3: 12.
  • Petruska JC, Napaporn J, Johnson RD, Gu JG, Cooper BY (2000) Subclassified acutely dissociated cells of rat DRG: histochemistry and patterns of capsaicin-, proton-, and ATP-activated currents. J Neurophysiol 84: 2365-2379.
  • Purves T, Middlemas A, Agthong S, Jude EB, Boulton AJ, Fernyhough P, Tomlinson DR (2001) A role for mitogen- activated protein kinases in the etiology of diabetic neu­ropathy. FASEB J 15: 2508-2514.
  • Renganathan M, Cummins TR, Waxman SG (2001) Contribution of Na(v)1.8 sodium channels to action potential electrogenesis in DRG neurons. J Neurophysiol 86: 629-640.
  • Ristoiu V, Pluteanu F, Flonta ML, Reid G (2002) Few cul­tured rat primary sensory neurons express a tolbu- tamide-sensitive K+ current. J Cell Mol Med 6: 271-274.
  • Ristoiu V, Dinu E, Flonta M (2006) Cultured rat primary sensory neurons exposed to hypoxic/hyperglicemic con­ditions exhibit altered Na+ and TRPV1 currents. Europ J Pain 10: S49.
  • Ristoiu V, Shibazaki K, Flonta M, Tominaga M (2009) Identification of critical determinants which potentiate TRPV1 activity under diabetic conditions. J Physiol Sci 59: 376.
  • Rogers M, Tang L, Madge DJ, Stevens EB (2006) The role of sodium channels in neuropathic pain. Semin Cell Dev Biol 17: 571-581.
  • Rush AM, Brau ME, Elliott AA, Elliott JR (1998) Electrophysiological properties of sodium current sub­types in small cells from adult rat dorsal root ganglia. J Physiol 511: 771-789.
  • Semenov DG, Samoilov MO, Lazarewicz JW (2008) Preconditioning reduces hypoxia-evoked alterations in glutamatergic Ca2+ signaling in rat cortex. Acta Neurobiol Exp (Wars) 68: 169-179
  • Scott JN, Clark AW, Zochodne DW (1999) Neurofilament and tubulin gene expression in progressive experimental diabetes: failure of synthesis and export by sensory neu­rons. Brain 122: 2109-2118.
  • Vijayaragavan K, Boutjdir M, Chahine M (2004) Modulation of Nav1.7 and Nav1.8 peripheral nerve sodium channels by protein kinase A and protein kinase C. J Neurophysiol 91: 1556-1569.
  • Wittmack EK, Rush AM, Hudmon A, Waxman SG, Dib-Hajj SD (2005) Voltage-gated sodium channel Nav1.6 is modulated by p38 mitogen-activated protein kinase. J Neurosci 25: 6621-6630.
  • Woolf CJ, Costigan M (1999) Transcriptional and posttrans- lational plasticity and the generation of inflammatory pain. Proc Natl Acad Sci USA 96: 7723-30.
  • Zhang YL, Tavakoli H, Chachisvilis M (2010) Apparent PKA Activity Responds to Intermittent Hypoxia in Bone Cells: A Redox Pathway. Am J Physiol Heart Circ Physiol 299: H225-H235
  • Zhang Z, Apse K, Pang J, Stanton RC (2000) High glucose inhibits glucose-6-phosphate dehydrogenase via cAMP in aortic endothelial cells. J Biol Chem 275: 40042­40047.
  • Zochodne DW, Ho LT, Allison JA (1994) Dorsal root gan­glia microenvironment of female BB Wistar diabetic rats with mild neuropathy. J Neurol Sci 127: 36-42.
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