Toshihiko Yanagita

Summary

Affiliation: University of Miyazaki
Country: Japan

Publications

  1. doi request reprint Transcriptional up-regulation of cell surface Na V 1.7 sodium channels by insulin-like growth factor-1 via inhibition of glycogen synthase kinase-3β in adrenal chromaffin cells: enhancement of 22Na+ influx, 45Ca2+ influx and catecholamine secretion
    Toshihiko Yanagita
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, 5200 Kihara Kiyotake, Miyazaki 889 1692, Japan
    Neuropharmacology 61:1265-74. 2011
  2. doi request reprint Chronic lithium treatment up-regulates cell surface Na(V)1.7 sodium channels via inhibition of glycogen synthase kinase-3 in adrenal chromaffin cells: enhancement of Na(+) influx, Ca(2+) influx and catecholamine secretion after lithium withdrawal
    Toshihiko Yanagita
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Kiyotake, Miyazaki 889 1692, Japan
    Neuropharmacology 57:311-21. 2009
  3. ncbi request reprint Lithium inhibits function of voltage-dependent sodium channels and catecholamine secretion independent of glycogen synthase kinase-3 in adrenal chromaffin cells
    Toshihiko Yanagita
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki 889 1692, Japan
    Neuropharmacology 53:881-9. 2007
  4. doi request reprint Nav1.7-Ca2+ influx-induced increased phosphorylations of extracellular signal-regulated kinase (ERK) and p38 attenuate tau phosphorylation via glycogen synthase kinase-3beta: priming of Nav1.7 gating by ERK and p38
    Takayuki Nemoto
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki 889 1692, Japan
    Eur J Pharmacol 640:20-8. 2010
  5. ncbi request reprint Lysophosphatidic acid-LPA1 receptor-Rho-Rho kinase-induced up-regulation of Nav1.7 sodium channel mRNA and protein in adrenal chromaffin cells: enhancement of 22Na+ influx, 45Ca2+ influx and catecholamine secretion
    Toyoaki Maruta
    Departments of Pharmacology, and Anesthesiology, Miyazaki Medical College, University of Miyazaki, Miyazaki, Japan
    J Neurochem 105:401-12. 2008
  6. ncbi request reprint Destabilization of Na(v)1.7 sodium channel alpha-subunit mRNA by constitutive phosphorylation of extracellular signal-regulated kinase: negative regulation of steady-state level of cell surface functional sodium channels in adrenal chromaffin cells
    Toshihiko Yanagita
    Department of Pharmacology, Miyazaki Medical College, Kiyotake, Japan
    Mol Pharmacol 63:1125-36. 2003
  7. doi request reprint Nav1.7 sodium channel-induced Ca2+ influx decreases tau phosphorylation via glycogen synthase kinase-3beta in adrenal chromaffin cells
    Tasuku Kanai
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki 889 1692, Japan
    Neurochem Int 54:497-505. 2009
  8. doi request reprint Proteasomal degradation of IRS-2, but not IRS-1 by calcineurin inhibition: attenuation of insulin-like growth factor-I-induced GSK-3beta and ERK pathways in adrenal chromaffin cells
    Shinya Satoh
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki 889 1692, Japan
    Neuropharmacology 55:71-9. 2008
  9. ncbi request reprint Glycogen synthase kinase-3beta: homologous regulation of cell surface insulin receptor level via controlling insulin receptor mRNA stability in adrenal chromaffin cells
    Hiroki Yokoo
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki, Japan
    J Neurochem 103:1883-96. 2007
  10. doi request reprint Regulation of Akt mRNA and protein levels by glycogen synthase kinase-3beta in adrenal chromaffin cells: effects of LiCl and SB216763
    Takayuki Nemoto
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki 889 1692, Japan
    Eur J Pharmacol 586:82-9. 2008

Collaborators

Detail Information

Publications39

  1. doi request reprint Transcriptional up-regulation of cell surface Na V 1.7 sodium channels by insulin-like growth factor-1 via inhibition of glycogen synthase kinase-3β in adrenal chromaffin cells: enhancement of 22Na+ influx, 45Ca2+ influx and catecholamine secretion
    Toshihiko Yanagita
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, 5200 Kihara Kiyotake, Miyazaki 889 1692, Japan
    Neuropharmacology 61:1265-74. 2011
    ..Thus, inhibition of GSK-3β caused by IGF-1 up-regulates cell surface expression of functional Na(+) channels via acceleration of α-subunit gene transcription...
  2. doi request reprint Chronic lithium treatment up-regulates cell surface Na(V)1.7 sodium channels via inhibition of glycogen synthase kinase-3 in adrenal chromaffin cells: enhancement of Na(+) influx, Ca(2+) influx and catecholamine secretion after lithium withdrawal
    Toshihiko Yanagita
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Kiyotake, Miyazaki 889 1692, Japan
    Neuropharmacology 57:311-21. 2009
    ..Thus, GSK-3 inhibition by LiCl up-regulated cell surface Na(V)1.7 via acceleration of alpha-subunit gene transcription, enhancing veratridine-induced Na(+) influx, Ca(2+) influx and catecholamine secretion...
  3. ncbi request reprint Lithium inhibits function of voltage-dependent sodium channels and catecholamine secretion independent of glycogen synthase kinase-3 in adrenal chromaffin cells
    Toshihiko Yanagita
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki 889 1692, Japan
    Neuropharmacology 53:881-9. 2007
    ..These results suggest that lithium selectively inhibits Na(+) influx thorough Na(+) channels and subsequent Ca(2+) influx and catecholamine secretion, independent of GSK-3 inhibition...
  4. doi request reprint Nav1.7-Ca2+ influx-induced increased phosphorylations of extracellular signal-regulated kinase (ERK) and p38 attenuate tau phosphorylation via glycogen synthase kinase-3beta: priming of Nav1.7 gating by ERK and p38
    Takayuki Nemoto
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki 889 1692, Japan
    Eur J Pharmacol 640:20-8. 2010
    ..In veratridine-nontreated cells, basal constitutive activities of ERK1/ERK2 and p38 primed Nav1.7 to increase 22Na+ influx...
  5. ncbi request reprint Lysophosphatidic acid-LPA1 receptor-Rho-Rho kinase-induced up-regulation of Nav1.7 sodium channel mRNA and protein in adrenal chromaffin cells: enhancement of 22Na+ influx, 45Ca2+ influx and catecholamine secretion
    Toyoaki Maruta
    Departments of Pharmacology, and Anesthesiology, Miyazaki Medical College, University of Miyazaki, Miyazaki, Japan
    J Neurochem 105:401-12. 2008
    ..LPA raised Nav1.7 mRNA level by approximately 37%. Thus, LPA-LPA(1) receptor-Rho/Rho kinase pathway up-regulated cell surface Nav1.7 and Nav1.7 mRNA levels, enhancing veratridine-induced Ca2+ influx and catecholamine secretion...
  6. ncbi request reprint Destabilization of Na(v)1.7 sodium channel alpha-subunit mRNA by constitutive phosphorylation of extracellular signal-regulated kinase: negative regulation of steady-state level of cell surface functional sodium channels in adrenal chromaffin cells
    Toshihiko Yanagita
    Department of Pharmacology, Miyazaki Medical College, Kiyotake, Japan
    Mol Pharmacol 63:1125-36. 2003
    ....
  7. doi request reprint Nav1.7 sodium channel-induced Ca2+ influx decreases tau phosphorylation via glycogen synthase kinase-3beta in adrenal chromaffin cells
    Tasuku Kanai
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki 889 1692, Japan
    Neurochem Int 54:497-505. 2009
    ....
  8. doi request reprint Proteasomal degradation of IRS-2, but not IRS-1 by calcineurin inhibition: attenuation of insulin-like growth factor-I-induced GSK-3beta and ERK pathways in adrenal chromaffin cells
    Shinya Satoh
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki 889 1692, Japan
    Neuropharmacology 55:71-9. 2008
    ..Thus, calcineurin inhibition decreased IRS-2 level via proteasomal IRS-2 degradation, attenuating IGF-I-induced GSK-3beta and ERK pathways...
  9. ncbi request reprint Glycogen synthase kinase-3beta: homologous regulation of cell surface insulin receptor level via controlling insulin receptor mRNA stability in adrenal chromaffin cells
    Hiroki Yokoo
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki, Japan
    J Neurochem 103:1883-96. 2007
    ..Thus, GSK-3beta regulates IR level via controlling IR mRNA stability...
  10. doi request reprint Regulation of Akt mRNA and protein levels by glycogen synthase kinase-3beta in adrenal chromaffin cells: effects of LiCl and SB216763
    Takayuki Nemoto
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki 889 1692, Japan
    Eur J Pharmacol 586:82-9. 2008
    ....
  11. doi request reprint Distinct regulation of insulin receptor substrate-1 and -2 by 90-kDa heat-shock protein in adrenal chromaffin cells
    Norie Yoshikawa
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki, Japan
    Neurochem Int 56:42-50. 2010
    ..Hsp90 inhibitors oppositely altered insulin receptor substrate-1 and -2 levels via proteasomal degradation and gene transcription...
  12. ncbi request reprint Constitutive activity of glycogen synthase kinase-3beta: positive regulation of steady-state levels of insulin receptor substrates-1 and -2 in adrenal chromaffin cells
    Takayuki Nemoto
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki, Japan
    Brain Res 1110:1-12. 2006
    ..These results suggest that constitutive activity of GSK-3beta in quiescent cells positively maintains steady-state levels of IRS-1 and IRS-2 via regulating proteasomal degradation and/or synthesis of IRS-1 and IRS-2 proteins...
  13. doi request reprint Homologous posttranscriptional regulation of insulin-like growth factor-I receptor level via glycogen synthase kinase-3beta and mammalian target of rapamycin in adrenal chromaffin cells: effect on tau phosphorylation
    Takayuki Nemoto
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki, Japan
    Neuropharmacology 58:1097-108. 2010
    ..Thus, IGF-I down-regulated functional IGF-I receptor via GSK-3beta inhibition and mTOR activation; constitutive activity of GSK-3beta maintained IGF-I receptor level in nonstimulated cells...
  14. doi request reprint Endothelin-1-induced down-regulation of NaV1.7 expression in adrenal chromaffin cells: attenuation of catecholamine secretion and tau dephosphorylation
    Takayuki Nemoto
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki, Japan
    FEBS Lett 587:898-905. 2013
    ..These findings suggest that the endothelin-1-induced down-regulation of NaV1.7 diminishes NaV1.7-related catecholamine secretion and dephosphorylation of tau...
  15. ncbi request reprint Enhancement of insulin-induced PI3K/Akt/GSK-3beta and ERK signaling by neuronal nicotinic receptor/PKC-alpha/ERK pathway: up-regulation of IRS-1/-2 mRNA and protein in adrenal chromaffin cells
    Takashi Sugano
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki, Japan
    J Neurochem 98:20-33. 2006
    ..Thus, stimulation of nAChRs up-regulated expression of IRS-1/IRS-2 via Ca(2+)-dependent sequential activation of cPKC-alpha and ERK, and enhanced insulin-induced PI3K/Akt/GSK-3beta and ERK signaling pathways...
  16. ncbi request reprint Differential effects of bupivacaine enantiomers, ropivacaine and lidocaine on up-regulation of cell surface voltage-dependent sodium channels in adrenal chromaffin cells
    Seiji Shiraishi
    Department of Pharmacology, Miyazaki Medical College, Miyazaki 889 1692, Kiyotake, Japan
    Brain Res 966:175-84. 2003
    ....
  17. doi request reprint Dexmedetomidine and clonidine inhibit the function of Na(v)1.7 independent of α(2)-adrenoceptor in adrenal chromaffin cells
    Toyoaki Maruta
    Department of Anesthesiology, Miyazaki Medical College, University of Miyazaki, Miyazaki 889 1692, Japan
    J Anesth 25:549-57. 2011
    ..In the present study, we examined whether dexmedetomidine and clonidine could inhibit the function of tetrodotoxin-sensitive Na(+) channels, which play important roles in the generation of pain...
  18. ncbi request reprint Distinct effects of ketone bodies on down-regulation of cell surface insulin receptor and insulin receptor substrate-1 phosphorylation in adrenal chromaffin cells
    Hiroki Yokoo
    Department of Pharmacology, Miyazaki Medical College, Miyazaki, Japan
    J Pharmacol Exp Ther 304:994-1002. 2003
    ..These results suggest that chronic treatment with acetoacetate selectively down-regulated the density of cell surface functional IR via lowering IR mRNA levels and IR synthesis, thereby retarding insulin-induced activation of IRS-1...
  19. ncbi request reprint Regulation of cell surface expression of voltage-dependent Nav1.7 sodium channels: mRNA stability and posttranscriptional control in adrenal chromaffin cells
    Akihiko Wada
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki 889 1692, Japan
    Front Biosci 9:1954-66. 2004
    ..Neuroprotective, antiepiletic, antipsychotic, and local anesthetic drugs up-regulated Na+ channels via transcriptional/translational events...
  20. doi request reprint New insights concerning insulin synthesis and its secretion in rat hippocampus and cerebral cortex: amyloid-β1-42-induced reduction of proinsulin level via glycogen synthase kinase-3β
    Takayuki Nemoto
    Department of Pharmacology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan Electronic address
    Cell Signal 26:253-9. 2014
    ....
  21. doi request reprint Up-regulation of NaV1.7 sodium channels expression by tumor necrosis factor-α in cultured bovine adrenal chromaffin cells and rat dorsal root ganglion neurons
    Ryuji Tamura
    From the Departments of Anesthesiology and Intensive Care and Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki, Japan Department of Anesthesiology, Division of Basic Research, Washington University School of Medicine, St Louis, Missouri Department of Sports Health and Welfare, Faculty of Social Welfare, Kyusyu University of Health and Welfare, Miyazaki, Japan
    Anesth Analg 118:318-24. 2014
    ..However, it remains unknown whether TNF-α affects the function and expression of the TTX-S NaV1.7 Na channel, which plays crucial roles in pain generation...
  22. ncbi request reprint Serum deprivation-induced upregulation of voltage-dependent sodium channels in adrenal chromaffin cells: selective involvement of extracellular signal-regulated kinase pathway
    Toshihiko Yanagita
    Department of Pharmacology, Miyazaki Medical College, Miyazaki 889 1692, Japan
    Ann N Y Acad Sci 971:153-5. 2002
    ....
  23. ncbi request reprint Regulation of voltage-dependent sodium channel expression in adrenal chromaffin cells: involvement of multiple calcium signaling pathways
    Hideyuki Kobayashi
    Department of Pharmacology, Miyazaki Medical College, Miyazaki 889 1692, Japan
    Ann N Y Acad Sci 971:127-34. 2002
    ....
  24. ncbi request reprint Drug development targeting the glycogen synthase kinase-3beta (GSK-3beta)-mediated signal transduction pathway: the role of GSK-3beta in the maintenance of steady-state levels of insulin receptor signaling molecules and Na(v)1.7 sodium channel in adrenal
    Takayuki Nemoto
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Japan
    J Pharmacol Sci 109:157-61. 2009
    ..g., lithium) up-regulated the voltage-dependent Na(v)1.7 sodium channel...
  25. doi request reprint Insulin-induced neurite-like process outgrowth: acceleration of tau protein synthesis via a phosphoinositide 3-kinase~mammalian target of rapamycin pathway
    Takayuki Nemoto
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki, Japan
    Neurochem Int 59:880-8. 2011
    ..Taken together, these results suggest that insulin-induced activation of PI3K∼mTOR pathway up-regulated tau protein via acceleration of protein synthesis, on which insulin promoted neurite-like process outgrowth...
  26. ncbi request reprint Down-regulation of cell surface insulin receptor and insulin receptor substrate-1 phosphorylation by inhibitor of 90-kDa heat-shock protein family: endoplasmic reticulum retention of monomeric insulin receptor precursor with calnexin in adrenal chromaffin
    Tomokazu Saitoh
    Department of Pharmacology, Miyazaki Medical College, Miyazaki, Japan
    Mol Pharmacol 62:847-55. 2002
    ....
  27. doi request reprint Involvement of the orexin system in adrenal sympathetic regulation
    Takayuki Nemoto
    Department of Pharmacology, Graduate School of Medicine, University of Miyazaki, Miyazaki, Japan
    Pharmacology 91:250-8. 2013
    ..Our results indicate involvement of the orexin system in the sympathetic regulation of the adrenal medulla...
  28. pmc Brain RVD-haemopressin, a haemoglobin-derived peptide, inhibits bombesin-induced central activation of adrenomedullary outflow in the rat
    Kenjiro Tanaka
    Department of Pharmacology, Kochi University School of Medicine, Nankoku, Japan
    Br J Pharmacol 171:202-13. 2014
    ..c.v. bombesin in the rat. Here, we investigated the effects of two haemoglobin-derived peptides on this bombesin-induced response..
  29. ncbi request reprint New twist on neuronal insulin receptor signaling in health, disease, and therapeutics
    Akihiko Wada
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki 889 1692, Japan
    J Pharmacol Sci 99:128-43. 2005
    ..More importantly, much remains unknown about the quality control mechanisms ensuring correct conformational maturation of the insulin receptor, and the cellular mechanisms regulating density of cell surface functional insulin receptors...
  30. doi request reprint Angiotensin II acting on brain AT1 receptors induces adrenaline secretion and pressor responses in the rat
    Kumiko Nakamura
    Department of Pharmacology, Kochi Medical School, Kochi University, Nankoku 783 8505, Japan
    Sci Rep 4:7248. 2014
    ..We propose that the central angiotensinergic system can activate central adrenomedullary outflow and modulate blood pressure. ..
  31. ncbi request reprint Induction of aquaporin 1 by dexamethasone in lipid rafts in immortalized brain microvascular endothelial cells
    Hideyuki Kobayashi
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki 889 1692, Japan
    Brain Res 1123:12-9. 2006
    ..Since glucocorticoid therapy has well known beneficial effects in the treatment of brain edema, the induction of AQP1 by dexamethasone raises a possibility that AQP1 plays a role in ameliorating brain edema...
  32. ncbi request reprint Pathophysiological function of adrenomedullin and proadrenomedullin N-terminal peptides in adrenal chromaffin cells
    Hideyuki Kobayashi
    Department of Pharmacology, Miyazaki Medical College, 5200 Kihara, Kiyotake, Miyazaki 889 1692, Japan
    Hypertens Res 26:S71-8. 2003
    ..PAMP20 and PAMP12 are endogenous peptides that modulate chromaffin cell function in an autocrine manner, whereas AM may mainly regulate vascular cell function in a paracrine manner...
  33. ncbi request reprint Beyond vasodilation: the antioxidant effect of adrenomedullin in Dahl salt-sensitive rat aorta
    Yuan Ning Cao
    First Department of Internal Medicine, Miyazaki Medical College, University of Miyazaki, Japan
    Biochem Biophys Res Commun 332:866-72. 2005
    ..AM possesses significant antioxidant properties that improve endothelial function...
  34. ncbi request reprint Molecular mechanisms and drug development in aquaporin water channel diseases: aquaporins in the brain
    Hideyuki Kobayashi
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Kiyotake, Japan
    J Pharmacol Sci 96:264-70. 2004
    ..Changes in AQP expression may be correlated with edema formation of the brain. In this review, we describe the physiological function of AQPs and the regulatory mechanism of their expression in the brain...
  35. ncbi request reprint Lithium: potential therapeutics against acute brain injuries and chronic neurodegenerative diseases
    Akihiko Wada
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki, Japan
    J Pharmacol Sci 99:307-21. 2005
    ..g., excitotoxicity, p53, Bax, caspase, cytochrome c release, beta-amyloid peptide production, and tau hyperphosphorylation), thus preventing or even reversing neuronal cell death and neurogenesis retardation...
  36. ncbi request reprint [Expression of insulin receptor and its signaling molecules: regulatory mechanisms in neuronal cells]
    Hiroki Yokoo
    Nihon Yakurigaku Zasshi 125:141-6. 2005
  37. ncbi request reprint Expression of adrenomedullin and its receptor by chondrocyte phenotype cells
    Etsuo Chosa
    Department of Orthopaedic Surgery, Miyazaki Medical College, 5200 Kihara, Kiyotake, Miyazaki 889 1692, Japan
    Biochem Biophys Res Commun 303:379-86. 2003
    ....
  38. ncbi request reprint [Regulation of brain microvessel function]
    Hideyuki Kobayashi
    Department of Pharmacology, Miyazaki Medical College, 5200 Kihara, Kiyotake, Miyazaki 889 1692, Japan
    Nihon Yakurigaku Zasshi 119:281-6, 309. 2002
    ....
  39. ncbi request reprint Differential effects of short and prolonged exposure to carvedilol on voltage-dependent Na(+) channels in cultured bovine adrenal medullary cells
    Koji Kajiwara
    Second Department of Internal Medicine, School of Medicine, 1 1 Iseigaoka, Yahatanishiku, Kitakyushu 807 8555, Japan
    J Pharmacol Exp Ther 302:212-8. 2002
    ..This may add new pharmacological effects of carvedilol to our understanding in the treatment of heart failure and hypertension...