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162 results on '"Tazaki, Masakazu"'

8. Ca2+ Extrusion via Na+-Ca2+ Exchangers in Rat Odontoblasts

Author

Tsumura, Maki, Okumura, Reijiro, Tatsuyama, Shoko, Ichikawa, Hideki, Muramatsu, Takashi, Matsuda, Toshio, Baba, Akemichi, Suzuki, Keiko, Kajiya, Hiroshi, Sahara, Yoshinori, Tokuda, Masayuki, Momose, Yasunori, Tazaki, Masakazu, Shimono, Masaki, and Shibukawa, Yoshiyuki

Published
2010
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11. Intracellular Ca2+ mobilization pathway via bradykinin B1 receptor activation in rat trigeminal ganglion neurons

Author

Terashima, Reiko, Kimura, Maki, Higashikawa, Asuka, Kojima, Yuki, Ichinohe, Tatsuya, Tazaki, Masakazu, and Shibukawa, Yoshiyuki

Subjects
Neurons, Bradykinin, G proteins, Cyclic adenylic acid, Ganglion, Psychology and mental health
Abstract

Bradykinin (BK) and its receptors, B.sub.1 and B.sub.2, in trigeminal ganglion (TG) neurons are involved in the regulation of pain. Recent studies have revealed that B.sub.1 receptors are expressed in neonatal rat TG neurons; however, the intracellular signaling pathway following B.sub.1 receptor activation remains to be elucidated. To investigate the mechanism by which B.sub.1 receptor activation leads to intracellular Ca.sup.2+ mobilization, we measured the intracellular free Ca.sup.2+ concentration ([Ca.sup.2+].sub.i) in primary-cultured TG neurons. The application of Lys-[Des-Arg.sup.9]BK (B.sub.1 receptor agonist) increased the [Ca.sup.2+].sub.i in these TG neurons even in the absence of extracellular Ca.sup.2+. Pretreatment with inhibitors of ryanodine receptors or sarco/endoplasmic reticulum Ca.sup.2+-ATPase suppressed the increase in Lys-[Des-Arg.sup.9]BK-induced [Ca.sup.2+].sub.i. The Lys-[Des-Arg.sup.9]BK-induced [Ca.sup.2+].sub.i increase was unaffected by phospholipase-C inhibitor. B.sub.1 receptor activation-induced [Ca.sup.2+].sub.i increase was suppressed by phosphodiesterase inhibitor and enhanced by adenylyl cyclase inhibitor. These results suggest that B.sub.1 receptor activation suppresses intracellular cAMP production via adenylyl cyclase inhibition and mobilizes intracellular Ca.sup.2+ via ryanodine receptors that access intracellular Ca.sup.2+ stores. Keywords: Adenylyl cyclase, Ca.sup.2+ mobilization, Cyclic AMP, G protein, Ryanodine receptors, Trigeminal ganglion neuron, Author(s): Reiko Terashima[sup.1,2], Maki Kimura[sup.2], Asuka Higashikawa[sup.2], Yuki Kojima[sup.2], Tatsuya Ichinohe[sup.1], Masakazu Tazaki[sup.2] and Yoshiyuki Shibukawa[sup.2] Introduction Bradykinin (BK) and related peptides play important roles in the modulation of physiological [...]

Published
2018
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23. Intracellular Ca2+ mobilization pathway via bradykinin B1 receptor activation in rat trigeminal ganglion neurons.

Author

Terashima, Reiko, Kimura, Maki, Higashikawa, Asuka, Kojima, Yuki, Ichinohe, Tatsuya, Tazaki, Masakazu, and Shibukawa, Yoshiyuki

Abstract

Bradykinin (BK) and its receptors, B1 and B2, in trigeminal ganglion (TG) neurons are involved in the regulation of pain. Recent studies have revealed that B1 receptors are expressed in neonatal rat TG neurons; however, the intracellular signaling pathway following B1 receptor activation remains to be elucidated. To investigate the mechanism by which B1 receptor activation leads to intracellular Ca2+ mobilization, we measured the intracellular free Ca2+ concentration ([Ca2+]i) in primary-cultured TG neurons. The application of Lys-[Des-Arg9]BK (B1 receptor agonist) increased the [Ca2+]i in these TG neurons even in the absence of extracellular Ca2+. Pretreatment with inhibitors of ryanodine receptors or sarco/endoplasmic reticulum Ca2+-ATPase suppressed the increase in Lys-[Des-Arg9]BK-induced [Ca2+]i. The Lys-[Des-Arg9]BK-induced [Ca2+]i increase was unaffected by phospholipase-C inhibitor. B1 receptor activation-induced [Ca2+]i increase was suppressed by phosphodiesterase inhibitor and enhanced by adenylyl cyclase inhibitor. These results suggest that B1 receptor activation suppresses intracellular cAMP production via adenylyl cyclase inhibition and mobilizes intracellular Ca2+ via ryanodine receptors that access intracellular Ca2+ stores. [ABSTRACT FROM AUTHOR]

Published
2019
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26. High pH-Sensitive Store-Operated Ca2+ Entry Mediated by Ca2+ Release-Activated Ca2+ Channels in Rat Odontoblasts.

Author

Kimura, Maki, Nishi, Koichi, Higashikawa, Asuka, Ohyama, Sadao, Sakurai, Kaoru, Tazaki, Masakazu, and Shibukawa, Yoshiyuki

Subjects
ODONTOBLASTS, INTRACELLULAR calcium, LABORATORY rats, THAPSIGARGIN, ENDOPLASMIC reticulum, LANTHANUM, DENTINOGENESIS
Abstract

Odontoblasts play a crucial role in dentin formation and sensory transduction following the application of stimuli to the dentin surface. Various exogenous and endogenous stimuli elicit an increase in the intracellular free calcium concentration ([Ca2+]i) in odontoblasts, which is mediated by Ca2+ release from intracellular Ca2+ stores and/or Ca2+ influx from the extracellular medium. In a previous study, we demonstrated that the depletion of Ca2+ stores in odontoblasts activated store-operated Ca2+ entry (SOCE), a Ca2+ influx pathway. However, the precise biophysical and pharmacological properties of SOCE in odontoblasts have remained unclear. In the present study, we examined the functional expression and pharmacological properties of Ca2+ release-activated Ca2+ (CRAC) channels that mediate SOCE and evaluated the alkali sensitivity of SOCE in rat odontoblasts. In the absence of extracellular Ca2+, treatment with thapsigargin (TG), a sarco/endoplasmic reticulum Ca2+-ATPase inhibitor, induced an increase in [Ca2+]i. After [Ca2+]i returned to near-resting levels, the subsequent application of 2.5 mM extracellular Ca2+ resulted in an increase in [Ca2+]i which is a typical of SOCE activation. Additionally, application of 2-methylthioadenosine diphosphate trisodium salt (2-MeSADP), a P2Y1,12,13 receptor agonist, or carbachol (CCh), a muscarinic cholinergic receptor agonist, in the absence of extracellular Ca2+, induced a transient increase in [Ca2+]i. The subsequent addition of extracellular Ca2+ resulted in significantly higher [Ca2+]i in 2-MeSADP- or CCh-treated odontoblasts than in untreated cells. SOCE, that is activated by addition of extracellular Ca2+ in the TG pretreated odontoblasts was then suppressed by Synta66, BTP2, or lanthanum, which are CRAC channel inhibitors. Treatment with an alkaline solution enhanced SOCE, while treatment with HC030031, a TRPA1 channel antagonist, inhibited it. The amplitude of SOCE at pH 9 in the presence of HC030031 was higher than that at pH 7.4 in the absence of HC030031. These findings indicate that CRAC channel-mediated alkali-sensitive SOCE occurs in odontoblasts. SOCE is mediated by P2Y and muscarinic-cholinergic receptors, which are activated by endogenous ligands in odontoblasts. [ABSTRACT FROM AUTHOR]

Published
2018
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27. Intracellular Ca2+mobilization pathway via bradykinin B1receptor activation in rat trigeminal ganglion neurons

Author

Terashima, Reiko, Kimura, Maki, Higashikawa, Asuka, Kojima, Yuki, Ichinohe, Tatsuya, Tazaki, Masakazu, and Shibukawa, Yoshiyuki

Abstract

Bradykinin (BK) and its receptors, B1and B2, in trigeminal ganglion (TG) neurons are involved in the regulation of pain. Recent studies have revealed that B1receptors are expressed in neonatal rat TG neurons; however, the intracellular signaling pathway following B1receptor activation remains to be elucidated. To investigate the mechanism by which B1receptor activation leads to intracellular Ca2+mobilization, we measured the intracellular free Ca2+concentration ([Ca2+]i) in primary-cultured TG neurons. The application of Lys-[Des-Arg9]BK (B1receptor agonist) increased the [Ca2+]iin these TG neurons even in the absence of extracellular Ca2+. Pretreatment with inhibitors of ryanodine receptors or sarco/endoplasmic reticulum Ca2+-ATPase suppressed the increase in Lys-[Des-Arg9]BK-induced [Ca2+]i. The Lys-[Des-Arg9]BK-induced [Ca2+]iincrease was unaffected by phospholipase-C inhibitor. B1receptor activation-induced [Ca2+]iincrease was suppressed by phosphodiesterase inhibitor and enhanced by adenylyl cyclase inhibitor. These results suggest that B1receptor activation suppresses intracellular cAMP production via adenylyl cyclase inhibition and mobilizes intracellular Ca2+via ryanodine receptors that access intracellular Ca2+stores.

Published
2019
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31. Transient Receptor Potential Cation Channel Subfamily Vanilloid Member 3 is not Involved in Plasma Membrane Stretch-induced Intracellular Calcium Signaling in Merkel Cells

Author

Higashikawa, Asuka, primary, Kojima, Yuki, additional, Sato, Masaki, additional, Kimura, Maki, additional, Ogura, Kazuhiro, additional, Mochizuki, Hiroyuki, additional, Sase, Toshiyuki, additional, Shinya, Akinori, additional, Kobune, Kunio, additional, Furuya, Tadashi, additional, Sato, Toru, additional, Shibukawa, Yoshiyuki, additional, and Tazaki, Masakazu, additional

Published
2015
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32. Depolarization-induced Intracellular Free Calcium Concentration Increases Show No Desensitizing Effect in Rat Odontoblasts

Author

Kojima, Yuki, primary, Higashikawa, Asuka, additional, Kimura, Maki, additional, Sato, Masaki, additional, Mochizuki, Hiroyuki, additional, Ogura, Kazuhiro, additional, Sase, Toshiyuki, additional, Shinya, Akinori, additional, Kobune, Kunio, additional, Furuya, Tadashi, additional, Sato, Toru, additional, Shibukawa, Yoshiyuki, additional, and Tazaki, Masakazu, additional

Published
2015
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33. Odontoblasts as sensory receptors: transient receptor potential channels, pannexin-1, and ionotropic ATP receptors mediate intercellular odontoblast-neuron signal transduction

Author

Shibukawa, Yoshiyuki, primary, Sato, Masaki, additional, Kimura, Maki, additional, Sobhan, Ubaidus, additional, Shimada, Miyuki, additional, Nishiyama, Akihiro, additional, Kawaguchi, Aya, additional, Soya, Manabu, additional, Kuroda, Hidetaka, additional, Katakura, Akira, additional, Ichinohe, Tatsuya, additional, and Tazaki, Masakazu, additional

Published
2014
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