Abstract：
:Hydrogen sulfide (H(2)S), a gasotransmitter, induces neuronal differentiation characterized by neuritogenesis and functional up-regulation of high voltage-activated Ca(2+) channels, via activation of T-type Ca(2+) channels in NG108-15 cells. We thus analyzed signaling mechanisms for the H(2)S-evoked neuronal differentiation. NaHS, a donor for H(2)S, facilitated T-type Ca(2+) channel-dependent membrane currents, an effect blocked by ascorbic acid that selectively inhibits Ca(v)3.2 among three T-type channel isoforms. NaHS, applied once at a high concentration (13.5 mM) or repetitively at a relatively low concentration (1.5 mM), as well as ionomycin, a Ca(2+) ionophore, evoked neuritogenesis. The neuritogenesis induced by NaHS, but not by ionomycin, was abolished by mibefradil, a T-type Ca(2+) channel blocker. PP2, a Src kinase inhibitor, completely suppressed the neuritogenesis caused by NaHS or ionomycin, while it only partially blocked neuritogenesis caused by dibutyryl cAMP, a differentiation inducer. NaHS, but not dibutyryl cAMP, actually caused phosphorylation of Src, an effect blocked by 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid acetoxymethyl, an intracellular Ca(2+) chelator, mibefradil or ascorbic acid. The up-regulation of high voltage-activated currents in the cells treated with NaHS was also inhibited by PP2. Together, our data reveal that Src kinase participates in the T-type Ca(2+) channel-dependent neuronal differentiation caused by NaHS/H(2)S in NG108-15 cells.
journal_name
J Neurochemjournal_title
Journal of neurochemistryauthors
Tarui T,Fukami K,Nagasawa K,Yoshida S,Sekiguchi F,Kawabata Adoi
10.1111/j.1471-4159.2010.06774.xsubject
Has Abstractpub_date
2010-07-01 00:00:00pages
512-9issue
2eissn
0022-3042issn
1471-4159pii
JNC6774journal_volume
114pub_type
杂志文章abstract：:As a consequence of intracerebral hemorrhage (ICH), blood components enter brain parenchyma causing progressive damage to the surrounding brain. Unless hematoma is cleared, the reservoirs of blood continue to inflict injury to neurovascular structures and blunt the brain repair processes. Microglia/macrophages (MMΦ) r...
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journal_title：Journal of neurochemistry
pub_type： 杂志文章,评审
doi：10.1111/jnc.14256
更新日期：2018-02-01 00:00:00
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doi：10.1046/j.1471-4159.1999.0732321.x
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更新日期：2007-12-01 00:00:00
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pub_type： 杂志文章
doi：10.1111/j.1471-4159.2007.05066.x
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journal_title：Journal of neurochemistry
pub_type： 杂志文章
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journal_title：Journal of neurochemistry
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journal_title：Journal of neurochemistry
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journal_title：Journal of neurochemistry
pub_type： 杂志文章,评审
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journal_title：Journal of neurochemistry
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journal_title：Journal of neurochemistry
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更新日期：1989-01-01 00:00:00
