Abstract:
:A small GTPase, Rac1, is recognized as an important modulator of the inflammatory responses to bacterial lipopolysaccharide (LPS) by affecting the processes of phospholipase C activation. The activation of Rac1 involves the exchange of GDP for GTP and is catalyzed by the guanine nucleotide exchange factors (GEFs). Here, we report on the gastric mucosal GEF, Dock180, activation in response to H. pylori PS, and the hormone, ghrelin. We show that stimulation of gastric mucosal cells with the LPS leads to up-regulation in Dock180 phosphorylation on Tyr and Ser that is accompanied by a massive rise in Rac1-GTP level, while the effect of ghrelin, manifested by a drop in Dock180 phosphorylation on Ser, is associated with a decrease in Rac1-GTP formation. Furthermore, we demonstrate that phosphorylation on Tyr remains under the control of the Src family protein tyrosine kinases (SFK-PTKs), and is accompanied by Dock180 membrane translocation, while phosphorylation of the membrane-localized Dock180 on Ser represents the stimulatory contribution of protein kinase Cδ (PKCδ) to Dock180 activation. Moreover, we reveal that the interaction between Dock180 and PKCδ is dependent on Dock180 Tyr phosphorylation as well as the activity of PKCδ. Thus, our findings point to the involvement of PKCδ in the LPS-induced up-regulation of Dock180 activation, and suggest the modulatory mechanism of ghrelin influence on the gastric mucosal inflammatory responses to H. pylori.
journal_name
Inflammopharmacologyjournal_title
Inflammopharmacologyauthors
Slomiany BL,Slomiany Adoi
10.1007/s10787-015-0235-2subject
Has Abstractpub_date
2015-06-01 00:00:00pages
111-8issue
2-3eissn
0925-4692issn
1568-5608journal_volume
23pub_type
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pub_type: 杂志文章,评审
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更新日期:2008-10-01 00:00:00
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pub_type: 杂志文章
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更新日期:2007-12-01 00:00:00
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pub_type: 杂志文章
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更新日期:2003-01-01 00:00:00
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pub_type: 杂志文章,评审
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更新日期:2018-06-01 00:00:00
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pub_type: 杂志文章,评审
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pub_type: 杂志文章
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更新日期:1998-01-01 00:00:00
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pub_type: 杂志文章,已发布勘误
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更新日期:2019-02-01 00:00:00
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pub_type: 杂志文章,随机对照试验
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pub_type: 杂志文章,评审
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更新日期:2019-02-01 00:00:00
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