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Faculty of Dentistry
Document Details
Document Type
:
Article In Journal
Document Title
:
CD38 cleavage in fMLP- and IL-8-induced chemotaxis is dependent on p38 MAP kinase but independent of p44/42 MAP kinase
CD38 cleavage in fMLP- and IL-8-induced chemotaxis is dependent on p38 MAP kinase but independent of p44/42 MAP kinase
Document Language
:
English
Abstract
:
In this study, we examined the mechanism by which CD38 cleavage is regulated through the mitogen-activated protein (MAP) kinases after stimulation by tMLP and interleukin-8 (IL-8) in neutrophils. Both tMLP and IL-8 increased chemotaxis and decreased CD38 protein in neutrophils, but did not change CD38 mRNA levels. Both tMLP and IL-8 increased CD38 in supematants, which was inhibitable with PMSF. tMLP stimulation resulted in phosphorylation of p38 MAP kinase and p42/44 MAP kinase (ERK.). SB20358, a p38 MAP kinase inhibitor, down-regulated neutrophil chemotaxis. Conversely, PD98059, an ERK inhibitor, did not influence chemotaxis to either agonist. The addition of SB20358 blocked the decrease of CD38 on neutrophils and the increase in supematants induced by tMLP or IL-8, whereas PD98059 did not. These findings suggest that CD38-mediated chemotaxis to tMLP or IL-8 is characterized by proteolytic cleavage ofCD38 and signaling through p38 MAP kinase. Activation of the protease for cleavage appears to be a postreceptor event that is dependent on p38 MAP kinase signaling.
ISSN
:
0
Journal Name
:
science direct
Volume
:
17
Issue Number
:
1
Publishing Year
:
2005 AH
2005 AD
Article Type
:
Article
Added Date
:
Thursday, December 6, 2007
Researchers
Researcher Name (Arabic)
Researcher Name (English)
Researcher Type
Dr Grade
Email
خالد زواوي
zwawi, Khalid
Investigator
Doctorate
kzawawi@kau.edu.sa
Files
File Name
Type
Description
CD38cleavage in fMLP.pdf
pdf
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