Document Detail


Cross-desensitization among CXCR1, CXCR2, and CCR5: role of protein kinase C-epsilon.
MedLine Citation:
PMID:  15905535     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The IL-8 (or CXCL8) chemokine receptors, CXCR1 and CXCR2, activate protein kinase C (PKC) to mediate leukocyte functions. To investigate the roles of different PKC isoforms in CXCL8 receptor activation and regulation, human mononuclear phagocytes were treated with CXCL8 or CXCL1 (melanoma growth-stimulating activity), which is specific for CXCR2. Plasma membrane association was used as a measure of PKC activation. Both receptors induced time-dependent association of PKCalpha, -beta1, and -beta2 to the membrane, but only CXCR1 activated PKCepsilon. CXCL8 also failed to activate PKCepsilon in RBL-2H3 cells stably expressing CXCR2. DeltaCXCR2, a cytoplasmic tail deletion mutant of CXCR2 that is resistant to internalization, activated PKCepsilon as well as CXCR1. Expression of the PKCepsilon inhibitor peptide epsilonV1 in RBL-2H3 cells blocked PKCepsilon translocation and inhibited receptor-mediated exocytosis, but not phosphoinositide hydrolysis or peak intracellular Ca(2+) mobilization. epsilonV1 also inhibited CXCR1-, CCR5-, and DeltaCXCR2-mediated cross-regulatory signals for GTPase activity, Ca(2+) mobilization, and internalization. Peritoneal macrophages from PKCepsilon-deficient mice (PKCepsilon(-/-)) also showed decreased CCR5-mediated cross-desensitization of G protein activation and Ca(2+) mobilization. Taken together, the results indicate that CXCR1 and CCR5 activate PKCepsilon to mediate cross-inhibitory signals. Inhibition or deletion of PKCepsilon decreases receptor-induced exocytosis and cross-regulatory signals, but not phosphoinositide hydrolysis or peak intracellular Ca(2+) mobilization, suggesting that cross-regulation is a Ca(2+)-independent process. Because DeltaCXCR2, but not CXCR2, activates PKCepsilon and cross-desensitizes CCR5, the data further suggest that signal duration leading to activation of novel PKC may modulate receptor-mediated cross-inhibitory signals.
Authors:
Mohd W Nasser; Robin J Marjoram; Stephan L Brown; Ricardo M Richardson
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  174     ISSN:  0022-1767     ISO Abbreviation:  J. Immunol.     Publication Date:  2005 Jun 
Date Detail:
Created Date:  2005-05-20     Completed Date:  2005-08-08     Revised Date:  2012-06-25    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  6927-33     Citation Subset:  AIM; IM    
Affiliation:
Julius L. Chambers Biomedical/Biotechnology Research Institute, North Carolina Central University, Durham, 27707, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Calcium Signaling / genetics,  immunology
Cell Line, Tumor
Endocytosis / genetics,  immunology
Enzyme Activation / genetics,  immunology
Genetic Vectors
Humans
Isoenzymes / deficiency,  metabolism,  physiology
Macrophages, Peritoneal / enzymology,  immunology,  metabolism
Mice
Mice, Knockout
Protein Kinase C / deficiency,  genetics,  metabolism,  physiology*
Protein Kinase C-epsilon
Rats
Receptors, CCR5 / genetics,  metabolism,  physiology*
Receptors, Interleukin-8A / metabolism,  physiology*
Receptors, Interleukin-8B / metabolism,  physiology*
Transfection
Grant Support
ID/Acronym/Agency:
AI38910/AI/NIAID NIH HHS; CA92077/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Isoenzymes; 0/Receptors, CCR5; 0/Receptors, Interleukin-8A; 0/Receptors, Interleukin-8B; EC 2.7.1.-/Prkce protein, mouse; EC 2.7.1.-/Prkce protein, rat; EC 2.7.11.13/PRKCE protein, human; EC 2.7.11.13/Protein Kinase C; EC 2.7.11.13/Protein Kinase C-epsilon

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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