Granulocyte chemotaxis and disease expression are differentially regulated by GRK subtype in an acute inflammatory arthritis model (K/BxN)

OBJECTIVE: Chemokine receptors are G-protein coupled receptors (GPCRs) phosphorylated by G-protein receptor kinases (GRKs) after ligand-mediated activation. We hypothesized that GRK subtypes differentially regulate granulocyte chemotaxis and clinical disease expression in the K/BxN model

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 129(2008), 1 vom: 18. Okt., Seite 115-22
1. Verfasser: Tarrant, Teresa K (VerfasserIn)
Weitere Verfasser: Rampersad, Rishi R, Esserman, Denise, Rothlein, Lisa R, Liu, Peng, Premont, Richard T, Lefkowitz, Robert J, Lee, David M, Patel, Dhavalkumar D
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2008
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Interleukin-6 Leukotriene B4 1HGW4DR56D Complement C5a 80295-54-1 GRK2 protein, mouse EC 2.7.11.15 mehr... G-Protein-Coupled Receptor Kinase 2 EC 2.7.11.16 G-Protein-Coupled Receptor Kinases G-protein-coupled receptor kinase 6
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100 1 |a Tarrant, Teresa K  |e verfasserin  |4 aut 
245 1 0 |a Granulocyte chemotaxis and disease expression are differentially regulated by GRK subtype in an acute inflammatory arthritis model (K/BxN) 
264 1 |c 2008 
336 |a Text  |b txt  |2 rdacontent 
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500 |a Date Revised 20.10.2021 
500 |a published: Print-Electronic 
500 |a Citation Status MEDLINE 
520 |a OBJECTIVE: Chemokine receptors are G-protein coupled receptors (GPCRs) phosphorylated by G-protein receptor kinases (GRKs) after ligand-mediated activation. We hypothesized that GRK subtypes differentially regulate granulocyte chemotaxis and clinical disease expression in the K/BxN model 
520 |a METHODS: Clinical, histologic, and cytokine responses in GRK6-/-, GRK5-/-, GRK2+/-, and wildtype mice were evaluated using K/BxN serum transfer. Granulocyte chemotaxis was analyzed by transendothelial migration assays 
520 |a RESULTS: Both GRK6-/- and GRK2+/- mice had increased arthritis disease severity (p<0.001); whereas GRK5-/- was not different from controls. Acute weight loss was enhanced in GRK6-/- and GRK2+/- mice (p<0.001, days 3-10). However, GRK6-/- mice uniquely had more weight loss (>10%), elevated serum IL-6, and enhanced migration toward LTB4 and C5a in vitro 
520 |a CONCLUSIONS: GRK6 and -2, but not GRK5, are involved in the pathogenesis of acute arthritis in the K/BxN model. In particular, GRK6 may dampen inflammatory responses by regulating granulocyte trafficking toward chemoattractants 
650 4 |a Journal Article 
650 4 |a Research Support, N.I.H., Extramural 
650 4 |a Research Support, Non-U.S. Gov't 
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700 1 |a Rampersad, Rishi R  |e verfasserin  |4 aut 
700 1 |a Esserman, Denise  |e verfasserin  |4 aut 
700 1 |a Rothlein, Lisa R  |e verfasserin  |4 aut 
700 1 |a Liu, Peng  |e verfasserin  |4 aut 
700 1 |a Premont, Richard T  |e verfasserin  |4 aut 
700 1 |a Lefkowitz, Robert J  |e verfasserin  |4 aut 
700 1 |a Lee, David M  |e verfasserin  |4 aut 
700 1 |a Patel, Dhavalkumar D  |e verfasserin  |4 aut 
773 0 8 |i Enthalten in  |t Clinical immunology (Orlando, Fla.)  |d 1999  |g 129(2008), 1 vom: 18. Okt., Seite 115-22  |w (DE-627)NLM098196855  |x 1521-7035  |7 nnns 
773 1 8 |g volume:129  |g year:2008  |g number:1  |g day:18  |g month:10  |g pages:115-22 
856 4 0 |u http://dx.doi.org/10.1016/j.clim.2008.06.008  |3 Volltext 
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