J Neuroimmunol 2003 Apr;137(1-2):79-86
Vroon A, Lombardi MS, Kavelaars A, Heijnen CJ.
Laboratory for Psychoneuroimmunology, Department of Immunology, University Medical Center Utrecht, Room KC03.068.0, Lundlaan 6, 3584 EA, Utrecht, The Netherlands
G-protein-coupled receptors (GPCR) play an important role in inflammation.
Their responsiveness is regulated by G-protein-coupled receptor kinases (GRKs) and beta-arrestins.
We show here that induction of experimental autoimmune encephalomyelitis (EAE) by myelin oligodendrocyte glycoprotein (MOG) resulted in a profound decrease in GRK2 and GRK6 protein in splenocytes during all phases of disease.
GRK2 mRNA was also lower during EAE, although the decrease in mRNA was less pronounced than the decrease in GRK2 protein.
Interestingly, beta-arrestin protein expression was significantly increased.
Downregulation of GRK2 was restricted to the spleen and mesenteric lymph nodes and was not observed in peritoneal macrophages.
Furthermore, EAE did not induce alterations in GRK2 expression in heart, liver and pituitary.