Changes in the G-protein-coupled receptor desensitization machinery during relapsing–progressive experimental allergic encephalomyelitis

Autor: Anne Vroon, Annemieke Kavelaars, Maria Stella Lombardi, Cobi Jacoba Johanna Heijnen
Rok vydání: 2003
Předmět:
medicine.medical_specialty
Encephalomyelitis
Autoimmune
Experimental
Arrestins
Encephalomyelitis
Immunology
Receptors
Cell Surface
Protein Serine-Threonine Kinases
Myelin oligodendrocyte glycoprotein
Downregulation and upregulation
GTP-Binding Proteins
Internal medicine
medicine
Animals
Immunology and Allergy
Mesenteric lymph nodes
RNA
Messenger
Receptor
beta-Arrestins
G protein-coupled receptor
G protein-coupled receptor kinase
biology
Chemistry
Experimental autoimmune encephalomyelitis
G-Protein-Coupled Receptor Kinases
medicine.disease
Cyclic AMP-Dependent Protein Kinases
Rats
Myelin-Associated Glycoprotein
medicine.anatomical_structure
Endocrinology
Neurology
beta-Adrenergic Receptor Kinases
biology.protein
Myelin-Oligodendrocyte Glycoprotein
Lymph Nodes
Neurology (clinical)
Myelin Proteins
Spleen
Zdroj: Journal of Neuroimmunology. 137:79-86
ISSN: 0165-5728
DOI: 10.1016/s0165-5728(03)00050-x
Popis: 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.
Databáze: OpenAIRE
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