Microglial expression of chemokine receptor CCR5 during rat forebrain development and after perinatal hypoxia-ischemia.
The chemokine macrophage inflammatory protein 1alpha (CCL3) is expressed by immune cells in the normal and injured perinatal brain. To determine whether the chemokine receptor CCR5 is a relevant target for CCL3 in the brain, we used RT-PCR and immunocytochemistry to assess changes in CCR5 expression and localization in developing normal and injured rat forebrain. CCR5 protein was expressed predominately by resting and activated microglia until 2 weeks of age. Neonatal hypoxia-ischemia increased CCR5 mRNA expression while causing CCR5 internalization, indicating receptor activation. These data implicate CCR5 in microglial recruitment and activation during brain development and after neonatal brain injury.
Cowell
Rita M
RM
Department of Neurology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Xu
Haiyan
H
Parent
Jack M
JM
Silverstein
Faye S
FS
D000818:Animals; D000831:Animals, Newborn; D020925:Hypoxia-Ischemia, Brain / Q000503:physiopathology*; D007150:Immunohistochemistry; D017628:Microglia / Q000378:metabolism*; D018613:Microscopy, Confocal; D016548:Prosencephalon / Q000254:growth & development* / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D019713:Receptors, CCR5 / Q000096:biosynthesis*; D020133:Reverse Transcriptase Polymerase Chain Reaction
D012333:RNA, Messenger; D019713:Receptors, CCR5