title: Up-regulation of CD81 (target of the antiproliferative antibody; TAPA) by reactive microglia and astrocytes after spinal cord injury in the rat.
abstract: We examined the expression of CD81 (also known as TAPA, or target of the antiproliferative antibody) after traumatic spinal cord injury in the rat. CD81, a member of the tetraspanin family of proteins, is thought to be involved in reactive gliosis. This is based on the antiproliferative and antiadhesive effects of antibodies against CD81 on cultured astrocytes, as well as its up-regulation after penetrating brain injury. CD81 expression following dorsal hemisection of the spinal cord was determined immunohistochemically at time points ranging from 1 day to 2 months postlesion (p.l.). In the unlesioned cord a low background level of CD81 was observed, with the exception of the ependyma of the central canal and the pia mater, which were strongly CD81-positive. One day p.l., CD81 was diffusely up-regulated in the spinal cord parenchyma surrounding the lesion site. From 3 days onward, intensely CD81-positive round cells entered the lesion site, completely filling it by 7 days p.l. Staining with the microglial markers OX-42 and Iba1 revealed that these cells were reactive microglia/macrophages. At this time, no significant CD81 expression by GFAP-positive reactive astrocytes was noted. From the second week onward, CD81 was gradually down-regulated; i.e., its spatial distribution became more restricted. The CD81-positive microglia/macrophages disappeared from the lesion site, leaving behind large cavities. After 2 months, astrocytes that formed the wall of these cavities were strongly CD81-positive. In addition, CD81 was present on reactive astrocytes in the dorsal funiculus distal from the lesion in degenerated white matter tracts. In conclusion, the spatiotemporal expression pattern of CD81 by reactive microglia and astrocytes indicates that CD81 is involved in the glial response to spinal cord injury.
authors.affiliation: Department of Experimental Neurology, RMI for Neurosciences, University Medical Centre, 3508 GA Utrecht, The Netherlands. s.dijkstra@neuro.azu.nl
authors.forename: S
authors.initials: S
authors.lastname: Dijkstra
authors.forename: J R
authors.initials: JR
authors.lastname: Geisert EE
authors.forename: W H
authors.initials: WH
authors.lastname: Gispen
authors.forename: P R
authors.initials: PR
authors.lastname: Bär
authors.forename: E A
authors.initials: EA
authors.lastname: Joosten
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000378:metabolism*; D001253:Astrocytes / Q000378:metabolism*; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism*; D047908:Intracellular Signaling Peptides and Proteins; D008297:Male; D008565:Membrane Proteins; D017628:Microglia / Q000378:metabolism*; D011506:Proteins / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D013119:Spinal Cord Injuries / Q000378:metabolism*; D060225:Tetraspanin 28; D013997:Time Factors; D015854:Up-Regulation
chemical_list: D015703:Antigens, CD; C554798:CD81 protein, human; C554797:Cd81 protein, rat; D005904:Glial Fibrillary Acidic Protein; D047908:Intracellular Signaling Peptides and Proteins; D008565:Membrane Proteins; D011506:Proteins; D060225:Tetraspanin 28; C110461:ZBTB7C protein, human