title: CD36 is involved in astrocyte activation and astroglial scar formation.
abstract: Inflammation is an essential component for glial scar formation. However, the upstream mediator(s) that triggers the process has not been identified. Previously, we showed that the expression of CD36, an inflammatory mediator, occurs in a subset of astcotyes in the peri-infarct area where the glial scar forms. This study investigates a role for CD36 in astrocyte activation and glial scar formation in stroke. We observed that the expression of CD36 and glial fibrillary acidic protein (GFAP) coincided in control and injured astrocytes and in the brain. Furthermore, GFAP expression was attenuated in CD36 small interfering RNA transfected astrocytes or in the brain of CD36 knockout (KO) mice, suggesting its involvement in GFAP expression. Using an in-vitro model of wound healing, we found that CD36 deficiency attenuated the proliferation of astrocytes and delayed closure of the wound gap. Furthermore, stroke-induced GFAP expression and scar formation were significantly attenuated in the CD36 KO mice compared with wild type. These findings identify CD36 as a novel mediator for injury-induced astrogliosis and scar formation. Targeting CD36 may serve as a potential strategy to reduce glial scar formation in stroke.
authors.affiliation: Burke-Cornell Medical Research Institute, White Plains, New York, USA.
authors.forename: Yi
authors.initials: Y
authors.lastname: Bao
authors.forename: Luye
authors.initials: L
authors.lastname: Qin
authors.forename: Eunhee
authors.initials: E
authors.lastname: Kim
authors.forename: Sangram
authors.initials: S
authors.lastname: Bhosle
authors.forename: Hengchang
authors.initials: H
authors.lastname: Guo
authors.forename: Maria
authors.initials: M
authors.lastname: Febbraio
authors.forename: Renee E
authors.initials: RE
authors.lastname: Haskew-Layton
authors.forename: Rajiv
authors.initials: R
authors.lastname: Ratan
authors.forename: Sunghee
authors.initials: S
authors.lastname: Cho
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D018955:CD36 Antigens / Q000235:genetics / Q000378:metabolism*; D018929:Cell Culture Techniques; D002460:Cell Line; D049109:Cell Proliferation; D002921:Cicatrix / Q000378:metabolism* / Q000473:pathology; D004195:Disease Models, Animal; D005904:Glial Fibrillary Acidic Protein; D005911:Gliosis / Q000378:metabolism* / Q000473:pathology; D002546:Ischemic Attack, Transient / Q000150:complications / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009419:Nerve Tissue Proteins / Q000096:biosynthesis / Q000378:metabolism; D009457:Neuroglia; D020521:Stroke / Q000209:etiology / Q000378:metabolism / Q000473:pathology*
chemical_list: D018955:CD36 Antigens; D005904:Glial Fibrillary Acidic Protein; D009419:Nerve Tissue Proteins; C528900:glial fibrillary astrocytic protein, mouse