title: Potential role of fibronectin in microglia/macrophage activation following cryoinjury in the rat brain: an immunohistochemical study.
abstract: To investigate whether fibronectin, a high-molecular weight glycoprotein of the extracellular matrix (ECM), plays a role in the activation of microglia/macrophages after brain injury, we examined the changes in fibronectin and arginase-1, a marker for alternatively activated macrophages, in a rat cryoinjury model using Western blot analysis, real-time reverse transcription PCR and immunohistochemistry. The protein and mRNA level of fibronectin and arginase-1 significantly increased in the injury site of the ipsilateral cerebral cortex at days 4 and 7 after cryoinjury but was decreased at day 14. The immunohistochemical analysis revealed fibronectin expression in ED1-positive microglia/macrophages and reactive astrocytes, in the lesion core and periphery, respectively. Fibronectin immunoreactivity in the lesion was similar to arginase-1 except that fibronectin was detected in the ECM after cryoinjury. The present results suggest that fibronectin was extravasated into injured brain lesions via an impaired blood-brain barrier and stimulated glial cells including microglia and infiltrating macrophages in the lesion core and periphery to become alternatively activated microglia/macrophages, which modulated CNS inflammation after brain injury.
authors: Laboratory of Veterinary Anatomy, College of Veterinary Medicine and Veterinary Medical Research Institute, Jeju National University, Jeju 690-756, Republic of Korea.
authors: Heechul
authors: H
authors: Kim
authors: Meejung
authors: M
authors: Ahn
authors: Sungyoung
authors: S
authors: Choi
authors: Minsoo
authors: M
authors: Kim
authors: Ki-Bum
authors: KB
authors: Sim
authors: Juhwan
authors: J
authors: Kim
authors: Changjong
authors: C
authors: Moon
authors: Taekyun
authors: T
authors: Shin
mesh_terms: D000818:Animals; D001119:Arginase / Q000235:genetics / Q000378:metabolism; D001930:Brain Injuries / Q000209:etiology / Q000276:immunology* / Q000473:pathology*; D004195:Disease Models, Animal; D053331:Ectodysplasins / Q000235:genetics / Q000378:metabolism; D005353:Fibronectins / Q000235:genetics / Q000378:metabolism*; D005786:Gene Expression Regulation / Q000502:physiology; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D007150:Immunohistochemistry; D037102:Lectins / Q000378:metabolism; D008262:Macrophage Activation; D008297:Male; D017628:Microglia / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D044366:Transition Temperature
chemical_list: D053331:Ectodysplasins; D005353:Fibronectins; D005904:Glial Fibrillary Acidic Protein; D037102:Lectins; D012333:RNA, Messenger; D001119:Arginase; C542908:arginase I, rat