Roles of reactive glial cells after brain injury

Research Project

Project/Area Number	13671448
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Single-year Grants
Section	一般
Research Field	Cerebral neurosurgery
Research Institution	OITA MEDICAL UNIVERSITY
Principal Investigator	ISONO Mitsuo Oita University, School of Medicine, Assistant Professor, 医学部, 助教授 (60151437)
Co-Investigator(Kenkyū-buntansha)	KAMIDA Tohru Oita University, School of Medicine, Associate Professor, 医学部, 講師 (90315333)
Project Period (FY)	2001 – 2002
Project Status	Completed (Fiscal Year 2002)
Budget Amount *help	¥2,500,000 (Direct Cost: ¥2,500,000) Fiscal Year 2002: ¥1,400,000 (Direct Cost: ¥1,400,000) Fiscal Year 2001: ¥1,100,000 (Direct Cost: ¥1,100,000)
Keywords	TGF / astrocyte / microglia / BrDU / TGF2 / astrogliosis / IL-6
Research Abstract	To determine the exact role of TGF-α in glial activation after traumatic brain injury, we investigated the astroglial and microglial responses after cortical stab wound injury in TGF-α overexpressing mice. Adult male B6D2-TgN (MMTVTGFA) 29RjC transgenic mice were used for the subjects. This transgenic line carries a TGF-alpha cDNA under the control of the dexamethasone-inducible MMTV promoter. Thus, exogenous administration of dexamethasone induces TGF-α overexpression. Male B6D2F1/J mice at the same age served as wild-type animals. After the cortical stab wound injury, expression of glial fibrilary acidic protein, CD-11b and interleukine-6 were investigated immunohistochemically. The results indicate that TGF-α might affect astrocytic hypertrophy without affecting microgliosis not only in the normal condition, but also in the pathological condition. Moreover, overexpression of TGF-α induced obvious expression of IL-6 around the lesion. This fact might indicate possible role of TGF-α in affecting neuronal function.