TY - JOUR
T1 - FABP7 expression in normal and stab-injured brain cortex and its role in astrocyte proliferation
AU - Sharifi, Kazem
AU - Morihiro, Yusuke
AU - Maekawa, Motoko
AU - Yasumoto, Yuki
AU - Hoshi, Hisae
AU - Adachi, Yasuhiro
AU - Sawada, Tomoo
AU - Tokuda, Nobuko
AU - Kondo, Hisatake
AU - Yoshikawa, Takeo
AU - Suzuki, Michiyasu
AU - Owada, Yuji
N1 - Funding Information:
Acknowledgments We thank Professor W. Stallcup for the gift of the anti-NG2 and anti-PDGFRα antibodies and his comments, Dr. K Fukunaga for the gift of NG108 cells, Dr. L. Koshy for proof reading, and Dr. T. Tuerxun, Dr. K. Udo, Dr. M. Okuda, Mr. M. Tamechika, Mr. M. Ebrahimi, Mr. Y. Kagawa, Mr. T. Hara, Ms. T. Nakamura and Mr. A. Islam for their technical assistance. This work was supported by grants from Ministry of Education, Culture, Sports, Science and Technology of Japan (no. 21590215) to Y.O., and from the Yamaguchi University Research Project on STRESS.
PY - 2011/11
Y1 - 2011/11
N2 - Reactive gliosis, in which astrocytes as well as other types of glial cells undergo massive proliferation, is a common hallmark of all brain pathologies. Brain-type fatty acid-binding protein (FABP7) is abundantly expressed in neural stem cells and astrocytes of developing brain, suggesting its role in differentiation and/or proliferation of glial cells through regulation of lipid metabolism and/or signaling. However, the role of FABP7 in proliferation of glial cells during reactive gliosis is unknown. In this study, we examined the expression of FABP7 in mouse cortical stab injury model and also the phenotype of FABP7-KO mice in glial cell proliferation. Western blotting showed that FABP7 expression was increased significantly in the injured cortex compared with the contralateral side. By immunohistochemistry, FABP7 was localized to GFAP + astrocytes (21% of FABP7 + cells) and NG 2+ oligodendrocyte progenitor cells (62%) in the normal cortex. In the injured cortex there was no change in the population of FABP7 +/NG2 + cells, while there was a significant increase in FABP7 +/GFAP + cells. In the stab-injured cortex of FABP7-KO mice there was decrease in the total number of reactive astrocytes and in the number of BrdU? astrocytes compared with wild-type mice. Primary cultured astrocytes from FABP7-KO mice also showed a significant decrease in proliferation and omega-3 fatty acid incorporation compared with wild-type astrocytes. Overall, these data suggest that FABP7 is involved in the proliferation of astrocytes by controlling cellular fatty acid homeostasis.
AB - Reactive gliosis, in which astrocytes as well as other types of glial cells undergo massive proliferation, is a common hallmark of all brain pathologies. Brain-type fatty acid-binding protein (FABP7) is abundantly expressed in neural stem cells and astrocytes of developing brain, suggesting its role in differentiation and/or proliferation of glial cells through regulation of lipid metabolism and/or signaling. However, the role of FABP7 in proliferation of glial cells during reactive gliosis is unknown. In this study, we examined the expression of FABP7 in mouse cortical stab injury model and also the phenotype of FABP7-KO mice in glial cell proliferation. Western blotting showed that FABP7 expression was increased significantly in the injured cortex compared with the contralateral side. By immunohistochemistry, FABP7 was localized to GFAP + astrocytes (21% of FABP7 + cells) and NG 2+ oligodendrocyte progenitor cells (62%) in the normal cortex. In the injured cortex there was no change in the population of FABP7 +/NG2 + cells, while there was a significant increase in FABP7 +/GFAP + cells. In the stab-injured cortex of FABP7-KO mice there was decrease in the total number of reactive astrocytes and in the number of BrdU? astrocytes compared with wild-type mice. Primary cultured astrocytes from FABP7-KO mice also showed a significant decrease in proliferation and omega-3 fatty acid incorporation compared with wild-type astrocytes. Overall, these data suggest that FABP7 is involved in the proliferation of astrocytes by controlling cellular fatty acid homeostasis.
KW - Astrocyte
KW - Brain injury
KW - FABP7
KW - Oligodendrocyte progenitor cell
KW - Reactive gliosis
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U2 - 10.1007/s00418-011-0865-4
DO - 10.1007/s00418-011-0865-4
M3 - Article
C2 - 21938553
AN - SCOPUS:84855493587
VL - 136
SP - 501
EP - 513
JO - Histochemistry and Cell Biology
JF - Histochemistry and Cell Biology
SN - 0948-6143
IS - 5
ER -