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Enhanced proliferation of astrocytes from β 2 ‐adrenergic receptor knockout mice is influenced by the IGF system
Author(s) -
Chesik Daniel,
Glazenburg Lisa,
De Keyser Jacques,
Wilczak Nadine
Publication year - 2007
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2006.04289.x
Subject(s) - knockout mouse , receptor , endocrinology , medicine , astrocyte , adrenergic receptor , beta (programming language) , biology , microbiology and biotechnology , chemistry , central nervous system , computer science , programming language
In the present study, we investigated the IGF system in neonatal astrocytes derived from mice with a targeted disruption of the beta‐2 adrenergic receptor (β 2 AR). β 2 AR knockout astrocytes demonstrated higher proliferation rates and increased expression of the astrogliotic marker GFAP, as compared with wild‐type cells. β 2 AR deletion also regulated molecules of the IGF system. Although IGF‐1 levels remained unaltered, IGF‐2 and type 1 IGF receptor expression was increased in β 2 AR knockout cells. Furthermore, conditioned medium from knockout astrocytes contained lower levels of IGF binding protein‐2 and ‐4. Our data suggest a deficit of β 2 AR on astrocytes, as previously reported in multiple sclerosis, may have implications on proliferative status of astrocytes, a feature that might be attributed to regulation of IGF mitogenic actions.