@article{oai:kanazawa-u.repo.nii.ac.jp:00014187,
 author = {Sugimoto, Naotoshi and Miwa, Shinji and Nakamura, Hiroyuki and Tsuchiya, Hiroyuki and Yachie, Akihiro},
 issue = {4},
 journal = {Archives of Biological Sciences},
 month = {Jan},
 note = {Cyclic adenosine monophosphate (cAMP) controls differentiation in several types of cells during brain development. However, the molecular mechanism of cAMP-controlled differentiation is not fully understood. We investigated the role of protein kinase A (PKA) and exchange protein directly activated by cAMP (Epac) on cAMP-induced glial fibrillary acidic protein (GFAP), an astrocyte marker, in cultured glial cells. B92 glial cells were treated with cAMP-elevating drugs, an activator of adenylate cyclase, phosphodiesterase inhibitor and a β adrenal receptor agonist. These cAMP-elevating agents induced dramatic morphological changes and expression of GFAP. A cAMP analog, 8-Br-cAMP, which activates Epac as well as PKA, induced GFAP expression and morphological changes, while another cAMP analog, 8-CPT-cAMP, which activates Epac with greater efficacy when compared to PKA, induced GFAP expression but very weak morphological changes. Most importantly, the treatment with a PKA inhibitor partially reduced cAMP-induced GFAP expression. Taken together, these results indicate that cAMP-elevating drugs lead to the induction of GFAP via PKA and/or Epac activation in B92 glial cells. © 2016 by the Serbian Biological Society.},
 pages = {795--801},
 title = {Protein kinase A and Epac activation by cAMP regulateS the expression of glial fibrillary acidic protein in glial cells},
 volume = {68},
 year = {2016}
}