
Fibroblast growth factor 2 upregulates ecto-5′-nucleotidase and adenosine deaminase via MAPK pathways in cultured rat spinal cord astrocytes
Author(s) -
Ryota Eguchi,
Taisuke Kitano,
Ken-ichi Otsuguro
Publication year - 2020
Publication title -
purinergic signalling
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.064
H-Index - 59
eISSN - 1573-9546
pISSN - 1573-9538
DOI - 10.1007/s11302-020-09731-0
Subject(s) - adenosine deaminase , adenosine , adenosine kinase , extracellular , biology , mapk/erk pathway , astrocyte , microbiology and biotechnology , nucleotidase , kinase , purinergic signalling , fibroblast growth factor , protein kinase a , signal transduction , purine metabolism , biochemistry , enzyme , adenosine receptor , endocrinology , central nervous system , receptor , agonist
Adenosine triphosphate (ATP) and adenosine are neurotransmitters and neuromodulators in the central nervous system. Astrocytes regulate extracellular concentration of purines via ATP release and its metabolisms via ecto-enzymes. The expression and activity of purine metabolic enzymes in astrocytes are increased under pathological conditions. We previously showed that fibroblast growth factor 2 (FGF2) upregulates the expression and activity of the enzymes ecto-5'-nucleotidase (CD73) and adenosine deaminase (ADA). Here, we further demonstrate that this occurs in concentration- and time-dependent manners in cultured rat spinal cord astrocytes and is suppressed by inhibitors of the FGF receptor as well as the mitogen-activated protein kinases (MAPKs). We also found that FGF2 increased the phosphorylation of MAPKs, including extracellular signal-regulated kinase, c-Jun N-terminal kinase, and p38 MAPK, leading to the increased expression and activity of CD73 and ADA. Our findings reveal the involvement of FGF2/MAPK pathways in the regulation of purine metabolic enzymes in astrocytes. These pathways may contribute to the control of extracellular purine concentrations under physiological and pathological conditions.