{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T02:50:06Z","timestamp":1791946206400,"version":"4.3.4"},"reference-count":58,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2018,10,28]],"date-time":"2018-10-28T00:00:00Z","timestamp":1540684800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2019,5]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    We have previously shown that knockout of fibroblast growth factor\u20102 (FGF\u20102) and potential compensatory effects of other growth factors result in amelioration of disease symptoms in a transgenic mouse model of amyotrophic lateral sclerosis (ALS). ALS is a rapidly progressive neurological disorder leading to degeneration of cortical, brain stem, and spinal motor neurons followed by subsequent denervation and muscle wasting. Mutations in the superoxide dismutase 1 (SOD1) gene are responsible for approximately 20% of familial ALS cases and SOD1 mutant mice still are among the models best mimicking clinical and neuropathological characteristics of ALS. The aim of the present study was a thorough characterization of FGF\u20102 and other growth factors and signaling effectors in vivo in the SOD1\n                    <jats:sup>G93A<\/jats:sup>\n                    mouse model. We observed tissue\u2010specific opposing gene regulation of FGF\u20102 and overall dysregulation of other growth factors, which in the gastrocnemius muscle was associated with reduced downstream extracellular\u2010signal\u2010regulated kinases (ERK) and protein kinase B (AKT) activation. To further investigate whether the effects of FGF\u20102 on motor neuron death are mediated by glial cells, astrocytes lacking FGF\u20102 were cocultured together with mutant SOD1\n                    <jats:sup>G93A<\/jats:sup>\n                    motor neurons. FGF\u20102 had an impact on motor neuron maturation indicating that astrocytic FGF\u20102 affects motor neurons at a developmental stage. Moreover, neuronal gene expression patterns showed FGF\u20102\u2010 and SOD1\n                    <jats:sup>G93A<\/jats:sup>\n                    \u2010dependent changes in ciliary neurotrophic factor, glial\u2010cell\u2010line\u2010derived neurotrophic factor, and ERK2, implying a potential involvement in ALS pathogenesis before the onset of clinical symptoms.\n                  <\/jats:p>","DOI":"10.1002\/jcp.27498","type":"journal-article","created":{"date-parts":[[2018,10,29]],"date-time":"2018-10-29T00:50:11Z","timestamp":1540774211000},"page":"7395-7410","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Characterizing the multiple roles of FGF\u20102 in SOD1\n                    <sup>G93A<\/sup>\n                    ALS mice in vivo and in vitro"],"prefix":"10.1002","volume":"234","author":[{"given":"Ekaterini","family":"Kefalakes","sequence":"first","affiliation":[{"name":"Department of Neurology Hannover 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