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We reported previously that GDF-15 increased delayed rectifier outward K+ currents and Kv2.1 \u03b1 subunit expression through T\u03b2RII (TGF-\u03b2 receptor II) to activate Src kinase and Akt\/mTOR (mammalian target of rapamycin) signalling in rat CGNs (cerebellar granule neurons). In the present study, we found that treatment of CGNs with GDF-15 for 24\u00a0h increased the intracellular Ca2+ concentration ([Ca2+]i) in response to membrane depolarization, as determined by Ca2+ imaging. Whole-cell current recordings indicated that GDF-15 increased the inward Ca2+ current (ICa) without altering steady-state activation of Ca2+ channels. Treatment with nifedipine, an inhibitor of L-type Ca2+ channels, abrogated GDF-15-induced increases in [Ca2+]i and ICa. The GDF-15-induced increase in ICa was mediated via up-regulation of the Cav1.3 \u03b1 subunit, which was attenuated by inhibiting Akt\/mTOR and ERK (extracellular-signal-regulated kinase) pathways and by pharmacological inhibition of Src-mediated T\u03b2RII phosphorylation. Given that Cav1.3 is not only a channel for Ca2+ influx, but also a transcriptional regulator, our data confirm that GDF-15 induces protein expression via T\u03b2RII and activation of a non-Smad pathway, and provide novel insight into the mechanism of GDF-15 function in neurons.<\/jats:p>","DOI":"10.1042\/bcj20160362","type":"journal-article","created":{"date-parts":[[2016,4,26]],"date-time":"2016-04-26T03:49:45Z","timestamp":1461642585000},"page":"1895-1904","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["GDF-15 enhances intracellular Ca2+ by increasing Cav1.3 expression in rat cerebellar granule neurons"],"prefix":"10.1042","volume":"473","author":[{"given":"Jun-Mei","family":"Lu","sequence":"first","affiliation":[{"name":"Institutes of Brain Science, State Key Laboratory of Medical Neurobiology and School of Life Sciences, Fudan University, Shanghai 200433, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chang-Ying","family":"Wang","sequence":"additional","affiliation":[{"name":"Institutes of Brain Science, State Key Laboratory of Medical Neurobiology and School of Life Sciences, Fudan University, Shanghai 200433, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Changlong","family":"Hu","sequence":"additional","affiliation":[{"name":"Institutes of Brain Science, State Key Laboratory of Medical Neurobiology and School of Life Sciences, Fudan University, Shanghai 200433, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yan-Jia","family":"Fang","sequence":"additional","affiliation":[{"name":"Institutes of Brain Science, State Key Laboratory of Medical Neurobiology and School of Life Sciences, Fudan University, Shanghai 200433, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yan-Ai","family":"Mei","sequence":"additional","affiliation":[{"name":"Institutes of Brain Science, State Key Laboratory of Medical Neurobiology and School of Life Sciences, Fudan University, Shanghai 200433, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2016,6,28]]},"reference":[{"key":"2021112216271810800_B1","doi-asserted-by":"publisher","first-page":"103","DOI":"10.1007\/s004410051337","article-title":"Expression of a novel member of the TGF-\u03b2 superfamily, growth\/differentiation factor-15\/macrophage-inhibiting cytokine-1 (GDF-15\/MIC-1) in adult rat tissues","volume":"297","author":"Bottner","year":"1999","journal-title":"Cell Tissue Res"},{"key":"2021112216271810800_B2","doi-asserted-by":"publisher","first-page":"626","DOI":"10.1002\/jcp.22196","article-title":"Divergent molecular mechanisms underlying the pleiotropic functions of macrophage inhibitory cytokine-1\u00a0in cancer","volume":"224","author":"Mimeault","year":"2010","journal-title":"J. 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