Basic fibroblast growth factor is pro‐adipogenic in rat skeletal muscle progenitor clone, <scp>2G11</scp> cells

<jats:title>Abstract</jats:title><jats:p>Intramuscular adipose tissue (<jats:styled-content style="fixed-case">IMAT</jats:styled-content>) formation is a hallmark of marbling in cattle. <jats:styled-content style="fixed-case">IMAT</jats:styled-content> is considered to originate from skeletal muscle progenitor cells with adipogenic potential. However, the mechanism involved in <jats:styled-content style="fixed-case">IMAT</jats:styled-content> formation from these progenitor cells <jats:italic>in vivo</jats:italic> remains unclear. In the present study, among the growth factors tested, which were known to be expressed in skeletal muscle, we found only basic fibroblast growth factor (<jats:styled-content style="fixed-case">bFGF</jats:styled-content>) has a pro‐adipogenic effect on skeletal muscle derived adipogenic progenitor clone, <jats:styled-content style="fixed-case">2G11</jats:styled-content> cells. Pre‐exposure of <jats:styled-content style="fixed-case">2G11</jats:styled-content> cells to <jats:styled-content style="fixed-case">bFGF</jats:styled-content> did not affect initial gene expressions of CCAAT/enhancer‐binding protein (<jats:styled-content style="fixed-case">C</jats:styled-content>/<jats:styled-content style="fixed-case">EBP)</jats:styled-content>β and <jats:styled-content style="fixed-case">C</jats:styled-content>/<jats:styled-content style="fixed-case">EBP</jats:styled-content>δ, while resulting in an enhancement of subsequent expressions of <jats:styled-content style="fixed-case">C</jats:styled-content>/<jats:styled-content style="fixed-case">EBP</jats:styled-content>α and proliferator‐activated receptor gamma (<jats:styled-content style="fixed-case">PPAR</jats:styled-content>γ) during adipogenesis, indicating that <jats:styled-content style="fixed-case">bFGF</jats:styled-content> is acting on the transcriptional regulation of <jats:styled-content style="fixed-case">C</jats:styled-content>/<jats:styled-content style="fixed-case">EBP</jats:styled-content>α and <jats:styled-content style="fixed-case">PPAR</jats:styled-content>γ. In addition, the effect of <jats:styled-content style="fixed-case">bFGF</jats:styled-content> is mediated via two types of <jats:styled-content style="fixed-case">FGF</jats:styled-content> receptor (<jats:styled-content style="fixed-case">FGFR</jats:styled-content>) isoforms: <jats:styled-content style="fixed-case">FGFR1</jats:styled-content> and <jats:styled-content style="fixed-case">FGFR2 IIIc</jats:styled-content>, and both receptors are prerequisite for <jats:styled-content style="fixed-case">bFGF</jats:styled-content> to express its pro‐adipogenic effect. These results suggest that <jats:styled-content style="fixed-case">bFGF</jats:styled-content> plays an important role as a key trigger of <jats:styled-content style="fixed-case">IMAT</jats:styled-content> formation <jats:italic>in vivo</jats:italic>.</jats:p>