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Disrupted\n                    <jats:styled-content style=\"fixed-case\">OEC<\/jats:styled-content>\n                    development is thought to be associated with abnormal\n                    <jats:styled-content style=\"fixed-case\">OB<\/jats:styled-content>\n                    morphogenesis, leading to anosmia, a defining characteristic of Kallmann syndrome. Hence, anosmin\u20101 encoded by Kallmann syndrome gene (\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">KAL<\/jats:styled-content>\n                      \u20101\n                    <\/jats:italic>\n                    ) might modulate\n                    <jats:styled-content style=\"fixed-case\">OEC<\/jats:styled-content>\n                    differentiation\/maturation in the\n                    <jats:styled-content style=\"fixed-case\">OB<\/jats:styled-content>\n                    . We performed\n                    <jats:italic>in ovo<\/jats:italic>\n                    electroporation of sh\n                    <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n                    in the olfactory placode to knock\u2010down\n                    <jats:italic>kal<\/jats:italic>\n                    in chick embryos, resulting in abnormal\n                    <jats:styled-content style=\"fixed-case\">OB<\/jats:styled-content>\n                    morphogenesis and loss of olfactory sensory axonal innervation into\n                    <jats:styled-content style=\"fixed-case\">OB<\/jats:styled-content>\n                    .\n                    <jats:styled-content style=\"fixed-case\">BLBP<\/jats:styled-content>\n                    \u2010expressing\n                    <jats:styled-content style=\"fixed-case\">OEC<\/jats:styled-content>\n                    s appeared to form a thinner and poorly organized outmost\n                    <jats:styled-content style=\"fixed-case\">OB<\/jats:styled-content>\n                    layer where\n                    <jats:styled-content style=\"fixed-case\">SOX<\/jats:styled-content>\n                    10 expressing\n                    <jats:styled-content style=\"fixed-case\">OEC<\/jats:styled-content>\n                    s were completely absent with emergence of\n                    <jats:styled-content style=\"fixed-case\">GFAP<\/jats:styled-content>\n                    \u2010expressing\n                    <jats:styled-content style=\"fixed-case\">OEC<\/jats:styled-content>\n                    s. Furthermore, in embryonic day 10 chick\n                    <jats:styled-content style=\"fixed-case\">OB<\/jats:styled-content>\n                    explant cultures,\n                    <jats:styled-content style=\"fixed-case\">GFAP<\/jats:styled-content>\n                    expression in\n                    <jats:styled-content style=\"fixed-case\">OEC<\/jats:styled-content>\n                    s accumulating along the\n                    <jats:styled-content style=\"fixed-case\">OB<\/jats:styled-content>\n                    nerve layers was dramatically reduced by recombinant anosmin\u20101. We then purified immature\n                    <jats:styled-content style=\"fixed-case\">OEC<\/jats:styled-content>\n                    s from embryonic day 10 chick\n                    <jats:styled-content style=\"fixed-case\">OB<\/jats:styled-content>\n                    . These cells express\n                    <jats:styled-content style=\"fixed-case\">GFAP<\/jats:styled-content>\n                    after 7\u00a0days in vitro, exhibiting a multipolar morphology. Overexpression of chick anosmin, exogenous anosmin\u20101 or\n                    <jats:styled-content style=\"fixed-case\">FGF<\/jats:styled-content>\n                    2 could inhibit\n                    <jats:styled-content style=\"fixed-case\">GFAP<\/jats:styled-content>\n                    expression with cells presenting elongated morphology, which was blocked by the\n                    <jats:styled-content style=\"fixed-case\">FGF<\/jats:styled-content>\n                    receptor inhibitor Su5402. These data demonstrate that anosmin\u20101 functions via\n                    <jats:styled-content style=\"fixed-case\">FGF<\/jats:styled-content>\n                    signalling in regulating\n                    <jats:styled-content style=\"fixed-case\">OEC<\/jats:styled-content>\n                    maturation, thereby providing a permissive glial environment for axonal innervation into the\n                    <jats:styled-content style=\"fixed-case\">OB<\/jats:styled-content>\n                    during development.\n                  <\/jats:p>","DOI":"10.1111\/ejn.14483","type":"journal-article","created":{"date-parts":[[2019,6,14]],"date-time":"2019-06-14T06:13:51Z","timestamp":1560492831000},"page":"3472-3486","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Extracellular matrix protein anosmin\u20101 modulates olfactory ensheathing cell maturation in chick olfactory bulb 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