Scientific Reports 4, SREP-13-04540, DOI: 10.1038\/srep04972 (2014).<\/p>\n
Kenji Suehiro1<\/sup>, Yuka Nakamura2<\/sup><\/b>, Shuai Xu<\/b>1<\/sup><\/b>, Youichi Uda<\/b>1<\/sup><\/b>, Takafumi Matsumura1<\/sup>, Yoshiaki Yamaguchi3<\/sup><\/b>, Hitoshi Okamura<\/b>3<\/sup><\/b>, Toshihide Yamashita2<\/sup> and Yoshinori Takei4<\/sup><\/b><\/b><\/p>\n 1<\/sup>Department of Genomic Drug Discovery Science, 3<\/sup>Department of Systems Biology, and 4<\/sup>Department of Nanobio Drug Discovery Science, Graduate School of Pharmaceutical Science, Kyoto University, Kyoto, Japan and 2<\/sup>Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Osaka, Japan 8<\/p>\n <\/p>\n The adult mammalian central nervous system (CNS) cannot be repaired spontaneously after injury, which is partly due to the myelin-associated proteins including Nogo-A, myelin-associated glycoprotein and oligodendrocyte myelin glycoprotein.\u00a0 Nogo-66 receptors (NgRs) are common receptors for those myelin-associated inhibitors of the regeneration, as well as chondroitin sulphate proteoglycans, another group of regeneration inhibitors.\u00a0 <\/p>\n (1) Takei, Y. Phosphorylation of nogo receptors suppresses nogo signaling, allowing neurite regeneration. Sci Signal 2, ra14 (2009).<\/p>\n","protected":false},"excerpt":{"rendered":" Ecto-domain phosphorylation promotes functional recovery from spinal cord injury Journal Paper Information Sci […]<\/p>\n","protected":false},"author":12,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"_bbp_topic_count":0,"_bbp_reply_count":0,"_bbp_total_topic_count":0,"_bbp_total_reply_count":0,"_bbp_voice_count":0,"_bbp_anonymous_reply_count":0,"_bbp_topic_count_hidden":0,"_bbp_reply_count_hidden":0,"_bbp_forum_subforum_count":0,"_crdt_document":"","_jetpack_memberships_contains_paid_content":false,"footnotes":"","jetpack_publicize_message":"","jetpack_publicize_feature_enabled":true,"jetpack_social_post_already_shared":false,"jetpack_social_options":{"image_generator_settings":{"template":"highway","default_image_id":0,"font":"","enabled":false},"version":2}},"categories":[15],"tags":[],"class_list":["post-6925","post","type-post","status-publish","format-standard","hentry","category-news-en"],"acf":[],"jetpack_publicize_connections":[],"jetpack_featured_media_url":"","jetpack_sharing_enabled":true,"_links":{"self":[{"href":"https:\/\/www.pharm.kyoto-u.ac.jp\/en\/wp-json\/wp\/v2\/posts\/6925","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.pharm.kyoto-u.ac.jp\/en\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.pharm.kyoto-u.ac.jp\/en\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.pharm.kyoto-u.ac.jp\/en\/wp-json\/wp\/v2\/users\/12"}],"replies":[{"embeddable":true,"href":"https:\/\/www.pharm.kyoto-u.ac.jp\/en\/wp-json\/wp\/v2\/comments?post=6925"}],"version-history":[{"count":2,"href":"https:\/\/www.pharm.kyoto-u.ac.jp\/en\/wp-json\/wp\/v2\/posts\/6925\/revisions"}],"predecessor-version":[{"id":6929,"href":"https:\/\/www.pharm.kyoto-u.ac.jp\/en\/wp-json\/wp\/v2\/posts\/6925\/revisions\/6929"}],"wp:attachment":[{"href":"https:\/\/www.pharm.kyoto-u.ac.jp\/en\/wp-json\/wp\/v2\/media?parent=6925"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.pharm.kyoto-u.ac.jp\/en\/wp-json\/wp\/v2\/categories?post=6925"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.pharm.kyoto-u.ac.jp\/en\/wp-json\/wp\/v2\/tags?post=6925"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}Outline<\/h3>\n
![\"nanobio-2014\"](\"http:\/\/www.pharm.kyoto-u.ac.jp\/wp-content\/uploads\/2014\/05\/nanobio-2014.jpg\")
<\/a> We previously reported that treatment of cells with protein kinase A (PKA) phosphorylated the ecto-domains of NgRs, which impedes the binding of the myelin-associated agonists1<\/sup>.\u00a0 Here, we found NgR1 expression in neural stem\/progenitor cells (NSPs) derived from the adult rat spinal cord. \u00a0Inhibition of NgR1 during differentiation of NSPs increased the proportion of neuronal cells in the differentiated cells, which indicate that NgR1 in NSPs can inhibit neuronal differentiation.\u00a0 As expected from those in vitro results, administration of PKA plus ATP to the injured spinal cord phosphorylated NgR1 in vivo.\u00a0 The treatment induced neuronal progenitor cells in the spinal cord, which is strictly inhibited without the treatment.\u00a0 Furthermore, paralysis caused by the spinal cord injury is significantly recovered by the administration of PKA plus ATP.\u00a0 These results suggest that activation of NgR1 in NSPs of the adult spinal cord can inhibit neuronal differentiation, which appears to be a critical reason for insufficient regeneration of the adult spinal cord.<\/p>\n