title: MicroRNA-223 expression in neutrophils in the early phase of secondary damage after spinal cord injury.
abstract: MicroRNA (miR)s are short non-coding RNAs that suppress the translation of target genes, and play an important role in gene regulation. Despite this prominence, there are few reports that refer to the expression of miRs after spinal cord injury (SCI). Previously, we reported on miR-223 expression after SCI in mice. The purpose of this study is to reveal the distribution of miR-223 and identify the cells that express miR-223 in the injured spinal cord. Quantitative polymerase chain reaction analysis revealed high expression of miR-223 at 12h after SCI. Double staining of in situ hybridization and immunohistochemistry showed that the signals of miR-223 merged with Gr-1 positive neutrophils. Our data indicate that miR-223 might regulate neutrophils in the early phase after SCI.
authors.affiliation: Department of Orthopaedic Surgery, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan. b-izumi730@hiroshima-u.ac.jp
authors.forename: Bunichiro
authors.initials: B
authors.lastname: Izumi
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Nakasa
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Tanaka
authors.forename: Kazuyoshi
authors.initials: K
authors.lastname: Nakanishi
authors.forename: Naosuke
authors.initials: N
authors.lastname: Kamei
authors.forename: Risako
authors.initials: R
authors.lastname: Yamamoto
authors.forename: Toshio
authors.initials: T
authors.lastname: Nakamae
authors.forename: Ryo
authors.initials: R
authors.lastname: Ohta
authors.forename: Yuki
authors.initials: Y
authors.lastname: Fujioka
authors.forename: Keiichiro
authors.initials: K
authors.lastname: Yamasaki
authors.forename: Mitsuo
authors.initials: M
authors.lastname: Ochi
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D022762:CCAAT-Enhancer-Binding Proteins / Q000378:metabolism; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D005786:Gene Expression Regulation / Q000502:physiology*; D051379:Mice; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D009456:Neurofibromatosis 1 / Q000378:metabolism; D009504:Neutrophils / Q000378:metabolism*; D011956:Receptors, Cell Surface / Q000378:metabolism; D013119:Spinal Cord Injuries / Q000473:pathology* / Q000503:physiopathology; D013997:Time Factors; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D022762:CCAAT-Enhancer-Binding Proteins; D016207:Cytokines; D035683:MicroRNAs; D011956:Receptors, Cell Surface; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C530718:CEBPA protein, mouse; C544877:MIRN223 microRNA, mouse; C551746:granulocyte receptor 1, mouse