title: Administration of antagomir-223 inhibits apoptosis, promotes angiogenesis and functional recovery in rats with spinal cord injury.
abstract: MicroRNAs (miRNAs) are recently described as a class of short non-coding RNAs, which play important roles in post-transcriptional gene regulation and involved in many physiological and pathological processes. MicroRNA-223 (miR-223) has been showed highly elevated in the injured spinal cord. However, the potential role and underlying mechanisms of miR-223 in spinal cord injury (SCI) were incompletely understood. In the present study, we observed the persistent high levels of miR-223 in the injured spinal cord at different time points (1, 3, 7, and 14 days) after SCI. Besides, inhibiting miR-223 by intrathecally injection with antagomir-223 significantly improved recovery in hindlimb motor function and attenuated cell apoptosis in spinal cord-injured rats. Additionally, antagomir-223 treatment markedly decreased the pro-apoptotic protein levels, including Bax and cleaved caspase-3, up-regulated the anti-apoptotic Bcl-2 protein level, as well as the expression of GluR2. Moreover, inhibition of miR-223 promoted angiogenesis, as evidenced by the increased CD31 expression and microvascular density. Taken together, our results indicate that inhibition of miR-223 with antagomir-223 exerts protective role in functional recovery, angiogenesis, and anti-apoptosis during SCI. Thereby, miR-223 may be a promising target of therapy for SCI.
authors.affiliation: Department of Orthopaedic Surgery, Shengjing Hospital of China Medical University, 36 Sanhao Street, Shenyang, 110004, People's Republic of China, daliumail@163.com.
authors.forename: Da
authors.initials: D
authors.lastname: Liu
authors.forename: Ying
authors.initials: Y
authors.lastname: Huang
authors.forename: Changqing
authors.initials: C
authors.lastname: Jia
authors.forename: Yan
authors.initials: Y
authors.lastname: Li
authors.forename: Feng
authors.initials: F
authors.lastname: Liang
authors.forename: Qin
authors.initials: Q
authors.lastname: Fu
mesh_terms: D000818:Animals; D000070416:Antagomirs; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000378:metabolism; D007278:Injections, Spinal; D008297:Male; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism; D018919:Neovascularization, Physiologic / Q000187:drug effects*; D009841:Oligonucleotides / Q000008:administration & dosage* / Q000494:pharmacology*; D017207:Rats, Sprague-Dawley; D018091:Receptors, AMPA / Q000378:metabolism; D020127:Recovery of Function / Q000187:drug effects*; D013119:Spinal Cord Injuries / Q000503:physiopathology*; D015854:Up-Regulation / Q000187:drug effects; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D000070416:Antagomirs; D035683:MicroRNAs; D009841:Oligonucleotides; D018091:Receptors, AMPA; C000603521:antagomir-223; D051028:bcl-2-Associated X Protein; D053148:Caspase 3; C104722:glutamate receptor ionotropic, AMPA 2