| Hung KS |
------>authors3_c= ------>paper_class1=1 ------>Impact_Factor=None ------>paper_class3=1 ------>paper_class2=1 ------>vol=6 ------>confirm_bywho=shiemin ------>insert_bywho=wtchiu ------>Jurnal_Rank=None ------>authors4_c= ------>comm_author=1 ------>patent_EDate=None ------>authors5_c= ------>publish_day=1 ------>paper_class2Letter=None ------>page2=46 ------>medlineContent= ------>unit=E0110 ------>insert_date=20071219 ------>iam=7 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN= ------>authors_c= ------>score=500 ------>journal_name=Journal of Neurosurgery Spine ------>paper_name=Gene transfer of insulin-like growth factor-I providing neuroprotection after spinal cord injury in rats. ------>confirm_date=20071220 ------>tch_id=073010 ------>pmid=17233289 ------>page1=35 ------>fullAbstract=OBJECT: Insulin-like growth factor-I (IGF-I) has been shown to be a potent neurotrophic factor that promotes the growth of projection neurons, dendritic arborization, and synaptogenesis. Its neuroprotective roles may be coordinated by activation of Akt, inhibition of glycogen synthase kinase-3beta (GSK-3beta), and thus inhibition of tau phosphorylation. The authors investigated the role and mechanism of IGF-I gene transfer after spinal cord injury (SCI). METHODS: Studies were performed in 40 male Sprague-Dawley rats after spinal cord hemisection. The authors conducted hydrodynamics-based gene transfection in which an IGF-I plasmid was rapidly injected into the rat~s tail vein 30 minutes after SCI. The animals were randomly divided into four groups: Group I, sham operated; Group II, SCI treated with pCMV-IGF-I gene; Group III, SCI treated with vehicle pCMV-LacZ gene; and Group IV, SCI only. The results showed that IGF-I gene transfer promoted motor recovery, antiinflammatory responses, and antiapoptotic effects after SCI. Using techniques of Western blotting and immunohistochemistry, the authors assessed the mechanism of IGF-I gene transfer after SCI in terms of activation of Akt, inhibition of GSK-3beta, attenuation of p35, and inhibition of tau phosphorylation. Moreover, they found that IGF-I gene transfer could block caspase-9 cleavage, increase Bcl-2 formation, and thus inhibit apoptosis after SCI. CONCLUSIONS: The intravenous administration of IGF-I after SCI activated Akt, attenuated GSK-3beta, inhibited p35 activation, diminished tau hyperphosphorylation, ended microglia and astrocyte activation, inhibited neuron loss, and significantly improved neurological dysfunction. Furthermore, IGF-I attenuated caspase-9 cleavage, increased Bcl2, and thus inhibited apoptosis after SCI. ------>tmu_sno=None ------>sno=16496 ------>authors2=Tsai SH ------>authors3=Lin TC ------>authors4=Lin JW ------>authors5=Chang CK ------>authors6=Chiu WT ------>authors6_c= ------>authors=Hung KS ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c= ------>publish_area=0 ------>updateTitle=Gene transfer of insulin-like growth factor-I providing neuroprotection after spinal cord injury in rats. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=NULL ------>no=1 ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2007 ------>submit_flag=None ------>publish_month=1 |