Early NFΚB activation is inhibited during focal cerebral ischemia in interleukin-1Β-converting enzyme deficient mice
dc.contributor.author | Huang, Feng-Peng | en_US |
dc.contributor.author | Wang, Zhi-Qiu | en_US |
dc.contributor.author | Wu, Du-Chu | en_US |
dc.contributor.author | Schielke, Gerald P. | en_US |
dc.contributor.author | Sun, Yi | en_US |
dc.contributor.author | Yang, Guo-Yuan | en_US |
dc.date.accessioned | 2006-04-19T13:55:06Z | |
dc.date.available | 2006-04-19T13:55:06Z | |
dc.date.issued | 2003-09-01 | en_US |
dc.identifier.citation | Huang, Feng-Peng; Wang, Zhi-Qiu; Wu, Du-Chu; Schielke, Gerald P.; Sun, Yi; Yang, Guo-Yuan (2003)."Early NFΚB activation is inhibited during focal cerebral ischemia in interleukin-1Β-converting enzyme deficient mice." Journal of Neuroscience Research 73(5): 698-707. <http://hdl.handle.net/2027.42/34868> | en_US |
dc.identifier.issn | 0360-4012 | en_US |
dc.identifier.issn | 1097-4547 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/34868 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=12929137&dopt=citation | en_US |
dc.description.abstract | Our previous study demonstrated that the inhibition of interleukin-1Β (IL-1Β) reduces ischemic brain injury; however, the molecular mechanism of the action of IL-1 in cerebral ischemia is unclear. We are investigating currently the role of NFΚB during focal cerebral ischemia, using mutant mice deficient in the interleukin-1 converting enzyme gene (ICE KO) in a middle cerebral artery occlusion (MCAO) model. Adult male ICE KO and wild-type mice ( n = 120) underwent up to 24 hr of permanent MCAO. Cytoplasmic phospho-NFΚB/p65 expression in ischemic brain was examined using Western blot analysis and immunohistochemistry. NFΚB DNA-binding activity was detected using electrophoretic mobility shift assay (EMSA). Furthermore, ICAM-1 expression was examined in both the ICE KO and wild-type mice (WT). Western blot analysis and immunostaining showed that the level of cytosolic phosphorylated NFΚB/p65 increased after 2 and 4 hr of MCAO in WT mice; however, NFΚB/p65 was significantly reduced after MCAO in the ICE KO mice ( P < 0.05). EMSA showed that NFΚB DNA-binding activity increased after MCAO in WT mice; but this effect was reduced in the ICE KO mice. The number of ICAM-1-positive vessels in the ischemic hemisphere was greatly attenuated in the ICE KO mice ( P < 0.05), which paralleled the results of immunohistochemistry. Our results demonstrate that NFΚB phosphorylation is reduced in ICE KO mice, suggesting that ICE or IL-1 are involved in early NFΚB phosphorylation. Because cerebral ischemia induced infarction is significantly reduced in ICE KO mice, we conclude that early NFΚB phosphorylation plays a disruptive role in the ischemic process. © 2003 Wiley-Liss, Inc. | en_US |
dc.format.extent | 1512010 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Wiley Subscription Services, Inc., A Wiley Company | en_US |
dc.subject.other | Life and Medical Sciences | en_US |
dc.subject.other | Neuroscience, Neurology and Psychiatry | en_US |
dc.title | Early NFΚB activation is inhibited during focal cerebral ischemia in interleukin-1Β-converting enzyme deficient mice | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Molecular, Cellular and Developmental Biology | en_US |
dc.subject.hlbsecondlevel | Neurosciences | en_US |
dc.subject.hlbsecondlevel | Psychology | en_US |
dc.subject.hlbsecondlevel | Public Health | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.subject.hlbtoplevel | Social Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Surgery (Neurosurgery), University of Michigan, Ann Arbor ; Department of Neurosurgery, Institute of Neurology, Hua-Shan Hospital, Shanghai Medical School, Fudan University, Shanghai, China | en_US |
dc.contributor.affiliationum | Department of Surgery (Neurosurgery), University of Michigan, Ann Arbor ; Department of Neurosurgery, Institute of Neurology, Hua-Shan Hospital, Shanghai Medical School, Fudan University, Shanghai, China | en_US |
dc.contributor.affiliationum | Department of Surgery (Neurosurgery), University of Michigan, Ann Arbor | en_US |
dc.contributor.affiliationum | Department of Surgery (Neurosurgery), University of Michigan, Ann Arbor ; Department of CNS pharmacology, Pfizer Global Research and Development, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Department of Surgery (Neurosurgery), University of Michigan, Ann Arbor ; Departments of Anesthesia and Neurosurgery, Center for Cerebrovascular Research, San Francisco General Hospital, UCSF, Room 3C-38, 1001 Potrero Ave., San Francisco, CA 94110 | en_US |
dc.contributor.affiliationother | Department of Molecular Biology, Pfizer Global Research and Development, Ann Arbor, Michigan | en_US |
dc.identifier.pmid | 12929137 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/34868/1/10654_ftp.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1002/jnr.10654 | en_US |
dc.identifier.source | Journal of Neuroscience Research | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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