Linked Life Data

19119918

Source:http://linkedlifedata.com/resource/pubmed/id/19119918

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-7-9
pubmed:abstractText
Heme oxygenase (HO)-1 is an inducible cytoprotective enzyme that degrades heme to iron, carbon monoxide (CO), and biliverdin, the latter two of which are thought to mediate the anti-inflammatory and antioxidant actions of HO-1. Bach1 is a transcriptional repressor of the HO-1 gene (Hmox-1). Previous reports have demonstrated that the genetic ablation of Bach1 engenders an increased HO-1 expression and a marked reduction in the degree of oxidative tissue damage in vivo. However, the function of Bach1 in spinal cord injury is still not understood. In the present study, we examined whether Bach1 deficiency increases HO-1 expression and reduces neural tissue damage in a spinal cord injury model using Bach1 knock-out (KO) mice and wild-type (WT) mice. The expression of HO-1 protein in the spinal cord was significantly higher in the Bach1 KO mice than in the WT mice before and after injury. The KO mice also had significantly higher Basso mouse scale scores for locomotor function and larger areas of spared white matter than the WT mice at 6 weeks after injury. Neuronal loss and apoptotic cell death in the injured spinal cord was significantly reduced in the KO mice in comparison to the WT mice. These results suggest that Bach1 deficiency engenders a constitutively higher expression of HO-1 and a dramatic increase in cytoprotection against spinal cord injury.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1557-9042
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
31-9
pubmed:meshHeading
pubmed-meshheading:19119918-Animals, pubmed-meshheading:19119918-Apoptosis, pubmed-meshheading:19119918-Basic-Leucine Zipper Transcription Factors, pubmed-meshheading:19119918-Biological Markers, pubmed-meshheading:19119918-Caspase 3, pubmed-meshheading:19119918-Female, pubmed-meshheading:19119918-Gene Therapy, pubmed-meshheading:19119918-Heme Oxygenase-1, pubmed-meshheading:19119918-In Situ Nick-End Labeling, pubmed-meshheading:19119918-Lameness, Animal, pubmed-meshheading:19119918-Mice, pubmed-meshheading:19119918-Mice, Inbred C57BL, pubmed-meshheading:19119918-Mice, Knockout, pubmed-meshheading:19119918-Motor Activity, pubmed-meshheading:19119918-Nerve Tissue Proteins, pubmed-meshheading:19119918-Nuclear Proteins, pubmed-meshheading:19119918-Recovery of Function, pubmed-meshheading:19119918-Repressor Proteins, pubmed-meshheading:19119918-Spinal Cord, pubmed-meshheading:19119918-Spinal Cord Injuries, pubmed-meshheading:19119918-Up-Regulation
pubmed:year
2009
pubmed:articleTitle
Genetic ablation of transcription repressor Bach1 reduces neural tissue damage and improves locomotor function after spinal cord injury in mice.
pubmed:affiliation
Department of Orthopaedic Surgery, Tohoku University School of Medicine, Sendai, Japan. kanno-h@isis.ocn.ne.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't