Source:http://linkedlifedata.com/resource/pubmed/id/18271013
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
|
pubmed:dateCreated |
2008-5-20
|
pubmed:abstractText |
Bach 1 is a transcription factor that negatively regulates the transcription of heme oxygenase-1 (HO-1), a stress-responding protein. In this study, we investigated the reaction to oxidative stress in the meniscus of Bach 1 deficient mice, and the suppression of meniscal degeneration by the induction of HO-1. We carried out a comparative study between Bach 1 deficient mice and wild type mice, in which the oxidative stress reaction and age-related changes were investigated using the menisci of 6-, 12-, and 24-week-old mice. The degrees of meniscal degeneration and expression of HO-1 were evaluated using the menisci cultured under oxidative stress with cadmium chloride or interleukin-1 beta. The age-related changes in the meniscus were histologically examined. The expression of HO-1 was higher, and the degrees of histological degeneration were lower in the Bach 1 deficient mice than in wild type mice (HO-1 mRNA expression: In both the Cd group and the IL group, two-fourfold higher in the meniscus). The age-related changes were lower in the Bach 1 deficient mice than in wild type mice. In 24-week-old mice, a moderate decrease in the cell density and proteoglycan content was observed in wild type mice compared with Bach 1 deficient mice. In the menisci of Bach 1 deficient mice, the anti-oxidative stress activity was considered to be increased by abrogating the suppression of HO-1 expression, resulting in a reduction of histological degeneration. This finding showed a potential new strategy for the prevention and treatment of meniscal degeneration.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Bach1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Basic-Leucine Zipper Transcription...,
http://linkedlifedata.com/resource/pubmed/chemical/Cadmium Chloride,
http://linkedlifedata.com/resource/pubmed/chemical/Heme Oxygenase-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1beta,
http://linkedlifedata.com/resource/pubmed/chemical/Proteoglycans
|
pubmed:status |
MEDLINE
|
pubmed:month |
Jun
|
pubmed:issn |
1554-527X
|
pubmed:author | |
pubmed:copyrightInfo |
(c) 2008 Orthopaedic Research Society.
|
pubmed:issnType |
Electronic
|
pubmed:volume |
26
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
894-8
|
pubmed:meshHeading |
pubmed-meshheading:18271013-Age Factors,
pubmed-meshheading:18271013-Animals,
pubmed-meshheading:18271013-Apoptosis,
pubmed-meshheading:18271013-Basic-Leucine Zipper Transcription Factors,
pubmed-meshheading:18271013-Cadmium Chloride,
pubmed-meshheading:18271013-Heme Oxygenase-1,
pubmed-meshheading:18271013-Interleukin-1beta,
pubmed-meshheading:18271013-Menisci, Tibial,
pubmed-meshheading:18271013-Mice,
pubmed-meshheading:18271013-Mice, Inbred C57BL,
pubmed-meshheading:18271013-Mice, Mutant Strains,
pubmed-meshheading:18271013-Organ Culture Techniques,
pubmed-meshheading:18271013-Oxidative Stress,
pubmed-meshheading:18271013-Proteoglycans
|
pubmed:year |
2008
|
pubmed:articleTitle |
Oxidative stress reaction in the meniscus of Bach 1 deficient mice: potential prevention of meniscal degeneration.
|
pubmed:affiliation |
Department of Orthopaedic Surgery, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima, 734-8551 Japan.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|