Linked Life Data

20622466

Source:http://linkedlifedata.com/resource/pubmed/id/20622466

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2010-7-12
pubmed:abstractText
Global comparison of the colonic gene expression profiles between 14-month-old senescenceaccelerated mouse (SAM)-P6 mice and SAM-R1 mice, a wild-type control, was conducted with an oligonucleotide microarray containing more than 5,000 mouse genes. Eight genes were upregulated more than two-fold and 94 genes were downregulated more than two-fold in SAM-P6 mice. The three cell defense genes intelectin1 (Itln1), trefoil factor 3 (intestinal) (Tff3) and "deleted in malignant brain tumors 1" (Dmbt1) were among those extensively downregulated. Quantitative RT-PCR analysis confirmed that Itln1 mRNA was almost undetectable in SAM-P6 colon, whereas it was readily detected in SAM-R1 colon. Colonic expression of both Tff3 and Dmbt1 mRNA was also substantially decreased, to one third and two thirds of the levels in SAM-R1 mice, respectively. A 14 kDa Tff3 dimer was detected by Western blotting in the colon of all three SAM-R1 mice, but was not present in three SAM-P6 mice. No upregulation of 3 cell defense genes was detected in 3-month-old SAM-R1 as well as SAM-P6 mice. These results suggest that a diminution of the intestinal trefoil factor system may be involved in the acceleration of aging in SAM-P6 mice.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1880-313X
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
169-75
pubmed:dateRevised
2011-4-22
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Downregulation of trefoil factor 3 gene expression in the colon of the senescence-accelerated mouse (SAM)-P6 revealed by oligonucleotide microarray analysis.
pubmed:affiliation
Public Health and Nutrition, Graduate School of Human Health Science, Siebold University of Nagasaki.
pubmed:publicationType
Journal Article