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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
1998-12-14
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pubmed:abstractText |
Chronic intestinal radiation injury is associated with locally increased TGF-beta1 immunoreactivity that correlates with morphological alterations. However, the underlying mechanisms are not known. This study examined changes in intestinal TGF-beta1 immunoreactivity, steady-state TGF-beta1 mRNA levels, and cellular localization of TGF-beta1 mRNA during development of chronic radiation enteropathy in a rat model. A loop of small bowel was fixed inside the scrotum of orchiectomized male rats. The intestine was subsequently exposed locally to 0, 12 or 21 Gy X radiation. Intestine was procured at 24 h and 2, 6 and 26 weeks and subjected to histopathological analysis, quantitative immunohistochemistry with computerized image analysis, assessment of steady-state TGF-beta1 mRNA levels with quantitative reverse transcriptase polymerase chain reaction, and identification of cell types expressing TGF-beta1 mRNA with in situ hybridization. Intestine from the 21-Gy group exhibited more histopathological injury and increased TGF-beta immunoreactivity 2-26 weeks after irradiation compared to the 12-Gy group and sham-irradiated controls. TGF-beta1 mRNA in irradiated intestine increased up to six times relative to controls at 24 h and 2 weeks, was less at 6 weeks, and did not differ from controls at 26 weeks. In situ hybridization detected TGF-beta1 mRNA in epithelial and Paneth cells in control intestine. Irradiated intestine exhibited additional TGF-beta1 mRNA in inflammatory and fibroblast-like cells. We conclude that there is a radiation-induced shift in the cellular sources of TGF-beta1, and that Tgfb1 gene expression is increased mainly during the early phases of radiation enteropathy, preceding the increase in immunoreactivity and histopathological injury. Translational or post-translational mechanisms are likely involved in sustaining increased TGF-beta1 immunoreactivity levels during the chronic phase of radiation enteropathy.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0033-7587
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
150
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
673-80
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:9840187-Animals,
pubmed-meshheading:9840187-Base Sequence,
pubmed-meshheading:9840187-DNA Primers,
pubmed-meshheading:9840187-Gene Expression,
pubmed-meshheading:9840187-Immunohistochemistry,
pubmed-meshheading:9840187-In Situ Hybridization,
pubmed-meshheading:9840187-Intestine, Small,
pubmed-meshheading:9840187-Male,
pubmed-meshheading:9840187-Protein Biosynthesis,
pubmed-meshheading:9840187-RNA, Messenger,
pubmed-meshheading:9840187-Radiation Injuries, Experimental,
pubmed-meshheading:9840187-Rats,
pubmed-meshheading:9840187-Rats, Sprague-Dawley,
pubmed-meshheading:9840187-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:9840187-Transforming Growth Factor beta
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pubmed:year |
1998
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pubmed:articleTitle |
Changes in transforming growth factor beta1 gene expression and immunoreactivity levels during development of chronic radiation enteropathy.
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pubmed:affiliation |
Department of Surgery, University of Arkansas for Medical Sciences, Little Rock 72205, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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