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Fas ligand expression following normothermic liver ischemia-reperfusion.
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- Additional Information
- Source:
Publisher: Academic Press Country of Publication: United States NLM ID: 0376340 Publication Model: Print Cited Medium: Print ISSN: 0022-4804 (Print) Linking ISSN: 00224804 NLM ISO Abbreviation: J Surg Res Subsets: MEDLINE
- Publication Information:
Publication: New York, NY : Academic Press
Original Publication: Philadelphia [etc.]
- Subject Terms:
- Abstract:
Background: The aim of this study was to evaluate the role of the pro-apoptotic molecule Fas Ligand (FasL) in 120 min normothermic ischemia-reperfusion (I-R) induced apoptosis in rat liver treated or not with Z-Asp-cmk caspase inhibitor.
Materials and Methods: Rats were divided into two groups: group 1, control, PBS administration; group 2, Z-Asp-cmk treatment. Z-Asp-cmk was injected intravenously, 2 min before induction of 120 min of normothermic liver ischemia. Immunohistochemical detection of apoptotic liver cells was carried out using the TUNEL method. Fas and FasL expression were measured by qualitative reverse transcription polymerase chain reaction (RT-PCR), Northern and western blot, and by immunofluorescence labeling, in ischemic and non-ischemic liver lobes at different times after reperfusion.
Results: FasL mRNA and protein expression were increased in ischemic liver, while Fas receptor mRNA levels remained unchanged. Pre-treatment of rats with Z-Asp-cmk caspase inhibitor reduced liver apoptosis, but did not modify FasL mRNA levels.
Conclusions: These results suggest that the pro-apoptotic molecule FasL is involved in the induction of liver apoptosis following I-R.
- Accession Number:
0 (Amino Acid Chloromethyl Ketones)
0 (Fas Ligand Protein)
0 (Faslg protein, rat)
0 (Membrane Glycoproteins)
0 (RNA, Messenger)
0 (Z-Asp-2,6-dichlorobenzoyl-oxymethylketone)
EC 3.4.22.- (Caspases)
- Publication Date:
Date Created: 20050420 Date Completed: 20050602 Latest Revision: 20200914
- Publication Date:
20250114
- Accession Number:
10.1016/j.jss.2004.11.026
- Accession Number:
15836847
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