Source:http://linkedlifedata.com/resource/pubmed/id/10627584
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2000-1-27
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| pubmed:abstractText |
White light (5 klux for 2 hr) induces apoptosis of rod photoreceptors in wild-type mice (c-fos(+/+)) within 24 hr, whereas rods of c-fos knock-out mice (c-fos(-/-)) are protected (). The range of this protection was tested by analyzing retinas of c-fos(+/+) and c-fos(-/-) mice up to 10 d after exposure to threefold increased light intensities (15 klux for 2 hr). In c-fos(-/-) mice, rods were unaffected, whereas they were destroyed in c-fos(+/+) mice. After light exposure, mitochondrial damage in rods was observed exclusively in c-fos(+/+) mice. Electroretinograms recorded 48 hr after exposure revealed a decrease of all components in c-fos(+/+) mice but indicated no light-induced loss of function in c-fos(-/-) mice. Thus, in c-fos(-/-) mice, light-induced apoptosis is blocked or its threshold is elevated more than threefold. Increased activity of the transcription factor activator protein-1 (AP-1) in retinas of light-exposed c-fos(+/+) mice indicated an acute contribution of AP-1 to apoptosis induction. AP-1 activity increased already during exposure and peaked approximately 6 hr thereafter, coinciding with the appearance of major morphological signs of apoptosis. Activated AP-1 mainly consisted of c-Fos/Jun heterodimers. In c-fos(-/-) mice, AP-1 activity remained unchanged, indicating that no other Jun- or Fos-family member could substitute for c-Fos. Like damaging light, N-methyl-N-nitrosourea (MNU) induced AP-1 containing c-Fos in c-fos(+/+) mice and did not induce AP-1 in c-fos(-/-) mice. In contrast to light, however, MNU induced apoptosis in rods of c-fos(-/-) mice. Thus, c-Fos is essential for a specific premitochondrial "private apoptotic pathway" induced by light but not for the execution of apoptosis induced by other stimuli.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Alkylating Agents,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Methylnitrosourea,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-fos,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factor AP-1
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jan
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| pubmed:issn |
1529-2401
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:day |
1
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| pubmed:volume |
20
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
81-8
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:10627584-Alkylating Agents,
pubmed-meshheading:10627584-Animals,
pubmed-meshheading:10627584-Apoptosis,
pubmed-meshheading:10627584-DNA-Binding Proteins,
pubmed-meshheading:10627584-Dark Adaptation,
pubmed-meshheading:10627584-Disease Models, Animal,
pubmed-meshheading:10627584-Electroretinography,
pubmed-meshheading:10627584-Female,
pubmed-meshheading:10627584-Light,
pubmed-meshheading:10627584-Male,
pubmed-meshheading:10627584-Methylnitrosourea,
pubmed-meshheading:10627584-Mice,
pubmed-meshheading:10627584-Mice, Inbred C57BL,
pubmed-meshheading:10627584-Mice, Knockout,
pubmed-meshheading:10627584-Microscopy, Electron,
pubmed-meshheading:10627584-Mitochondria,
pubmed-meshheading:10627584-Proto-Oncogene Proteins c-fos,
pubmed-meshheading:10627584-Retinal Degeneration,
pubmed-meshheading:10627584-Retinal Rod Photoreceptor Cells,
pubmed-meshheading:10627584-Transcription Factor AP-1
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| pubmed:year |
2000
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| pubmed:articleTitle |
c-fos controls the "private pathway" of light-induced apoptosis of retinal photoreceptors.
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| pubmed:affiliation |
Department of Ophthalmology, University Hospital Zürich, CH-8091 Zürich, Switzerland. awenzel@opht.unizh.ch
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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