Source:http://linkedlifedata.com/resource/pubmed/id/11316763
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2001-4-24
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pubmed:abstractText |
PTH and PTH-related protein (PTHrP) are key mediators of skeletal development and homeostasis through their activation of the PTH-1 receptor. Previous studies have found that several AP-1 family members are regulated by PTH, such as c-fos, fra-1, and c-jun. There are numerous genes in the bone microenvironment that contain AP-1 sites, and different Fos family members are reported to have opposing transcriptional activities at AP-1 sites. The purpose of this study was to identify the effects of PTH on expression of the AP-1 protein complex member, fra-2, to extend our understanding of transcriptional regulators of PTH action. PTH induction of fra-2 messenger RNA (mRNA) levels in MC3T3-E1 preosteoblastic cells was maximal with 0.1 microM PTH (1-34). The expression in vitro was greatest 1 h after treatment and was present with N-terminal PTH but not PTH (7-34) or (53-84). Cycloheximide treatment induced fra-2 expression, and actinomycin D inhibited basal and PTHrP-induced expression. AP-1 protein in nuclear extracts of MC3T3-E1 cells was increased with PTH treatment at 3 h and consisted of high levels of Fra-2 protein, as evidenced by a supershift in an electrophoretic mobility shift assay and Western blot analysis. Up-regulation of steady-state fra-2 mRNA was also noted in vivo, where injection of PTH (1-34) (20 microgram) resulted in a more-than-7-fold maximal increase in fra-2 mRNA expression in the calvaria of mice, after 1 h of treatment. These data add to the transcriptional mediators induced by PTH and suggest that the interplay of AP-1 family members will provide insight into regulatory pathways of PTH and PTHrP for their anabolic and catabolic actions in bone.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cycloheximide,
http://linkedlifedata.com/resource/pubmed/chemical/DNA,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Fos-Related Antigen-2,
http://linkedlifedata.com/resource/pubmed/chemical/Fosl2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Parathyroid Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/Parathyroid Hormone-Related Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factor AP-1,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0013-7227
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
142
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1975-81
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:11316763-Animals,
pubmed-meshheading:11316763-Cells, Cultured,
pubmed-meshheading:11316763-Cycloheximide,
pubmed-meshheading:11316763-DNA,
pubmed-meshheading:11316763-DNA-Binding Proteins,
pubmed-meshheading:11316763-Fos-Related Antigen-2,
pubmed-meshheading:11316763-Gene Expression Regulation,
pubmed-meshheading:11316763-Genes, fos,
pubmed-meshheading:11316763-Mice,
pubmed-meshheading:11316763-Osteoblasts,
pubmed-meshheading:11316763-Parathyroid Hormone,
pubmed-meshheading:11316763-Parathyroid Hormone-Related Protein,
pubmed-meshheading:11316763-Proteins,
pubmed-meshheading:11316763-RNA, Messenger,
pubmed-meshheading:11316763-Transcription Factor AP-1,
pubmed-meshheading:11316763-Transcription Factors
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pubmed:year |
2001
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pubmed:articleTitle |
Parathyroid hormone stimulates fra-2 expression in osteoblastic cells in vitro and in vivo.
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pubmed:affiliation |
Department of Periodontics/Prevention/Geriatrics, University of Michigan, Ann Arbor, Michigan 48109-1078, 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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