Document Detail

Prostaglandin E2 increases proenkephalin mRNA level in rat astrocyte-enriched culture.
MedLine Citation:
PMID:  9757037     Owner:  NLM     Status:  MEDLINE    
The effect of prostaglandin E2 (PGE2) on proenkephalin (proENK) mRNA expression in primary cultured rat astrocytes was studied. The proENK mRNA level was significantly increased about 3.3-fold 4 h after PGE2 (10 microM) treatment and this increase was potentiated by the pre-treatment with cycloheximide (CHX; 15 microM) about 1.7-fold as much as PGE2 alone treated cells. The pretreatment with staurosporine (1 microM) completely inhibited the increase of PGE2-induced proENK mRNA level, although only a partial inhibition of PGE2-induced proENK mRNA level (approximately 1.5-fold) by H89 (10 microM) was observed. The increase of PGE2-induced proENK mRNA level was not affected by the pretreatment with PD98059 (1, 5, and 10 microM), omega-conotoxin GIVA (1 microM), nimodipine (1 microM), calmidazolium (1 microM), or KN-62 (1 microM). In addition to the proENK mRNA level, PGE2 also increased c-Fos (approximately 4.3-fold), Fra-1 ( approximately 3.8 fold), and Fra-2 (approximately 8.2-fold) protein levels at 4 h after drug treatment. However, c-Jun, JunB, and JunD protein levels were not affected by PGE2. Indeed, PGE2 failed to up-regulate c-jun mRNA expression as well as its protein product. Surprisingly, although three Jun proteins were not induced by PGE2, AP-1 and ENKCRE-2 DNA binding activities were increased by PGE2, (approximately 5 and approximately 2.8-fold, respectively) and which were effectively reduced by CHX (approximately 2.5 and 2-fold, respectively). In western blot analyses, PGE2 enhanced the phosphorylation of CREB (approximately 2.6-fold at 1 h), and CHX showed a potentiative effect on PGE2-induced CREB phosphorylation ( approximately 1.7 fold at 1 h) which is similar to the action on proENK mRNA regulation. Our results suggest that PGE2 increases proENK mRNA expression via activating serine/threonine protein kinase such as PKA, but not calcium/calmodulin dependent protein kinase and MAPK. In addition, phosphorylation of CREB rather than the increase of AP-1 may have a possible role at least early stage in PGE2-induced proENK mRNA level and CHX-evoked potentiation.
J S Won; H W Suh; Y H Kim; D K Song; S O Huh; J K Lee; K J Lee
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Brain research. Molecular brain research     Volume:  60     ISSN:  0169-328X     ISO Abbreviation:  Brain Res. Mol. Brain Res.     Publication Date:  1998 Oct 
Date Detail:
Created Date:  1998-12-07     Completed Date:  1998-12-07     Revised Date:  2013-06-03    
Medline Journal Info:
Nlm Unique ID:  8908640     Medline TA:  Brain Res Mol Brain Res     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  203-14     Citation Subset:  IM    
Copyright Information:
Copyright 1998 Elsevier Science B.V.
Department of Pharmacology and Institute of Natural Medicine, College of Medicine, Hallym University, 1 Okchun-Dong, Chunchon, Kangwon-Do 200-702, South Korea.
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MeSH Terms
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / analogs & derivatives,  pharmacology
Animals, Newborn
Astrocytes / cytology,  drug effects,  metabolism*
Cells, Cultured
Cerebral Cortex / cytology,  metabolism*
Cyclic AMP Response Element-Binding Protein / metabolism
Cycloheximide / pharmacology
Dinoprostone / pharmacology*
Enkephalins / biosynthesis,  genetics*
Enzyme Inhibitors / pharmacology*
Flavonoids / pharmacology
Imidazoles / pharmacology
Isoquinolines / pharmacology
Nimodipine / pharmacology
Peptides / pharmacology
Protein Precursors / biosynthesis,  genetics*
Proto-Oncogene Proteins c-jun / genetics
RNA, Messenger / biosynthesis*
Rats, Sprague-Dawley
Staurosporine / pharmacology
Transcription Factor AP-1 / biosynthesis,  genetics
Transcription, Genetic / drug effects*
omega-Conotoxin GVIA
Reg. No./Substance:
0/2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0/Cyclic AMP Response Element-Binding Protein; 0/Enkephalins; 0/Enzyme Inhibitors; 0/Flavonoids; 0/Imidazoles; 0/Isoquinolines; 0/Peptides; 0/Protein Precursors; 0/Proto-Oncogene Proteins c-jun; 0/RNA, Messenger; 0/Sulfonamides; 0/Transcription Factor AP-1; 0/proenkephalin; 127191-97-3/KN 62; 127243-85-0/N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide; 363-24-6/Dinoprostone; 57265-65-3/calmidazolium; 62996-74-1/Staurosporine; 66-81-9/Cycloheximide; 66085-59-4/Nimodipine; 84477-87-2/1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; 92078-76-7/omega-Conotoxin GVIA

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