| Decay-accelerating factor in the periovulatory rat ovary. | |
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MedLine Citation:
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PMID: 16079256 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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One of the most prominent inflammatory reactions is the activation of the complement system. The activated complement system does not distinguish between pathogens and the host cell. In order to prevent autologous complement-mediated attack, host cells express a variety of both membrane-bound and fluid-phase complement regulatory proteins which control activity of the complement cascade by acting on convertase enzymes or the membrane-attack complex. Although the process of ovulation is facilitated by the inflammatory reaction, this reaction has the potential to cause serious damage to growing follicles, ovulated follicles, and other important ovarian tissues. This study was undertaken to characterize the expression and regulation of decay-accelerating factor (DAF), a complement regulator, as a potential mediator of ovarian tissue protection from ovulatory inflammation. DNA microarray and Northern blot analyses showed that an ovulatory gonadotropin stimulus dramatically yet transiently induced DAF mRNA expression in the immature rat ovary. Northern blot and PCR analyses revealed that of the three known DAF isoforms, glycosylphosphatidylinositol (GPI)-, soluble-, and transmembrane-(TM) DAF, GPI-DAF was the predominant form. In situ hybridization localized GPI-DAF mRNA expression in the theca-interstitial cells of the periovulatory ovary. Neither the anti-progestin RU486 nor the cyclooxygenase inhibitor indomethacin significantly inhibited human chorionic gonadotropin (hCG)-induced GPI-DAF mRNA expression in vivo. In vitro theca cell culture studies indicated that hCG induces GPI-DAF mRNA expression through the protein kinase A pathway. This study suggests that gonadotropin-induced GPI-DAF may be involved in the protection of ovarian tissues from the potential attack by the complement system activated by the inflammatory response associated with ovulation. |
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Authors:
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Mary C Gieske; Gi Youn Na; Yongbum Koo; Misung Jo; Thomas E Curry; Chemyong Ko |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: The Journal of endocrinology Volume: 186 ISSN: 0022-0795 ISO Abbreviation: J. Endocrinol. Publication Date: 2005 Aug |
Date Detail:
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Created Date: 2005-08-04 Completed Date: 2005-09-22 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0375363 Medline TA: J Endocrinol Country: England |
Other Details:
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Languages: eng Pagination: 303-13 Citation Subset: IM |
Affiliation:
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Department of Clinical Sciences and Biological Sciences, University of Kentucky, Lexington, Kentucky 40506, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antigens, CD55 / genetics, metabolism* Blotting, Northern Chorionic Gonadotropin / pharmacology Cyclooxygenase Inhibitors / pharmacology Female Indomethacin / pharmacology Mifepristone / pharmacology Oligonucleotide Array Sequence Analysis Ovulation / physiology* Progestins / antagonists & inhibitors Protein Isoforms / genetics, metabolism* RNA, Messenger / analysis* Rats Rats, Sprague-Dawley Reverse Transcriptase Polymerase Chain Reaction Stimulation, Chemical Theca Cells / chemistry* |
| Grant Support | |
ID/Acronym/Agency:
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P20 RR15592/RR/NCRR NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antigens, CD55; 0/Chorionic Gonadotropin; 0/Cyclooxygenase Inhibitors; 0/Progestins; 0/Protein Isoforms; 0/RNA, Messenger; 53-86-1/Indomethacin; 84371-65-3/Mifepristone |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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