Document Detail

Prostaglandin expression profile in hypoxic osteoblastic cells.
MedLine Citation:
PMID:  19471853     Owner:  NLM     Status:  MEDLINE    
Conditions such as fracture and unloading have been shown to be associated with tissue and cellular hypoxia in bone. The effects of hypoxia on bone cell physiology and ultimately its impact on bone tissue repair and remodeling are not well understood. In this study, we investigated the role of hypoxia on prostaglandin release from osteoblastic cells cultured in 2% (hypoxia), 5% (potentially cellular normoxia), and 21% (normoxia for standard cell culture conditions) oxygen for up to 24 h. We quantified the effects of reduced oxygen tension on the release of prostaglandin (PG)E(2), PGF(2alpha), PGD(2), and PGI(2). The mechanism by which hypoxia increases PG production was investigated by examining the various regulatory components of the PG biosynthetic pathway. Our data show that PGE(2) levels alone are significantly elevated under hypoxic conditions. Also, we show that cyclooxygenase (COX)-1 and COX-2 play an important role in hypoxia-induced PGE(2) production, possibly via a mechanism involving changes in their respective activity levels under low oxygen conditions. The effect of hypoxia on PGE(2) levels was mimicked by dimethyloxaloglycine, a known activator of the HIF pathway. In addition, we confirmed that HIF-1alpha was stabilized in osteoblastic cells under hypoxia. Taken together these data suggest a role for the HIF pathway in regulation of PGE(2) levels under hypoxic conditions. Previous studies have detected release of prostaglandins from areas of damaged bone, such as a fracture site, and our data may contribute to an understanding of how this release is regulated.
Christina M Lee; Damian C Genetos; Alice Wong; Clare E Yellowley
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Publication Detail:
Type:  Journal Article     Date:  2009-05-28
Journal Detail:
Title:  Journal of bone and mineral metabolism     Volume:  28     ISSN:  1435-5604     ISO Abbreviation:  J. Bone Miner. Metab.     Publication Date:  2010  
Date Detail:
Created Date:  2009-12-24     Completed Date:  2010-03-11     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9436705     Medline TA:  J Bone Miner Metab     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  8-16     Citation Subset:  IM    
Department of Anatomy, Physiology and Cell Biology, School of Veterinary Medicine, University of California Davis, 1321 Haring Hall, One Shields Ave, Davis, CA 95616, USA.
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MeSH Terms
Bone Remodeling / physiology
Cell Hypoxia*
Cell Line
Culture Media, Conditioned / chemistry
Cyclooxygenase Inhibitors / pharmacology
Dinoprost / analysis,  metabolism
Dinoprostone / analysis,  metabolism*
Epoprostenol / analysis,  metabolism
Hydroxyprostaglandin Dehydrogenases / genetics,  metabolism
Hypoxia-Inducible Factor 1, alpha Subunit / agonists,  antagonists & inhibitors,  genetics,  metabolism*
Osteoblasts / metabolism,  physiology*
Oxygen / physiology*
Phospholipases A2 / genetics,  metabolism
Polymerase Chain Reaction
Prostaglandin D2 / analysis,  metabolism
RNA, Messenger
Time Factors
Reg. No./Substance:
0/Culture Media, Conditioned; 0/Cyclooxygenase Inhibitors; 0/Hif1a protein, mouse; 0/Hypoxia-Inducible Factor 1, alpha Subunit; 0/RNA, Messenger; 35121-78-9/Epoprostenol; 363-24-6/Dinoprostone; 41598-07-6/Prostaglandin D2; 551-11-1/Dinoprost; 7782-44-7/Oxygen; EC 1.1.1.-/Hydroxyprostaglandin Dehydrogenases; EC dehydrogenase; EC A2

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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