Document Detail


Apelin is decreased with human preterm and term labor and regulates prolabor mediators in human primary amnion cells.
MedLine Citation:
PMID:  23314958     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A critical role of proinflammatory mediators including cytokines, prostaglandins, and extracellular matrix remodeling enzymes in the processes of human labor and delivery, at term and preterm, has been demonstrated. In nongestational tissues, apelin plays an important role in a number of physiologic processes, including the regulation of inflammation. However, the role and regulation of apelin and the apelin receptor (APJ) in human gestational tissues are not known. The aims of this study were to determine the effect of (i) preterm and term labor on apelin and APJ expression in human gestational tissues and (ii) apelin small interfering RNA (siRNA) knockdown in human primary amnion cells on prolabor mediators. Human placenta and fetal membranes were collected from term nonlaboring women and women after spontaneous labor and delivery. Preterm and term spontaneous labor were associated with significantly lower apelin expression in fetal membranes. On the other hand, there was no effect of labor on APJ expression and no effect of term labor on placental apelin or APJ expression. Transfection of primary amnion cells with apelin siRNA was associated with significantly increased interleukin (IL)-1β-induced IL-6 and IL-8 release and cyclooxygenase-2 messenger RNA (mRNA) expression and resultant prostaglandin E2 and prostaglandin F2α release. There was no effect of apelin siRNA on matrix metalloproteinase (MMP)-9 mRNA expression and pro MMP-9 release. In summary, human labor downregulates apelin expression in human fetal membranes. Furthermore, a role of apelin in the regulation of proinflammatory and prolabor mediators in human fetal membranes is supported by our studies.
Authors:
Ratana Lim; Gillian Barker; Clyde Riley; Martha Lappas
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2013-01-11
Journal Detail:
Title:  Reproductive sciences (Thousand Oaks, Calif.)     Volume:  20     ISSN:  1933-7205     ISO Abbreviation:  Reprod Sci     Publication Date:  2013 Aug 
Date Detail:
Created Date:  2013-07-17     Completed Date:  2014-01-09     Revised Date:  2014-08-05    
Medline Journal Info:
Nlm Unique ID:  101291249     Medline TA:  Reprod Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  957-67     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Amnion / metabolism*
Cells, Cultured
Cyclooxygenase 2 / genetics,  metabolism
Dinoprost / metabolism
Dinoprostone / metabolism
Down-Regulation
Female
Humans
Inflammation Mediators / metabolism
Intercellular Signaling Peptides and Proteins / genetics,  metabolism*
Interleukin-1beta / genetics,  metabolism
Interleukin-6 / genetics,  metabolism
Interleukin-8 / genetics,  metabolism
Matrix Metalloproteinase 9 / genetics,  metabolism
Placenta / metabolism
Pregnancy
Premature Birth / genetics,  metabolism*
RNA Interference
RNA, Messenger / metabolism
Receptors, G-Protein-Coupled / metabolism
Signal Transduction
Term Birth / genetics,  metabolism*
Transfection
Chemical
Reg. No./Substance:
0/APLN protein, human; 0/APLNR protein, human; 0/IL6 protein, human; 0/IL8 protein, human; 0/Inflammation Mediators; 0/Intercellular Signaling Peptides and Proteins; 0/Interleukin-1beta; 0/Interleukin-6; 0/Interleukin-8; 0/RNA, Messenger; 0/Receptors, G-Protein-Coupled; B7IN85G1HY/Dinoprost; EC 1.14.99.1/Cyclooxygenase 2; EC 1.14.99.1/PTGS2 protein, human; EC 3.4.24.35/MMP9 protein, human; EC 3.4.24.35/Matrix Metalloproteinase 9; K7Q1JQR04M/Dinoprostone
Comments/Corrections

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


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