Document Detail


Prevention of inflammation-associated preterm birth by knockdown of the endothelin-1-matrix metalloproteinase-1 pathway.
MedLine Citation:
PMID:  20809048     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Premature delivery occurs in 12% of all births, accounts for nearly half of neonatal morbidity and is increasing in frequency. Current therapeutic approaches to preterm delivery are ineffective and present serious risks to both the mother and fetus. Although there are multiple factors that contribute to the etiology of preterm birth, the single most common cause is infection. Recently, using cDNA microarray analysis of human placental tissue, we demonstrated that human placental matrix metalloproteinase-1 (MMP-1) is upregulated during labor. In a separate line of investigation, we have shown that blockade of endothelin-1 (ET-1) action through the use of an endothelin-converting enzyme-1 (ECE-1) inhibitor, an established commercially available endothelin receptor antagonist or a novel quinolone-derived endothelin receptor antagonist synthesized by our group also prevents preterm labor and delivery in a mouse model. We have now shown that induction of preterm labor with lipopolysaccharide in our mouse model is associated with increased levels of MMP-1. Furthermore, we showed that silencing the ECE-1/ET-1 pathway by using ECE-1 RNA interference prevents both the onset of preterm labor and upregulation of MMP-1. The data indicate that ET-1 and MMP-1 act in the same molecular pathway in preterm labor.
Authors:
Wei Wang; Haoting Yen; Chih-Hung Chen; Nitesh Jasani; Rimabahen Soni; Karen Koscica; Sandra E Reznik
Related Documents :
1372508 - Premature rupture of the membranes: effect of penicillin prophylaxis and long-term outc...
8238158 - The efficacy of oral terbutaline after intravenous tocolysis.
11561908 - The epidemiology of preterm labor.
2496208 - Prostaglandins, inflammation, and preterm labor.
23562958 - Associations of prenatal exposure to phenols with birth outcomes.
1519138 - The proposed death certificate for south africa. part i. death certificate description.
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-08-18
Journal Detail:
Title:  Molecular medicine (Cambridge, Mass.)     Volume:  16     ISSN:  1528-3658     ISO Abbreviation:  Mol. Med.     Publication Date:    2010 Nov-Dec
Date Detail:
Created Date:  2010-11-05     Completed Date:  2011-02-17     Revised Date:  2013-05-28    
Medline Journal Info:
Nlm Unique ID:  9501023     Medline TA:  Mol Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  505-12     Citation Subset:  IM    
Affiliation:
Department of Pharmaceutical Sciences, College of Pharmacy and Allied Health Professions, St. John's University, Jamaica, New York, United States of America.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Aspartic Acid Endopeptidases / antagonists & inhibitors,  metabolism*
Endothelin-1 / antagonists & inhibitors,  metabolism
Female
Gene Knockdown Techniques
Inflammation / prevention & control*
Matrix Metalloproteinase 13 / metabolism
Metalloendopeptidases / antagonists & inhibitors,  metabolism*
Mice
Mice, Inbred C57BL
Models, Animal
Obstetric Labor, Premature
Placenta / metabolism
Pregnancy
Premature Birth / prevention & control*
RNA Interference*
Tocolysis
Uterus / metabolism
Grant Support
ID/Acronym/Agency:
1K08HD1209/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/Endothelin-1; EC 3.4.23.-/Aspartic Acid Endopeptidases; EC 3.4.24.-/Matrix Metalloproteinase 13; EC 3.4.24.-/Metalloendopeptidases; EC 3.4.24.-/Mmp13 protein, mouse; EC 3.4.24.71/endothelin-converting enzyme
Comments/Corrections

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


Previous Document:  A longitudinal, integrated, clinical, histological and mRNA profiling study of resistance exercise i...
Next Document:  Phosphorylation of extracellular signal-regulated kinase (ERK)-1/2 Is associated with the downregula...