Document Detail


MIR-210 modulates mitochondrial respiration in placenta with preeclampsia.
MedLine Citation:
PMID:  22840297     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Preeclampsia (PE) affects 5-8% of all pregnancies and is associated with significant maternal and fetal morbidity and mortality. Placental mitochondrial dysfunction has been reported in PE. MicroRNAs (miRNA) are small non-coding RNAs that regulate gene expression through mRNA degradation and translational repression. MiR-210 has been previously shown to be upregulated in placentas from pregnancies complicated by PE. We hypothesized that placental mitochondrial dysfunction during PE can be mediated by miR-210. Placentas were collected at term from normotensive pregnancies (CTRL) and those complicated by severe PE (n = 6 each) following c-section (no labor). Villous tissue from PE showed significantly increased levels of HIF-1α compared to CTRL with no change in corresponding mRNA expression but with reduced DNA-binding activity. Mitochondrial complex III was significantly decreased in PE along with significantly reduced protein expression in complex I and IV during PE. Among the four miRNAs tested, miR-210 showed significant up regulation in PE and significant downregulation of its target, ISCU mRNA. To understand the role of miR-210 in PE, loss- and gain-of-function studies were performed using primary trophoblasts. Trophoblasts were transfected with miR-210 inhibitor or pre-miR-210 and mitochondrial function was measured using Seahorse Extracellular Flux Analyzer. Cells transfected with pre-miR-210 showed significant reduction in oxygen consumption. In contrast, transfection of trophoblast with AntagomiR-210 was sufficient to prevent the DFO-mediated respiratory deficiency. These data collectively suggest that miR-210 overexpression during PE could be responsible for placental mitochondria dysfunction.
Authors:
S Muralimanoharan; A Maloyan; J Mele; C Guo; L G Myatt; L Myatt
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-07-26
Journal Detail:
Title:  Placenta     Volume:  33     ISSN:  1532-3102     ISO Abbreviation:  Placenta     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-09-11     Completed Date:  2013-01-25     Revised Date:  2013-10-17    
Medline Journal Info:
Nlm Unique ID:  8006349     Medline TA:  Placenta     Country:  England    
Other Details:
Languages:  eng     Pagination:  816-23     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Elsevier Ltd. All rights reserved.
Affiliation:
Center for Pregnancy and Newborn Research, Dept of Ob-Gyn, University of Texas Health Science Center, San Antonio, TX 78229, USA. muralimanoha@uthscsa.edu
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MeSH Terms
Descriptor/Qualifier:
Adult
Down-Regulation
Electron Transport Complex I / metabolism
Electron Transport Complex III / metabolism
Electron Transport Complex IV / metabolism
Female
Humans
Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
MicroRNAs / physiology*
Mitochondria / metabolism*
Placenta / physiopathology*
Pre-Eclampsia / physiopathology*
Pregnancy
Grant Support
ID/Acronym/Agency:
HL075297/HL/NHLBI NIH HHS; R01 HL075297/HL/NHLBI NIH HHS; UL1 RR025767/RR/NCRR NIH HHS; UL1 TR000149/TR/NCATS NIH HHS; UL1RR025767/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Hypoxia-Inducible Factor 1, alpha Subunit; 0/MIRN210 microRNA, human; 0/MicroRNAs; EC 1.10.2.2/Electron Transport Complex III; EC 1.6.5.3/Electron Transport Complex I; EC 1.9.3.1/Electron Transport Complex IV
Comments/Corrections

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


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