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TLR3‐induced expression patterns of human placental microRNAs (LB705)
Author(s) -
Jamison Ashley,
Jupiter Daniel,
Chatterjee Piyali
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.lb705
Subject(s) - ctbs , microrna , preeclampsia , placenta , andrology , gene expression , microarray , downregulation and upregulation , biology , medicine , bioinformatics , cancer research , pregnancy , gene , receptor , genetics , fetus , metaplasticity , synaptic plasticity
OBJECTIVE: Preeclampsia (PE) is a pregnancy‐specific hypertensive disorder that affects 5‐8% of women worldwide. The placenta is considered to be the main culprit as symptoms of PE typically reduce following delivery of the placenta. This study was designed to determine the effects of TLR3 activation on placental miRNA expression and whether these miRs are associated with PE in women. METHODS: Microarray for miRNAs was performed in human cytotrophoblasts (CTBs) treated with poly I:C for 24 hour and compared with vehicle‐treated CTBs. The expression of 10 miRNAs (5 upregulated and 5 downregulated) were confirmed by qRT‐PCR. Formalin fixed paraffin embedded placental tissues were obtained from patients with PE (n= 9‐11) and normal pregnant women (n = 6‐8) and the expression of these miRNAs were assessed by qPCR. RESULTS: Both human CTBs treated with poly I:C and placentas of PE women exhibited increased expression of miR‐155 and miR‐125a‐5p and decreased expression of miR‐575, miR‐149*, and miR‐145. Gene Ontology analysis of the target genes using miRTarBase revealed enrichment for specific biological process categories (chromatin binding and cell death: miR‐155; cell cycle and proliferation: miR‐145). CONCLUSIONS: Here we demonstrate that alterations in the expression of specific miRNAs induced by TLR3 activation in CTB were also observed in PE women. These data provide novel targets for further investigation into the pathophysiology of PE. Grant Funding Source : 13SDG14630018