Talk:Implantation microRNA
| About Discussion Pages |
|---|
Glossary Links
Cite this page: Hill, M.A. (2026, October 2) Embryology Implantation microRNA. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Implantation_microRNA |
2016
Inflammatory gene networks in term human decidual cells define a potential signature for cytokine-mediated parturition
Am J Obstet Gynecol. 2016 Feb;214(2):284.e1-284.e47. doi: 10.1016/j.ajog.2015.08.075. Epub 2015 Sep 5.
Ibrahim SA1, Ackerman WE 4th1, Summerfield TL1, Lockwood CJ1, Schatz F1, Kniss DA2.
Abstract
BACKGROUND: Inflammation is a proximate mediator of preterm birth and fetal injury. During inflammation several microRNAs (22 nucleotide noncoding ribonucleic acid (RNA) molecules) are up-regulated in response to cytokines such as interleukin-1β. MicroRNAs, in most cases, fine-tune gene expression, including both up-regulation and down-regulation of their target genes. However, the role of pro- and antiinflammatory microRNAs in this process is poorly understood. OBJECTIVE: The principal goal of the work was to examine the inflammatory genomic profile of human decidual cells challenged with a proinflammatory cytokine known to be present in the setting of preterm parturition. We determined the coding (messenger RNA) and noncoding (microRNA) sequences to construct a network of interacting genes during inflammation using an in vitro model of decidual stromal cells. STUDY DESIGN: The effects of interleukin-1β exposure on mature microRNA expression were tested in human decidual cell cultures using the multiplexed NanoString platform, whereas the global inflammatory transcriptional response was measured using oligonucleotide microarrays. Differential expression of select transcripts was confirmed by quantitative real time-polymerase chain reaction. Bioinformatics tools were used to infer transcription factor activation and regulatory interactions. RESULTS: Interleukin-1β elicited up- and down-regulation of 350 and 78 nonredundant transcripts (false discovery rate < 0.1), respectively, including induction of numerous cytokines, chemokines, and other inflammatory mediators. Whereas this transcriptional response included marked changes in several microRNA gene loci, the pool of fully processed, mature microRNA was comparatively stable following a cytokine challenge. Of a total of 6 mature microRNAs identified as being differentially expressed by NanoString profiling, 2 (miR-146a and miR-155) were validated by quantitative real time-polymerase chain reaction. Using complementary bioinformatics approaches, activation of several inflammatory transcription factors could be inferred downstream of interleukin-1β based on the overall transcriptional response. Further analysis revealed that miR-146a and miR-155 both target genes involved in inflammatory signaling, including Toll-like receptor and mitogen-activated protein kinase pathways. CONCLUSION: Stimulation of decidual cells with interleukin-1β alters the expression of microRNAs that function to temper proinflammatory signaling. In this setting, some microRNAs may be involved in tissue-level inflammation during the bulk of gestation and assist in pregnancy maintenance. Copyright © 2016 Elsevier Inc. All rights reserved. KEYWORDS: inflammation; microribonucleic acid; preterm birth; systems biology; transcription factor
PMID 26348374
- Stimulation of decidual cells with interleukin-1β alters the expression of transcripts and microRNAs
- Microarray profiling of cultured decidual cells challenged with IL-1β for 6 hours revealed an up-regulation of 448 and a down-regulation of 116 transcript clusters (350 and 78 nonredundant transcripts, respectively)
- highly up-regulated transcripts were numerous proinflammatory cytokines (eg, IL-1A, IL-6, and tumor necrosis factor); leukoattractants (including 8 chemokine ligand chemokines and 6 cysteine-cysteine chemokines); interferon-inducible genes (eg, MX1, GBP1, OAS2, and IFI44); inducible prostaglandin-synthesizing enzymes (eg, prostaglandin-endoperoxide synthase 2 and prostaglandin E synthase); and matrix metalloproteinases (e.g., MMP1, MMP3, and MMP12).
- microRNAs dampen gene expression. and In addition, some miRNAs target mRNAs whose gene products exert inhibitory activity, and in this case, these miRNAs may actually enhance expression of small subsets of genes. More than 2500 unique mature human miRNAs have been identified, each with the ability to regulate the expression of potentially hundreds of genes.
- microarray data set, transcript clusters associated with 15 miRNAs and 4 long, noncoding RNAs (lncRNAs) were up-regulated by at least ±1.5-fold (false discovery rate < 0.1), whereas those corresponding to 9 miRNAs and 3 lncRNAs were down-regulated.
- Up-regulated - MiRNA 147b
MiRNA 3142 MiRNA 146a MiRNA 155, MIR155 host gene (nonprotein coding) Long intergenic nonprotein coding RNA 944 Long intergenic nonprotein coding RNA 473 Long intergenic nonprotein coding RNA 1137 MiRNA 4632 MiRNA 154 MiRNA 3182 MiRNA 4683 MiRNA 1185-1 MiRNA 645 Long intergenic nonprotein coding RNA 312 MiRNA 889 MiRNA 3614 MiRNA 299 MiRNA 4751 MiRNA 1246
- Down-regulated
MiRNA 4680 MiRNA 452, miRNA 224 MiRNA 622 MiRNA 196b Long intergenic nonprotein coding RNA 339 Long intergenic nonprotein coding RNA 478 MiRNA 143, miRNA 145, MIR143 host gene (nonprotein coding) MiRNA 424 MiRNA 503 Long intergenic nonprotein coding RNA 1085
2012
miRNA signature and Dicer requirement during human endometrial stromal decidualization in vitro
PLoS One. 2012;7(7):e41080. doi: 10.1371/journal.pone.0041080. Epub 2012 Jul 20.
Estella C1, Herrer I, Moreno-Moya JM, Quiñonero A, Martínez S, Pellicer A, Simón C.
Abstract
Decidualization is a morphological and biochemical transformation of endometrial stromal fibroblast into differentiated decidual cells, which is critical for embryo implantation and pregnancy establishment. The complex regulatory networks have been elucidated at both the transcriptome and the proteome levels, however very little is known about the post-transcriptional regulation of this process. miRNAs regulate multiple physiological pathways and their de-regulation is associated with human disorders including gynaecological conditions such as endometriosis and preeclampsia. In this study we profile the miRNAs expression throughout human endometrial stromal (hESCs) decidualization and analyze the requirement of the miRNA biogenesis enzyme Dicer during this process. A total of 26 miRNAs were upregulated and 17 miRNAs downregulated in decidualized hESCs compared to non-decidualized hESCs. Three miRNAs families, miR-181, miR-183 and miR-200, are down-regulated during the decidualization process. Using miRNAs target prediction algorithms we have identified the potential targets and pathways regulated by these miRNAs. The knockdown of Dicer has a minor effect on hESCs during in vitro decidualization. We have analyzed a battery of decidualization markers such as cell morphology, Prolactin, IGFBP-1, MPIF-1 and TIMP-3 secretion as well as HOXA10, COX2, SP1, C/EBPß and FOXO1 expression in decidualized hESCs with decreased Dicer function. We found decreased levels of HOXA10 and altered intracellular organization of actin filaments in Dicer knockdown decidualized hESCs compared to control. Our results provide the miRNA signature of hESC during the decidualization process in vitro. We also provide the first functional characterization of Dicer during human endometrial decidualization although surprisingly we found that Dicer plays a minor role regulating this process suggesting that alternative biogenesis miRNAs pathways must be involved in human endometrial decidualization. PMID 22911744
