Downregulated miR-195 Detected in Preeclamptic Placenta Affects Trophoblast Cell Invasion via Modulating ActRIIA Expression

Preeclampsia (PE) is a pregnancy-specific syndrome manifested by on-set of hypertension and proteinuria after 20 weeks of gestation. Abnormal placenta development has been generally accepted as initial cause of the disorder. Recently, miR-195 was found to be down-regulated in preeclamptic placentas...

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Published inPloS one Vol. 7; no. 6; p. e38875
Main Authors Bai, Yang, Yang, Weiwei, Yang, Hui-xia, Liao, Qinping, Ye, Gang, Fu, Guodong, Ji, Lei, Xu, Peng, Wang, Hao, Li, Yu-xia, Peng, Chun, Wang, Yan-ling
Format Journal Article
LanguageEnglish
Published United States Public Library of Science 19.06.2012
Public Library of Science (PLoS)
Subjects
Aberration
Activin
Activin Receptors, Type II - genetics
Activin Receptors, Type II - metabolism
Adult
Angiogenesis
Assaying
Biology
Blood pressure
Breast cancer
Cell cycle
Cell Line
Comparative analysis
Cyclin D1 - genetics
Cyclin D1 - metabolism
Cyclin D3 - genetics
Cyclin D3 - metabolism
Epigenetics
Evolutionary biology
Female
Gene Expression
Gene Expression Regulation
Genes
Gestation
Gynecology
Humans
Hypertension
Laboratories
Medicine
MicroRNAs
MicroRNAs - genetics
Obstetrics
Pathogenesis
Placenta
Placenta - metabolism
Placenta - pathology
Pre-eclampsia
Pre-Eclampsia - genetics
Preeclampsia
Pregnancy
Pregnant women
Proteinuria
Ribonucleic acid
RNA
Signal transduction
Signaling
Tissues
Trophoblasts - metabolism
Trophoblasts - pathology
Western blotting
Young Adult
Zoology
Beijing China
China
Online AccessGet full text

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Abstract Preeclampsia (PE) is a pregnancy-specific syndrome manifested by on-set of hypertension and proteinuria after 20 weeks of gestation. Abnormal placenta development has been generally accepted as initial cause of the disorder. Recently, miR-195 was found to be down-regulated in preeclamptic placentas compared with normal pregnant ones, indicating possible association of this small molecule with placental pathology of preeclampsia. By far the function of miR-195 in the development of placenta remains unknown. Bioinformatic assay predicted ActRIIA as one of the targets for miR-195. By using Real-time PCR, Western blotting and Dual Luciferase Assay, we validated that ActRIIA was the direct target of miR-195 in human trophoblast cells. Transwell insert invasion assay showed that miR-195 could promote cell invasion in trophoblast cell line, HTR8/SVneo cells, and the effect could be abrogated by overexpressed ActRIIA. In preeclamptic placenta tissues, pri-miR-195 and mature miR-195 expressions were down-regulated, whereas ActRIIA level appeared to be increased when compared with that in gestational-week-matched normal placentas. This is the first report on the function of miR-195 in human placental trophoblast cells which reveals an invasion-promoting effect of the small RNA via repressing ActRIIA. Aberrant expression of miR-195 may contribute to the occurrence of preeclampsia through interfering with Activin/Nodal signaling mediated by ActRIIA in human placenta.
AbstractList Background Preeclampsia (PE) is a pregnancy-specific syndrome manifested by on-set of hypertension and proteinuria after 20 weeks of gestation. Abnormal placenta development has been generally accepted as initial cause of the disorder. Recently, miR-195 was found to be down-regulated in preeclamptic placentas compared with normal pregnant ones, indicating possible association of this small molecule with placental pathology of preeclampsia. By far the function of miR-195 in the development of placenta remains unknown. Methodology/Principal Findings Bioinformatic assay predicted ActRIIA as one of the targets for miR-195. By using Real-time PCR, Western blotting and Dual Luciferase Assay, we validated that ActRIIA was the direct target of miR-195 in human trophoblast cells. Transwell insert invasion assay showed that miR-195 could promote cell invasion in trophoblast cell line, HTR8/SVneo cells, and the effect could be abrogated by overexpressed ActRIIA. In preeclamptic placenta tissues, pri-miR-195 and mature miR-195 expressions were down-regulated, whereas ActRIIA level appeared to be increased when compared with that in gestational-week-matched normal placentas. Conclusions/Significance This is the first report on the function of miR-195 in human placental trophoblast cells which reveals an invasion-promoting effect of the small RNA via repressing ActRIIA. Aberrant expression of miR-195 may contribute to the occurrence of preeclampsia through interfering with Activin/Nodal signaling mediated by ActRIIA in human placenta.
Preeclampsia (PE) is a pregnancy-specific syndrome manifested by on-set of hypertension and proteinuria after 20 weeks of gestation. Abnormal placenta development has been generally accepted as initial cause of the disorder. Recently, miR-195 was found to be down-regulated in preeclamptic placentas compared with normal pregnant ones, indicating possible association of this small molecule with placental pathology of preeclampsia. By far the function of miR-195 in the development of placenta remains unknown.BACKGROUNDPreeclampsia (PE) is a pregnancy-specific syndrome manifested by on-set of hypertension and proteinuria after 20 weeks of gestation. Abnormal placenta development has been generally accepted as initial cause of the disorder. Recently, miR-195 was found to be down-regulated in preeclamptic placentas compared with normal pregnant ones, indicating possible association of this small molecule with placental pathology of preeclampsia. By far the function of miR-195 in the development of placenta remains unknown.Bioinformatic assay predicted ActRIIA as one of the targets for miR-195. By using Real-time PCR, Western blotting and Dual Luciferase Assay, we validated that ActRIIA was the direct target of miR-195 in human trophoblast cells. Transwell insert invasion assay showed that miR-195 could promote cell invasion in trophoblast cell line, HTR8/SVneo cells, and the effect could be abrogated by overexpressed ActRIIA. In preeclamptic placenta tissues, pri-miR-195 and mature miR-195 expressions were down-regulated, whereas ActRIIA level appeared to be increased when compared with that in gestational-week-matched normal placentas.METHODOLOGY/PRINCIPAL FINDINGSBioinformatic assay predicted ActRIIA as one of the targets for miR-195. By using Real-time PCR, Western blotting and Dual Luciferase Assay, we validated that ActRIIA was the direct target of miR-195 in human trophoblast cells. Transwell insert invasion assay showed that miR-195 could promote cell invasion in trophoblast cell line, HTR8/SVneo cells, and the effect could be abrogated by overexpressed ActRIIA. In preeclamptic placenta tissues, pri-miR-195 and mature miR-195 expressions were down-regulated, whereas ActRIIA level appeared to be increased when compared with that in gestational-week-matched normal placentas.This is the first report on the function of miR-195 in human placental trophoblast cells which reveals an invasion-promoting effect of the small RNA via repressing ActRIIA. Aberrant expression of miR-195 may contribute to the occurrence of preeclampsia through interfering with Activin/Nodal signaling mediated by ActRIIA in human placenta.CONCLUSIONS/SIGNIFICANCEThis is the first report on the function of miR-195 in human placental trophoblast cells which reveals an invasion-promoting effect of the small RNA via repressing ActRIIA. Aberrant expression of miR-195 may contribute to the occurrence of preeclampsia through interfering with Activin/Nodal signaling mediated by ActRIIA in human placenta.
Preeclampsia (PE) is a pregnancy-specific syndrome manifested by on-set of hypertension and proteinuria after 20 weeks of gestation. Abnormal placenta development has been generally accepted as initial cause of the disorder. Recently, miR-195 was found to be down-regulated in preeclamptic placentas compared with normal pregnant ones, indicating possible association of this small molecule with placental pathology of preeclampsia. By far the function of miR-195 in the development of placenta remains unknown. Bioinformatic assay predicted ActRIIA as one of the targets for miR-195. By using Real-time PCR, Western blotting and Dual Luciferase Assay, we validated that ActRIIA was the direct target of miR-195 in human trophoblast cells. Transwell insert invasion assay showed that miR-195 could promote cell invasion in trophoblast cell line, HTR8/SVneo cells, and the effect could be abrogated by overexpressed ActRIIA. In preeclamptic placenta tissues, pri-miR-195 and mature miR-195 expressions were down-regulated, whereas ActRIIA level appeared to be increased when compared with that in gestational-week-matched normal placentas. This is the first report on the function of miR-195 in human placental trophoblast cells which reveals an invasion-promoting effect of the small RNA via repressing ActRIIA. Aberrant expression of miR-195 may contribute to the occurrence of preeclampsia through interfering with Activin/Nodal signaling mediated by ActRIIA in human placenta.
Background Preeclampsia (PE) is a pregnancy-specific syndrome manifested by on-set of hypertension and proteinuria after 20 weeks of gestation. Abnormal placenta development has been generally accepted as initial cause of the disorder. Recently, miR-195 was found to be down-regulated in preeclamptic placentas compared with normal pregnant ones, indicating possible association of this small molecule with placental pathology of preeclampsia. By far the function of miR-195 in the development of placenta remains unknown. Methodology/Principal Findings Bioinformatic assay predicted ActRIIA as one of the targets for miR-195. By using Real-time PCR, Western blotting and Dual Luciferase Assay, we validated that ActRIIA was the direct target of miR-195 in human trophoblast cells. Transwell insert invasion assay showed that miR-195 could promote cell invasion in trophoblast cell line, HTR8/SVneo cells, and the effect could be abrogated by overexpressed ActRIIA. In preeclamptic placenta tissues, pri-miR-195 and mature miR-195 expressions were down-regulated, whereas ActRIIA level appeared to be increased when compared with that in gestational-week-matched normal placentas. Conclusions/Significance This is the first report on the function of miR-195 in human placental trophoblast cells which reveals an invasion-promoting effect of the small RNA via repressing ActRIIA. Aberrant expression of miR-195 may contribute to the occurrence of preeclampsia through interfering with Activin/Nodal signaling mediated by ActRIIA in human placenta.
Preeclampsia (PE) is a pregnancy-specific syndrome manifested by on-set of hypertension and proteinuria after 20 weeks of gestation. Abnormal placenta development has been generally accepted as initial cause of the disorder. Recently, miR-195 was found to be down-regulated in preeclamptic placentas compared with normal pregnant ones, indicating possible association of this small molecule with placental pathology of preeclampsia. By far the function of miR-195 in the development of placenta remains unknown. Bioinformatic assay predicted ActRIIA as one of the targets for miR-195. By using Real-time PCR, Western blotting and Dual Luciferase Assay, we validated that ActRIIA was the direct target of miR-195 in human trophoblast cells. Transwell insert invasion assay showed that miR-195 could promote cell invasion in trophoblast cell line, HTR8/SVneo cells, and the effect could be abrogated by overexpressed ActRIIA. In preeclamptic placenta tissues, pri-miR-195 and mature miR-195 expressions were down-regulated, whereas ActRIIA level appeared to be increased when compared with that in gestational-week-matched normal placentas. This is the first report on the function of miR-195 in human placental trophoblast cells which reveals an invasion-promoting effect of the small RNA via repressing ActRIIA. Aberrant expression of miR-195 may contribute to the occurrence of preeclampsia through interfering with Activin/Nodal signaling mediated by ActRIIA in human placenta.
Audience Academic
Author Li, Yu-xia
Xu, Peng
Ye, Gang
Yang, Weiwei
Yang, Hui-xia
Wang, Yan-ling
Bai, Yang
Ji, Lei
Liao, Qinping
Fu, Guodong
Peng, Chun
Wang, Hao
AuthorAffiliation Fudan University, China
3 Department of Biology, York University, Toronto, Ontario, Canada
4 Graduate School of Chinese Academy of Sciences, Beijing, China
2 Department of Obstetrics and Gynecology, Peking University First Hospital, Beijing, China
1 State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China
AuthorAffiliation_xml – name: 1 State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China
– name: 2 Department of Obstetrics and Gynecology, Peking University First Hospital, Beijing, China
– name: Fudan University, China
– name: 4 Graduate School of Chinese Academy of Sciences, Beijing, China
– name: 3 Department of Biology, York University, Toronto, Ontario, Canada
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  givenname: Yang
  surname: Bai
  fullname: Bai, Yang
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  givenname: Weiwei
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/22723898$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright COPYRIGHT 2012 Public Library of Science
2012 Bai et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
Bai et al. 2012
Copyright_xml – notice: COPYRIGHT 2012 Public Library of Science
– notice: 2012 Bai et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
– notice: Bai et al. 2012
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Conceived and designed the experiments: YB CP YLW. Performed the experiments: YB GY GF HW. Analyzed the data: YB WY LJ PX CP YLW. Contributed reagents/materials/analysis tools: HY QL GY GF YL. Wrote the paper: YB YLW.
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Snippet Preeclampsia (PE) is a pregnancy-specific syndrome manifested by on-set of hypertension and proteinuria after 20 weeks of gestation. Abnormal placenta...
Background Preeclampsia (PE) is a pregnancy-specific syndrome manifested by on-set of hypertension and proteinuria after 20 weeks of gestation. Abnormal...
Background Preeclampsia (PE) is a pregnancy-specific syndrome manifested by on-set of hypertension and proteinuria after 20 weeks of gestation. Abnormal...
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StartPage e38875
SubjectTerms Aberration
Activin
Activin Receptors, Type II - genetics
Activin Receptors, Type II - metabolism
Adult
Angiogenesis
Assaying
Biology
Blood pressure
Breast cancer
Cell cycle
Cell Line
Comparative analysis
Cyclin D1 - genetics
Cyclin D1 - metabolism
Cyclin D3 - genetics
Cyclin D3 - metabolism
Epigenetics
Evolutionary biology
Female
Gene Expression
Gene Expression Regulation
Genes
Gestation
Gynecology
Humans
Hypertension
Laboratories
Medicine
MicroRNAs
MicroRNAs - genetics
Obstetrics
Pathogenesis
Placenta
Placenta - metabolism
Placenta - pathology
Pre-eclampsia
Pre-Eclampsia - genetics
Preeclampsia
Pregnancy
Pregnant women
Proteinuria
Ribonucleic acid
RNA
Signal transduction
Signaling
Tissues
Trophoblasts - metabolism
Trophoblasts - pathology
Western blotting
Young Adult
Zoology
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Title Downregulated miR-195 Detected in Preeclamptic Placenta Affects Trophoblast Cell Invasion via Modulating ActRIIA Expression
URI https://www.ncbi.nlm.nih.gov/pubmed/22723898
https://www.proquest.com/docview/1326187235
https://www.proquest.com/docview/1021982304
https://pubmed.ncbi.nlm.nih.gov/PMC3378540
https://doaj.org/article/3da0d25526464329b4cedd123c302745
http://dx.doi.org/10.1371/journal.pone.0038875
Volume 7
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