PMID- 27176145
OWN - NLM
STAT- MEDLINE
DCOM- 20170808
LR  - 20181202
IS  - 1473-5598 (Electronic)
IS  - 0263-6352 (Linking)
VI  - 34
IP  - 7
DP  - 2016 Jul
TI  - MiR-195 participates in the placental disorder of preeclampsia via targeting 
      activin receptor type-2B in trophoblastic cells.
PG  - 1371-9
LID - 10.1097/HJH.0000000000000948 [doi]
AB  - OBJECTIVE: Preeclampsia is a pregnancy-related syndrome. Shallow invasion of 
      uterine wall by trophoblast cells has been generally accepted as the major 
      pathological change of this disorder. We previously found downregulation of 
      miR-195 in preeclamptic placentas. Bioinformatic analysis predicted a type II 
      activin receptor, activin receptor type-2B (ActRIIB), as one of the potential 
      targets of miR-195. Considering the key function of activin A on trophoblast cell 
      behaviors and placenta development, we proposed miR-195 may affect trophoblast 
      cell invasion by repressing the expression of ActRIIB. METHODS: The 
      colocalization of ActRIIB and miR-195 in human placenta was measured by in-situ 
      hybridization and immunohistochemistry. Western blotting, real-time PCR and dual 
      luciferase assay were performed in human trophoblast cell line, HTR8/SVneo cells, 
      to validate the targeting of ActRIIB by miR-195. Cell invasiveness was analyzed 
      using transwell insert invasion assay in HTR8/SVneo cells. RESULTS: In human 
      placenta, ActRIIB and miR-195 exhibited similar localization in various subtypes 
      of trophoblast cells, including villous and extravillous trophoblasts. The 
      protein expressions of ActRIIB in preeclamptic placenta were significantly higher 
      as compared with the normal controls, which was opposite to the changing pattern 
      of miR-195. In HTR8/SVneo cells, miR-195 could directly target and suppress the 
      expression of ActRIIB. Meanwhile, the invasion-promoting effect of miR-195 on 
      trophoblast cells could be largely impeded by ActRIIB overexpression. CONCLUSION: 
      In human trophoblast cells, miR-195 could promote cell invasion via directly 
      targeting ActRIIB. The impaired miR-195 expression may contribute to the 
      occurrence or development of preeclampsia through interfering with activin/nodal 
      signaling in the placenta.
FAU - Wu, Hairong
AU  - Wu H
AD  - aDepartment of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical 
      University, Guangzhou bDepartment of Obstetric and Gynecology, Aviation General 
      Hospital of China Medical University and Beijing Institute of Translational 
      Medicine cState Key Laboratory of Stem Cell and Reproductive Biology, Institute 
      of Zoology, Chinese Academy of Sciences dUniversity of Chinese Academy of 
      Sciences, Beijing, China eDepartment of Biology, York University, Toronto, 
      Ontario, Canada *HWu and HWang contributed equally to the writing of this 
      article.
FAU - Wang, Hao
AU  - Wang H
FAU - Liu, Ming
AU  - Liu M
FAU - Bai, Yang
AU  - Bai Y
FAU - Li, Yu-Xia
AU  - Li YX
FAU - Ji, Lei
AU  - Ji L
FAU - Peng, Chun
AU  - Peng C
FAU - Yu, Yanhong
AU  - Yu Y
FAU - Wang, Yan-Ling
AU  - Wang YL
LA  - eng
PT  - Journal Article
PL  - Netherlands
TA  - J Hypertens
JT  - Journal of hypertension
JID - 8306882
RN  - 0 (MIRN195 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - EC 2.7.11.30 (Activin Receptors, Type II)
RN  - EC 2.7.11.30 (activin receptor type II-B)
SB  - IM
MH  - Activin Receptors, Type II/analysis/genetics/*metabolism
MH  - Adult
MH  - Case-Control Studies
MH  - Cell Line
MH  - *Cell Movement
MH  - Female
MH  - Humans
MH  - In Situ Hybridization
MH  - MicroRNAs/analysis/genetics/*metabolism
MH  - Placenta/chemistry/*metabolism
MH  - Pre-Eclampsia/genetics/*metabolism
MH  - Pregnancy
MH  - Trophoblasts/*physiology
EDAT- 2016/05/14 06:00
MHDA- 2017/08/09 06:00
CRDT- 2016/05/14 06:00
PHST- 2016/05/14 06:00 [entrez]
PHST- 2016/05/14 06:00 [pubmed]
PHST- 2017/08/09 06:00 [medline]
AID - 10.1097/HJH.0000000000000948 [doi]
PST - ppublish
SO  - J Hypertens. 2016 Jul;34(7):1371-9. doi: 10.1097/HJH.0000000000000948.