Endothelin-1 down-regulates matrix metalloproteinase 14 and 15 expression in human first trimester trophoblasts via endothelin receptor type B

STUDY QUESTION Does endothelin-1 (ET-1) regulate matrix metalloproteinase (MMP) 14 and 15 production and invasion of human first trimester trophoblasts? SUMMARY ANSWER ET-1 in pathophysiological concentrations down-regulates MMP14 and MMP15 expression via endothelin receptor (ETR) type B and decreas...

Full description

Saved in:
Bibliographic Details
Published in:Human reproduction (Oxford) Vol. 32; no. 1; pp. 46 - 54
Main Authors: Majali-Martinez, Alejandro, Velicky, Philipp, Pollheimer, Jürgen, Knöfler, Martin, Yung, Hong wa, Burton, Graham J., Tabrizi-Wizsy, Nassim Ghaffari, Lang, Uwe, Hiden, Ursula, Desoye, Gernot, Dieber-Rotheneder, Martina
Format: Journal Article
Language:English
Published: England Oxford University Press 01.01.2017
Subjects:
ISSN:0268-1161, 1460-2350
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Abstract STUDY QUESTION Does endothelin-1 (ET-1) regulate matrix metalloproteinase (MMP) 14 and 15 production and invasion of human first trimester trophoblasts? SUMMARY ANSWER ET-1 in pathophysiological concentrations down-regulates MMP14 and MMP15 expression via endothelin receptor (ETR) type B and decreases trophoblast migration and invasion. WHAT IS KNOWN ALREADY MMP14 and MMP15 are involved in trophoblast invasion. Impairment of invasion has been linked to pregnancy complications such as pre-eclampsia (PE). ET-1 is up-regulated in PE. STUDY DESIGN, SIZE, DURATION In vitro study using primary human trophoblasts from 50 first trimester placentas (gestational week 7–12). PARTICIPANTS/MATERIALS, SETTING, METHODS Trophoblasts were cultured in the absence or presence of 10–100 nM ET-1. MMP14 and MMP15 mRNA and protein were quantified by RT-qPCR and Western blotting, respectively. Selective antagonists for ETRA (BQ-123) or ETRB (BQ-788) were used to identify ETR subtypes involved. Functional ET-1 effects were tested in first trimester chorionic villous explants and transwell invasion assays. The roles of tumor necrosis factor (TNF)-α (25 ng/ml) and oxygen (1%) in ET-1 regulation of MMP14 and 15 expression were assessed by Western blotting. MAIN RESULTS AND THE ROLE OF CHANCE ET-1 down-regulated MMP14 and MMP15 mRNA (−21% and −26%, respectively, P < 0.05) and protein levels (–18% and –22%, respectively, P < 0.05). This effect was mediated via ETRB. ET-1 decreased trophoblast outgrowth in placental explants (−24%, P < 0.05) and trophoblast invasion (−26%, P ≤ 0.01). TNF-α enhanced ET-1 mediated MMP15 down-regulation (by 10%, P < 0.05), whereas hypoxia abolished the effect of ET-1 on both MMPs. LARGE SCALE DATA N/A. LIMITATIONS, REASONS FOR CAUTION Only primary trophoblasts were used in this study. Since trophoblast yield from first trimester placental material is limited, further aspects of MMP14 and 15 regulation could not be characterized. Other anti-invasive factors may be altered by ET-1 in trophoblasts and, thus, contribute to the reduced invasion, but have not been investigated. Oxygen levels similar to those found in the decidua (5–8% O2) were not analyzed in this study. WIDER IMPLICATIONS OF THE FINDINGS ET-1 modifies placental function already during the first trimester of pregnancy, the time-window when the placental changes implicated in PE occur. Thus, our results improve the understanding of the placental mechanisms underlying trophoblast invasion and PE. STUDY FUNDING/COMPETING INTEREST(S) The study was funded by the Oesterreichische Nationalbank (Anniversary Fund, project number: 14796) and the Herzfelder'sche Familienstiftung (to J.P.; number: 00685). AMM received funding from the Austrian Science Fund FWF (W1241) and the Medical University Graz through the PhD Program Molecular Fundamentals of Inflammation (DK-MOLIN). The authors have no conflict of interest.
AbstractList Does endothelin-1 (ET-1) regulate matrix metalloproteinase (MMP) 14 and 15 production and invasion of human first trimester trophoblasts? ET-1 in pathophysiological concentrations down-regulates MMP14 and MMP15 expression via endothelin receptor (ETR) type B and decreases trophoblast migration and invasion. MMP14 and MMP15 are involved in trophoblast invasion. Impairment of invasion has been linked to pregnancy complications such as pre-eclampsia (PE). ET-1 is up-regulated in PE. In vitro study using primary human trophoblasts from 50 first trimester placentas (gestational week 7-12). Trophoblasts were cultured in the absence or presence of 10-100 nM ET-1. MMP14 and MMP15 mRNA and protein were quantified by RT-qPCR and Western blotting, respectively. Selective antagonists for ETRA (BQ-123) or ETRB (BQ-788) were used to identify ETR subtypes involved. Functional ET-1 effects were tested in first trimester chorionic villous explants and transwell invasion assays. The roles of tumor necrosis factor (TNF)-α (25 ng/ml) and oxygen (1%) in ET-1 regulation of MMP14 and 15 expression were assessed by Western blotting. ET-1 down-regulated MMP14 and MMP15 mRNA (-21% and -26%, respectively, P < 0.05) and protein levels (-18% and -22%, respectively, P < 0.05). This effect was mediated via ETRB. ET-1 decreased trophoblast outgrowth in placental explants (-24%, P < 0.05) and trophoblast invasion (-26%, P ≤ 0.01). TNF-α enhanced ET-1 mediated MMP15 down-regulation (by 10%, P < 0.05), whereas hypoxia abolished the effect of ET-1 on both MMPs. N/A. Only primary trophoblasts were used in this study. Since trophoblast yield from first trimester placental material is limited, further aspects of MMP14 and 15 regulation could not be characterized. Other anti-invasive factors may be altered by ET-1 in trophoblasts and, thus, contribute to the reduced invasion, but have not been investigated. Oxygen levels similar to those found in the decidua (5-8% O ) were not analyzed in this study. ET-1 modifies placental function already during the first trimester of pregnancy, the time-window when the placental changes implicated in PE occur. Thus, our results improve the understanding of the placental mechanisms underlying trophoblast invasion and PE. The study was funded by the Oesterreichische Nationalbank (Anniversary Fund, project number: 14796) and the Herzfelder'sche Familienstiftung (to J.P.; number: 00685). AMM received funding from the Austrian Science Fund FWF (W1241) and the Medical University Graz through the PhD Program Molecular Fundamentals of Inflammation (DK-MOLIN). The authors have no conflict of interest.
STUDY QUESTIONDoes endothelin-1 (ET-1) regulate matrix metalloproteinase (MMP) 14 and 15 production and invasion of human first trimester trophoblasts?SUMMARY ANSWERET-1 in pathophysiological concentrations down-regulates MMP14 and MMP15 expression via endothelin receptor (ETR) type B and decreases trophoblast migration and invasion.WHAT IS KNOWN ALREADYMMP14 and MMP15 are involved in trophoblast invasion. Impairment of invasion has been linked to pregnancy complications such as pre-eclampsia (PE). ET-1 is up-regulated in PE.STUDY DESIGN, SIZE, DURATIONIn vitro study using primary human trophoblasts from 50 first trimester placentas (gestational week 7-12).PARTICIPANTS/MATERIALS, SETTING, METHODSTrophoblasts were cultured in the absence or presence of 10-100 nM ET-1. MMP14 and MMP15 mRNA and protein were quantified by RT-qPCR and Western blotting, respectively. Selective antagonists for ETRA (BQ-123) or ETRB (BQ-788) were used to identify ETR subtypes involved. Functional ET-1 effects were tested in first trimester chorionic villous explants and transwell invasion assays. The roles of tumor necrosis factor (TNF)-α (25 ng/ml) and oxygen (1%) in ET-1 regulation of MMP14 and 15 expression were assessed by Western blotting.MAIN RESULTS AND THE ROLE OF CHANCEET-1 down-regulated MMP14 and MMP15 mRNA (-21% and -26%, respectively, P < 0.05) and protein levels (-18% and -22%, respectively, P < 0.05). This effect was mediated via ETRB. ET-1 decreased trophoblast outgrowth in placental explants (-24%, P < 0.05) and trophoblast invasion (-26%, P ≤ 0.01). TNF-α enhanced ET-1 mediated MMP15 down-regulation (by 10%, P < 0.05), whereas hypoxia abolished the effect of ET-1 on both MMPs.LARGE SCALE DATAN/A.LIMITATIONS, REASONS FOR CAUTIONOnly primary trophoblasts were used in this study. Since trophoblast yield from first trimester placental material is limited, further aspects of MMP14 and 15 regulation could not be characterized. Other anti-invasive factors may be altered by ET-1 in trophoblasts and, thus, contribute to the reduced invasion, but have not been investigated. Oxygen levels similar to those found in the decidua (5-8% O2) were not analyzed in this study.WIDER IMPLICATIONS OF THE FINDINGSET-1 modifies placental function already during the first trimester of pregnancy, the time-window when the placental changes implicated in PE occur. Thus, our results improve the understanding of the placental mechanisms underlying trophoblast invasion and PE.STUDY FUNDING/COMPETING INTERESTSThe study was funded by the Oesterreichische Nationalbank (Anniversary Fund, project number: 14796) and the Herzfelder'sche Familienstiftung (to J.P.; number: 00685). AMM received funding from the Austrian Science Fund FWF (W1241) and the Medical University Graz through the PhD Program Molecular Fundamentals of Inflammation (DK-MOLIN). The authors have no conflict of interest.
STUDY QUESTION Does endothelin-1 (ET-1) regulate matrix metalloproteinase (MMP) 14 and 15 production and invasion of human first trimester trophoblasts? SUMMARY ANSWER ET-1 in pathophysiological concentrations down-regulates MMP14 and MMP15 expression via endothelin receptor (ETR) type B and decreases trophoblast migration and invasion. WHAT IS KNOWN ALREADY MMP14 and MMP15 are involved in trophoblast invasion. Impairment of invasion has been linked to pregnancy complications such as pre-eclampsia (PE). ET-1 is up-regulated in PE. STUDY DESIGN, SIZE, DURATION In vitro study using primary human trophoblasts from 50 first trimester placentas (gestational week 7–12). PARTICIPANTS/MATERIALS, SETTING, METHODS Trophoblasts were cultured in the absence or presence of 10–100 nM ET-1. MMP14 and MMP15 mRNA and protein were quantified by RT-qPCR and Western blotting, respectively. Selective antagonists for ETRA (BQ-123) or ETRB (BQ-788) were used to identify ETR subtypes involved. Functional ET-1 effects were tested in first trimester chorionic villous explants and transwell invasion assays. The roles of tumor necrosis factor (TNF)-α (25 ng/ml) and oxygen (1%) in ET-1 regulation of MMP14 and 15 expression were assessed by Western blotting. MAIN RESULTS AND THE ROLE OF CHANCE ET-1 down-regulated MMP14 and MMP15 mRNA (−21% and −26%, respectively, P < 0.05) and protein levels (–18% and –22%, respectively, P < 0.05). This effect was mediated via ETRB. ET-1 decreased trophoblast outgrowth in placental explants (−24%, P < 0.05) and trophoblast invasion (−26%, P ≤ 0.01). TNF-α enhanced ET-1 mediated MMP15 down-regulation (by 10%, P < 0.05), whereas hypoxia abolished the effect of ET-1 on both MMPs. LARGE SCALE DATA N/A. LIMITATIONS, REASONS FOR CAUTION Only primary trophoblasts were used in this study. Since trophoblast yield from first trimester placental material is limited, further aspects of MMP14 and 15 regulation could not be characterized. Other anti-invasive factors may be altered by ET-1 in trophoblasts and, thus, contribute to the reduced invasion, but have not been investigated. Oxygen levels similar to those found in the decidua (5–8% O2) were not analyzed in this study. WIDER IMPLICATIONS OF THE FINDINGS ET-1 modifies placental function already during the first trimester of pregnancy, the time-window when the placental changes implicated in PE occur. Thus, our results improve the understanding of the placental mechanisms underlying trophoblast invasion and PE. STUDY FUNDING/COMPETING INTEREST(S) The study was funded by the Oesterreichische Nationalbank (Anniversary Fund, project number: 14796) and the Herzfelder'sche Familienstiftung (to J.P.; number: 00685). AMM received funding from the Austrian Science Fund FWF (W1241) and the Medical University Graz through the PhD Program Molecular Fundamentals of Inflammation (DK-MOLIN). The authors have no conflict of interest.
Author Burton, Graham J.
Knöfler, Martin
Hiden, Ursula
Majali-Martinez, Alejandro
Tabrizi-Wizsy, Nassim Ghaffari
Velicky, Philipp
Pollheimer, Jürgen
Desoye, Gernot
Dieber-Rotheneder, Martina
Yung, Hong wa
Lang, Uwe
Author_xml – sequence: 1
  givenname: Alejandro
  surname: Majali-Martinez
  fullname: Majali-Martinez, Alejandro
  organization: 1 Department of Obstetrics and Gynecology, Medical University of Graz, Auenbruggerplatz 14, Graz 8036, Austria
– sequence: 2
  givenname: Philipp
  surname: Velicky
  fullname: Velicky, Philipp
  organization: 2 Department of Obstetrics and Fetal-Maternal Medicine, Medical University of Vienna, Währinger Gürtel 18-20, Vienna 1090, Austria
– sequence: 3
  givenname: Jürgen
  surname: Pollheimer
  fullname: Pollheimer, Jürgen
  organization: 2 Department of Obstetrics and Fetal-Maternal Medicine, Medical University of Vienna, Währinger Gürtel 18-20, Vienna 1090, Austria
– sequence: 4
  givenname: Martin
  surname: Knöfler
  fullname: Knöfler, Martin
  organization: 2 Department of Obstetrics and Fetal-Maternal Medicine, Medical University of Vienna, Währinger Gürtel 18-20, Vienna 1090, Austria
– sequence: 5
  givenname: Hong wa
  surname: Yung
  fullname: Yung, Hong wa
  organization: 3 Department of Physiology, Development and Neuroscience, Centre for Trophoblast Research,  University of Cambridge, Downing Street, Cambridge CB2 3 EG, UK
– sequence: 6
  givenname: Graham J.
  surname: Burton
  fullname: Burton, Graham J.
  organization: 3 Department of Physiology, Development and Neuroscience, Centre for Trophoblast Research,  University of Cambridge, Downing Street, Cambridge CB2 3 EG, UK
– sequence: 7
  givenname: Nassim Ghaffari
  surname: Tabrizi-Wizsy
  fullname: Tabrizi-Wizsy, Nassim Ghaffari
  organization: 4 Institute of Pathophysiology and Immunology, SFL Chicken CAM Lab, Medical University of Graz, Heinrichstrasse 31a, Graz 8010, Austria
– sequence: 8
  givenname: Uwe
  surname: Lang
  fullname: Lang, Uwe
  organization: 1 Department of Obstetrics and Gynecology, Medical University of Graz, Auenbruggerplatz 14, Graz 8036, Austria
– sequence: 9
  givenname: Ursula
  surname: Hiden
  fullname: Hiden, Ursula
  email: ursula.hiden@medunigraz.at
  organization: 1 Department of Obstetrics and Gynecology, Medical University of Graz, Auenbruggerplatz 14, Graz 8036, Austria
– sequence: 10
  givenname: Gernot
  surname: Desoye
  fullname: Desoye, Gernot
  organization: 1 Department of Obstetrics and Gynecology, Medical University of Graz, Auenbruggerplatz 14, Graz 8036, Austria
– sequence: 11
  givenname: Martina
  surname: Dieber-Rotheneder
  fullname: Dieber-Rotheneder, Martina
  organization: 1 Department of Obstetrics and Gynecology, Medical University of Graz, Auenbruggerplatz 14, Graz 8036, Austria
BackLink https://www.ncbi.nlm.nih.gov/pubmed/27864359$$D View this record in MEDLINE/PubMed
BookMark eNpFUctOwzAQtFARfcCRK_KRS6jtOK8jVOUhVeIC52gTb2lQYgfboe1P8M0YtcBpR9rZ3ZmdKRlpo5GQS85uOCvi-WboLPZzhVtRJCdkwmXKIhEnbEQmTKR5xHnKx2Tq3DtjAebpGRmLLE9lnBQT8rXUyvgNto2OOFVmqyOLb0MLHh3twNtmRzv00Lamt8Zjo8Eh5ZKCVpQnFHe9Recao2mjaRADmq4b6zwNox06jzYg029M1YLzjn42QPHvJrVYY-9NIO17pHfn5HQNrcOLY52R1_vly-IxWj0_PC1uV1Et89RHUCCoTK1FXSkOkORSFZKnTNQqjmuBecygqutKIAJDxFQwrCqZoMogk1LFM3J92BtMfQxBZtk1rsa2BY1mcCXPJc-KokhEoF4dqUPVoSr74Avsvvz94f8uM_R_Xc7Kn3jKQzzlIZ74GxdniNc
CitedBy_id crossref_primary_10_1007_s00418_017_1608_y
crossref_primary_10_1161_ATVBAHA_125_321710
ContentType Journal Article
Copyright The Author 2016. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. 2016
The Author 2016. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology.
Copyright_xml – notice: The Author 2016. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. 2016
– notice: The Author 2016. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology.
DBID TOX
CGR
CUY
CVF
ECM
EIF
NPM
7U8
7X8
C1K
JXQ
DOI 10.1093/humrep/dew295
DatabaseName Oxford Academic Journals (Open Access)
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
TOXLINE
MEDLINE - Academic
Environmental Sciences and Pollution Management
Toxline
DatabaseTitle MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
TOXLINE
MEDLINE - Academic
Environmental Sciences and Pollution Management
DatabaseTitleList MEDLINE
TOXLINE

Database_xml – sequence: 1
  dbid: NPM
  name: PubMed
  url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 2
  dbid: TOX
  name: Oxford Journals Open Access Collection
  url: https://academic.oup.com/journals/
  sourceTypes: Publisher
– sequence: 3
  dbid: 7X8
  name: MEDLINE - Academic
  url: https://search.proquest.com/medline
  sourceTypes: Aggregation Database
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
Anatomy & Physiology
Pharmacy, Therapeutics, & Pharmacology
EISSN 1460-2350
EndPage 54
ExternalDocumentID 27864359
10.1093/humrep/dew295
Genre Research Support, Non-U.S. Gov't
Journal Article
GrantInformation_xml – fundername: Oesterreichische Nationalbank
  grantid: 14796
  funderid: http://dx.doi.org/10.13039/501100004061
– fundername: Herzfelder'sche Familienstiftung
  grantid: 00685
  funderid: http://dx.doi.org/10.13039/501100003494
– fundername: Medical University of Graz
– fundername: Doctorate program MOLIN
  grantid: W1241
– fundername: Austrian Science Fund FWF
  grantid: W 1241
GroupedDBID ---
-E4
.2P
.I3
.XZ
.ZR
0R~
1TH
29I
2WC
4.4
482
48X
53G
5GY
5RE
5VS
5WA
5WD
70D
AABZA
AACZT
AAIMJ
AAJKP
AAJQQ
AAMDB
AAMVS
AAOGV
AAPNW
AAPQZ
AAPXW
AARHZ
AASNB
AAUAY
AAUQX
AAVAP
AAVLN
ABEUO
ABIXL
ABJNI
ABKDP
ABMNT
ABNHQ
ABNKS
ABPTD
ABQLI
ABQNK
ABWST
ABXVV
ABZBJ
ACCCW
ACGFS
ACPRK
ACUFI
ACUTJ
ACUTO
ACYHN
ADBBV
ADEYI
ADEZT
ADGKP
ADGZP
ADHKW
ADHZD
ADIPN
ADJQC
ADOCK
ADQBN
ADRIX
ADRTK
ADVEK
ADYVW
ADZXQ
AEGPL
AEJOX
AEKSI
AELWJ
AEMDU
AENEX
AENZO
AEPUE
AETBJ
AEWNT
AFFZL
AFGWE
AFIYH
AFOFC
AFXAL
AFXEN
AGINJ
AGKEF
AGQXC
AGSYK
AGUTN
AHMBA
AHXPO
AIJHB
AJEEA
AKWXX
ALMA_UNASSIGNED_HOLDINGS
ALUQC
APIBT
APWMN
ARIXL
ATGXG
AXUDD
AYOIW
BAWUL
BAYMD
BCRHZ
BEYMZ
BHONS
BQDIO
BSWAC
BTRTY
BVRKM
C45
CDBKE
CS3
CZ4
DAKXR
DIK
DILTD
DU5
D~K
E3Z
EBS
EE~
EJD
EMOBN
ENERS
F5P
F9B
FECEO
FHSFR
FLUFQ
FOEOM
FOTVD
FQBLK
GAUVT
GJXCC
GX1
H13
H5~
HAR
HW0
HZ~
IOX
J21
JXSIZ
KAQDR
KBUDW
KOP
KQ8
KSI
KSN
L7B
M-Z
M49
MHKGH
ML0
N9A
NGC
NLBLG
NOMLY
NOYVH
NU-
NVLIB
O9-
OAUYM
OAWHX
OBOKY
OCZFY
ODMLO
OJQWA
OJZSN
OK1
OPAEJ
OVD
OWPYF
P2P
PAFKI
PEELM
PQQKQ
Q1.
Q5Y
R44
RD5
RIG
ROL
ROX
ROZ
RUSNO
RW1
RXO
TCN
TCURE
TEORI
TJX
TLC
TOX
TR2
W8F
WH7
WOQ
X7H
YAYTL
YKOAZ
YXANX
ZKX
~91
.55
.GJ
3O-
AAPGJ
AAWDT
ABDFA
ABEJV
ABGNP
ABIME
ABPIB
ABPQP
ABSMQ
ABVGC
ABXZS
ABZEO
ACFRR
ACPQN
ACVCV
ACZBC
ADMTO
ADNBA
AEHUL
AEKPW
AEMQT
AFFNX
AFFQV
AFSHK
AFYAG
AGKRT
AGMDO
AGORE
AGQPQ
AHGBF
AHMMS
AJBYB
AJDVS
AJNCP
ALXQX
ANFBD
APJGH
AQDSO
AQKUS
ASAOO
ASPBG
ATDFG
ATTQO
AVNTJ
AVWKF
AZFZN
BZKNY
C1A
CAG
CGR
COF
CUY
CVF
CXTWN
DFGAJ
ECM
EIF
EIHJH
ELUNK
FEDTE
HVGLF
MBLQV
MBTAY
NPM
NTWIH
O0~
OBFPC
OHT
O~Y
PB-
QBD
RNI
RZF
RZO
TMA
X7M
ZGI
ZXP
7U8
7X8
C1K
JXQ
ID FETCH-LOGICAL-c486t-a9ead7df2cbd1aa584d941602cd33c2e830abccb2eea0eee620ebb45ed7a744d3
IEDL.DBID TOX
ISICitedReferencesCount 17
ISICitedReferencesURI http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000394815100007&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN 0268-1161
IngestDate Sat Sep 27 21:52:35 EDT 2025
Mon Jul 21 06:01:41 EDT 2025
Wed Sep 11 04:47:55 EDT 2024
IsDoiOpenAccess true
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 1
Keywords hypoxia
invasion
inflammation
MMPs
pre-eclampsia
endothelin-1
trophoblast
Language English
License This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
The Author 2016. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology.
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c486t-a9ead7df2cbd1aa584d941602cd33c2e830abccb2eea0eee620ebb45ed7a744d3
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
OpenAccessLink https://dx.doi.org/10.1093/humrep/dew295
PMID 27864359
PQID 1841799952
PQPubID 23479
PageCount 9
ParticipantIDs proquest_miscellaneous_1841799952
pubmed_primary_27864359
oup_primary_10_1093_humrep_dew295
PublicationCentury 2000
PublicationDate 2017-01-01
PublicationDateYYYYMMDD 2017-01-01
PublicationDate_xml – month: 01
  year: 2017
  text: 2017-01-01
  day: 01
PublicationDecade 2010
PublicationPlace England
PublicationPlace_xml – name: England
PublicationTitle Human reproduction (Oxford)
PublicationTitleAlternate Hum Reprod
PublicationYear 2017
Publisher Oxford University Press
Publisher_xml – name: Oxford University Press
SSID ssj0016186
Score 2.3243783
Snippet STUDY QUESTION Does endothelin-1 (ET-1) regulate matrix metalloproteinase (MMP) 14 and 15 production and invasion of human first trimester trophoblasts?...
Does endothelin-1 (ET-1) regulate matrix metalloproteinase (MMP) 14 and 15 production and invasion of human first trimester trophoblasts? ET-1 in...
STUDY QUESTIONDoes endothelin-1 (ET-1) regulate matrix metalloproteinase (MMP) 14 and 15 production and invasion of human first trimester trophoblasts?SUMMARY...
SourceID proquest
pubmed
oup
SourceType Aggregation Database
Index Database
Publisher
StartPage 46
SubjectTerms Cell Proliferation - drug effects
Dose-Response Relationship, Drug
Down-Regulation - drug effects
Endothelin-1 - pharmacology
Female
Humans
Matrix Metalloproteinase 14 - genetics
Matrix Metalloproteinase 14 - metabolism
Matrix Metalloproteinase 15 - genetics
Matrix Metalloproteinase 15 - metabolism
Placenta - drug effects
Placenta - metabolism
Pregnancy
Pregnancy Trimester, First - metabolism
Receptor, Endothelin B - genetics
Receptor, Endothelin B - metabolism
Trophoblasts - drug effects
Trophoblasts - metabolism
Tumor Necrosis Factor-alpha - pharmacology
Title Endothelin-1 down-regulates matrix metalloproteinase 14 and 15 expression in human first trimester trophoblasts via endothelin receptor type B
URI https://www.ncbi.nlm.nih.gov/pubmed/27864359
https://www.proquest.com/docview/1841799952
Volume 32
WOSCitedRecordID wos000394815100007&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV1Lb9QwELagQogLjy2U8qgGCfVUq4njbOJjQa24dNnDIu0t8mOi5rDOapMt3T_Bb2bshEWiHHqJksiOI80k882M5xvGPhtZ54hacCmLjAcGLq7rpOa2CFk-Z6VKTWw2Ucxm5XKp5mO8o_tPCl9l5zfb1QbX5w5_ChWqydO8DAq9-L7cpwsC6fsQTCGXiK5GMs17s_-pYrsHJqNRuXrx8Nd5yZ6PwBEuBkm_Yo_QT9jhhSenebWDU4hbOWOMfMKeXo8Z8wk7nQ_c1LszWPwtterO4ow9a_XukP269C5UYxHs5Ck4cs75ZuhTjx2sApH_HaywD3n6yO3QeLJ_kErQ3kGaA96NW2o9NB5i6z-oG8KW0IcOAoGPgc7a9U1rCLD3Hdw2GnC_JtCfF9d9S4PIM4Yvr9mPq8vF1298bNbArSynPdeKdLJwtbDGpVoTrnGKwF4irMsyK7DMEm2sNYI0I0HEqUjQGJmjK3QhpcvesAPfenzLQETQ5zCbSiUJoJjU5Cqts4LuJSXiMftEUqzWAx1HNaTRs2oQTDUIhsb8kXFFH0zIgmiP7baryKUNLHgqF8fsaBD-_lGiKAmh5erdA1Z4z56JYOJjOOYDO-g3W_zIntjbvuk2J-xxsSzpOJtfn0Rd_Q2bsurF
linkProvider Oxford University Press
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Endothelin-1+down-regulates+matrix+metalloproteinase+14+and+15+expression+in+human+first+trimester+trophoblasts+via+endothelin+receptor+type+B&rft.jtitle=Human+reproduction+%28Oxford%29&rft.au=Majali-Martinez%2C+Alejandro&rft.au=Velicky%2C+Philipp&rft.au=Pollheimer%2C+J%C3%BCrgen&rft.au=Kn%C3%B6fler%2C+Martin&rft.date=2017-01-01&rft.pub=Oxford+University+Press&rft.issn=0268-1161&rft.eissn=1460-2350&rft.volume=32&rft.issue=1&rft.spage=46&rft.epage=54&rft_id=info:doi/10.1093%2Fhumrep%2Fdew295&rft.externalDocID=10.1093%2Fhumrep%2Fdew295
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0268-1161&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0268-1161&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0268-1161&client=summon