Evidence map›Paper›PMID 23116176›Full record

ArticleVirology journal2012

Human cytomegalovirus infection inhibits CXCL12- mediated migration and invasion of human extravillous cytotrophoblasts.

Jessica A Warner, Kevin J Zwezdaryk, Bonita Day, Deborah E Sullivan, Gabriella Pridjian, Cindy A Morris

Abstract read
In one paragraph

Article in Virology journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed.

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  17. Expression of KIR2DS1 by decidual natural killer cells increases their ability to control placental HCMV infection.Proceedings of the National Academy of Sciences of the United States of America · 2016
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Jessica A WarnerDepartment of Microbiology and Immunology, Tulane University School of Medicine, New Orleans, LA, USA.
Kevin J Zwezdaryk
Bonita Day
Deborah E Sullivan
Gabriella Pridjian
Cindy A Morris

Funding

Human Cytomegalovirus-Induced Inhibition of Cytotrophoblast InvasionR01HD051998 · NICHD · TULANE UNIVERSITY OF LOUISIANA · PI MORRIS, CINDY ANNE · 2008 to 2012
$1.5M
NICHD NIH HHS 5R01HD051998-04NICHD NIH HHS R01 HD051998
6 · The paper itself

Abstract

backgroundDuring the first trimester of pregnancy, a series of tightly regulated interactions govern the formation of a highly invasive population of fetal-derived extravillous cytotrophoblasts (EVT). Successful pregnancy is dependent on efficient invasion of the uterine wall and maternal spiral arteries by EVT. Dysregulated trophoblast invasion is associated with intrauterine growth restriction, birth defects, spontaneous abortion and preeclampsia. A number of soluble growth factors, cytokines, and chemokines modulate this process, fine-tuning the temporal and spatial aspects of cytotrophoblast invasion. In particular, the CXCL12/CXCR4 axis has been shown to specifically modulate cytotrophoblast differentiation, invasion, and survival throughout early pregnancy. Infection with human cytomegalovirus (HCMV) has been associated with impaired differentiation of cytotrophoblasts down the invasive pathway, specifically dysregulating the response to mitogens including epidermal growth factor (EGF) and hepatocyte growth factor (HGF). In this study, the effect of HCMV infection on the CXCL12-mediated migration and invasion of the EVT cell line SGHPL-4 was investigated.

resultsInfection with HCMV significantly decreased secretion of CXCL12 by SGHPL-4 cells, and induced a striking perinuclear accumulation of the chemokine. HCMV infection significantly increased mRNA and total cell surface expression of the two known receptors for CXCL12: CXCR4 and CXCR7. Functionally, HCMV-infected SGHPL-4 cells were unable to migrate or invade in response to a gradient of soluble CXCL12 in transwell assays.

conclusionsCollectively, these studies demonstrate that HCMV impairs EVT migration and invasion induced by CXCL12. As HCMV has the ability to inhibit EVT migration and invasion through dysregulation of other relevant signaling pathways, it is likely that the virus affects multiple signaling pathways to impair placentation and contribute to some of the placental defects seen in HCMV-positive pregnancies.

Indexed as

CytomegalovirusCell LineCell MovementChemokine CXCL12Cytomegalovirus InfectionsFemaleGene ExpressionHumansPregnancyReceptors, CXCRReceptors, CXCR4RNA, MessengerTrophoblastsACKR3 protein, humanChemokine CXCL12Receptors, CXCRReceptors, CXCR4RNA, Messenger

Identifiers

PMID23116176
PMCPMC3545970

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.