Evidence map›Paper›PMID 20930069›Full record

ArticleBlood2011

IL-6 in human cytomegalovirus secretome promotes angiogenesis and survival of endothelial cells through the stimulation of survivin.

Sara Botto, Daniel N Streblow, Victor DeFilippis, Laura White, Craig N Kreklywich, Patricia P Smith, Patrizia Caposio

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
5.7field-weighted citation impact, top 4% of its field
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

57 citing papers in PubMed, 109 citations in OpenAlex.

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  19. Immunological Considerations forFrontiers in immunology · 2021
    Review
  20. Frontiers in oncology · 2021
    Article
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

7 authors at 2 institutions in 1 country.

Sara BottoVaccine and Gene Therapy Institute, Oregon Health & Science University, Portland, OR 97006, USA.
Daniel N Streblow
Victor DeFilippis
Laura White
Craig N Kreklywich
Patricia P Smith
Patrizia Caposio
Vaccine and Gene Therapy InstituteOregon Health & Science University · US

Funding

The role of CMV secretome in the acceleration of transplant vascular sclerosisR01HL088603 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI NELSON, JAY A · 2008 to 2012
$3.6M
Mechanisms of CMV latency in accelerated vascular diseaseR01HL083194 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI STREBLOW, DANIEL N · 2006 to 2010
$1.5M
NHLBI NIH HHS HL 083194NHLBI NIH HHS HL 088603NHLBI NIH HHS R01 HL083194NHLBI NIH HHS R01 HL088603
6 · The paper itself

Abstract

Human cytomegalovirus (HCMV) is linked to the acceleration of vascular diseases such as atherosclerosis and transplant vasculopathy. One of the hallmarks of these diseases is angiogenesis (AG) and neovessel formation. Endothelial cells (ECs) are an integral part of AG and are sites of HCMV persistence. AG requires multiple synchronous processes that include EC proliferation, migration, and vessel stabilization. Virus-free supernatant (secretome) from HCMV-infected ECs induces AG. To identify factor(s) involved in this process, we performed a human cytokine array. Several cytokines were significantly induced in the HCMV secretomes including interleukin-6 (IL-6), granulocyte macrophage colony-stimulating factor, and IL-8/CXCL8. Using in vitro AG assays, neutralization of IL-6 significantly reduced neovessel formation. Addition of the HCMV secretome to preformed vessels extended neovessel survival, but this effect was blocked by neutralization of IL-6. In these cells, IL-6 prevented apoptosis by blocking caspase-3 and -7 activation through the induction of survivin. Neutralization of IL-6 receptor on ECs abolished the ability of HCMV secretome to increase survivin expression and activated effector caspases. Moreover, survivin shRNA expression induced rapid regression of tubule capillary networks in ECs stimulated with HCMV secretome and activated effector caspases. These observations may explain how CMV accelerates vascular disease despite limited infection in tissues.

Indexed as

Angiogenesis Inducing AgentsApoptosisBlotting, WesternCaspase 3Cell AdhesionCell MovementCell ProliferationCells, CulturedCytomegalovirusCytomegalovirus InfectionsEndothelium, VascularHumansInhibitor of Apoptosis ProteinsInterleukin-6Interleukin-8Macrophage Colony-Stimulating FactorAngiogenesis Inducing AgentsBIRC5 protein, humanCaspase 3Inhibitor of Apoptosis ProteinsInterleukin-6Interleukin-8Macrophage Colony-Stimulating FactorMicrotubule-Associated ProteinsReceptors, Interleukin-6RNA, MessengerRNA, Small InterferingSurvivin

Identifiers

PMID20930069
PMCPMC3037756
OpenAlexW1998779041

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.