Evidence map›Paper›PMID 18239193›Full record

ArticleAmerican journal of respiratory cell and molecular biology2008

Macrophage migration inhibitory factor governs endothelial cell sensitivity to LPS-induced apoptosis.

Rachel L Damico, Alan Chesley, Laura Johnston, Eric P Bind, Eric Amaro, Julie Nijmeh, Bedri Karakas, Laura Welsh, David B Pearse, Joe G N Garcia and 1 more

Abstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Functional Impact of Human Genetic Variants ofAmerican journal of respiratory cell and molecular biology · 2020
    Article
  2. A nonapoptotic endothelial barrier-protective role for caspase-3.American journal of physiology. Lung cellular and molecular physiology · 2019
    Article
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  9. Endothelial CD74 mediates macrophage migration inhibitory factor protection in hyperoxic lung injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
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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

11 authors at 1 institution in 1 country.

Rachel L DamicoDepartment of Medicine, Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, MD 21224, USA.
Alan Chesley
Laura Johnston
Eric P Bind
Eric Amaro
Julie Nijmeh
Bedri Karakas
Laura Welsh
David B Pearse
Joe G N Garcia
Michael T Crow
Johns Hopkins University · US

Funding

ARC REGULATES MITOCHONDRIAL DEATH SIGNALING IN HEARTR01HL073935 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI CROW, MICHAEL T · 2004 to 2007
$1.6M
The Role of MIF in Endothelial ApoptosisF32HL078113 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI DAMICO, RACHEL L · 2004 to 2005
$96k
NHLBI NIH HHS HL073935NHLBI NIH HHS HL078113
6 · The paper itself

Abstract

Human endothelial cells (EC) are typically resistant to the apoptotic effects of stimuli associated with lung disease. The determinants of this resistance remain incompletely understood. Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine produced by human pulmonary artery EC (HPAEC). Its expression increases in response to various death-inducing stimuli, including lipopolysaccharide (LPS). We show here that silencing MIF expression by RNA interference (MIF siRNA) dramatically reduces MIF mRNA expression and the LPS-induced increase in MIF protein levels, thereby sensitizing HPAECs to LPS-induced cell death. Addition of recombinant human MIF (rhMIF) protein prevents the death-sensitizing effect of MIF siRNA. A common mediator of apoptosis resistance in ECs is the death effector domain (DED)-containing protein, FLIP (FLICE-like inhibitory protein). We show that LPS induces a transcription-independent increase in the short isoform of FLIP (FLIP(s)). This increase is blocked by MIF siRNA but restored with the addition of recombinant MIF protein (rHMIF). While FLIP(s) siRNA also sensitizes HPAECs to LPS-induced death, the addition of rhMIF does not affect this sensitization, placing MIF upstream of FLIP(s) in preventing HPAEC death. These studies demonstrate that MIF is an endogenous pro-survival factor in HPAECs and identify a novel mechanism for its role in apoptosis resistance through the regulation of FLIP(s). These results show that MIF can protect vascular endothelial cells from inflammation-associated cell damage.

Indexed as

ApoptosisCASP8 and FADD-Like Apoptosis Regulating ProteinCell DeathDNA PrimersEndothelium, VascularGene Expression RegulationHumansLipopolysaccharidesMacrophage Migration-Inhibitory FactorsPulmonary ArteryRespiratory MucosaReverse Transcriptase Polymerase Chain ReactionRNA InterferenceRNA, MessengerRNA, Small InterferingCASP8 and FADD-Like Apoptosis Regulating ProteinDNA PrimersLipopolysaccharidesMacrophage Migration-Inhibitory FactorsRNA, MessengerRNA, Small Interfering

Identifiers

PMID18239193
PMCPMC2438450
OpenAlexW2022767114

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.