Evidence map›Paper›PMID 24318111›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2014

HIV envelope protein gp120-induced apoptosis in lung microvascular endothelial cells by concerted upregulation of EMAP II and its receptor, CXCR3.

Linden A Green, Ru Yi, Daniela Petrusca, Ting Wang, Alhasan Elghouche, Samir K Gupta, Irina Petrache, Matthias Clauss

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

32 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Role of HIV-encoded proteins in cardiovascular disease.American journal of physiology. Cell physiology · 2025
    Review
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  6. Article
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  18. Review
  19. Effects of HIV-1 gp120 and TAT-derived microvesicles on endothelial cell function.Journal of applied physiology (Bethesda, Md. : 1985) · 2019
    Article
  20. 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

8 authors at 2 institutions in 1 country.

Linden A GreenIndiana University School of Medicine, Cellular and Integrative Physiology, Indianapolis, IN 46202. MClauss@iupui.edu.
Ru Yi
Daniela Petrusca
Ting Wang
Alhasan Elghouche
Samir K Gupta
Irina Petrache
Matthias Clauss
Indiana University – Purdue University Indianapolis · USIndiana University School of Medicine

Funding

Ceramide-induced Lung Destruction in EmphysemaR01HL077328 · NHLBI · NATIONAL JEWISH HEALTH · PI PETRACHE, IRINA · 2006 to 2024
$8.0M
HIV, Inflammation, and Endothelial DysfunctionR01HL095149 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI CLAUSS, MATTHIAS, GUPTA, SAMIR KUMAR · 2008 to 2012
$4.1M
Training in Vascular Biology and MedicineT32HL079995 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI MARCH, KEITH LEONARD · 2005 to 2014
$2.2M
Direct and Bone-Marrow Mediated Effects of Adipose Stem Cells in EmphysemaR01HL105772 · NHLBI · NATIONAL JEWISH HEALTH · PI MARCH, KEITH LEONARD, PETRACHE, IRINA · 2012 to 2015
$1.5M
EMAP II, a molecular link of inflammation and apoptosis in pulmonary emphysema.R01HL090950 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI CLAUSS, MATTHIAS, PETRACHE, IRINA · 2008 to 2011
$1.5M
Endothelial mechanisms of impaired lung gas exchange by HIVR56HL125043 · NHLBI · NATIONAL JEWISH HEALTH · PI CROTHERS, KRISTINA ANNE, PETRACHE, IRINA · 2014 to 2014
$684k
NHLBI NIH HHS R01-HL-077328NHLBI NIH HHS R01-HL-090950NHLBI NIH HHS R01-HL-095149NHLBI NIH HHS R01 HL105772NHLBI NIH HHS T32-HL-079995
6 · The paper itself

Abstract

Chronic lung diseases, such as pulmonary emphysema, are increasingly recognized complications of infection with the human immunodeficiency virus (HIV). Emphysema in HIV may occur independent of cigarette smoking, via mechanisms that are poorly understood but may involve lung endothelial cell apoptosis induced by the HIV envelope protein gp120. Recently, we have demonstrated that lung endothelial apoptosis is an important contributor to the development of experimental emphysema, via upregulation of the proinflammatory cytokine endothelial monocyte-activating polypeptide II (EMAP II) in the lung. Here we investigated the role of EMAP II and its receptor, CXCR3, in gp120-induced lung endothelial cell apoptosis. We could demonstrate that gp120 induces a rapid and robust increase in cell surface expression of EMAP II and its receptor CXCR3. This surface expression occurred via a mechanism involving gp120 signaling through its CXCR4 receptor and p38 MAPK activation. Both EMAP II and CXCR3 were essentially required for gp120-induced apoptosis and exposures to low gp120 concentrations enhanced the susceptibility of endothelial cells to undergo apoptosis when exposed to soluble cigarette smoke extract. These data indicate a novel mechanism by which HIV infection causes endothelial cell loss involved in lung emphysema formation, independent but potentially synergistic with smoking, and suggest therapeutic targets for emphysema prevention and/or treatment.

Indexed as

ApoptosisAnimalsCHO CellsCricetinaeCricetulusCytokinesEndothelial CellsHIV Envelope Protein gp120HIV InfectionsHumansLungMicrovesselsNeoplasm Proteinsp38 Mitogen-Activated Protein KinasesPulmonary EmphysemaReceptors, CXCR3CXCR3 protein, humanCXCR4 protein, humanCytokinesHIV Envelope Protein gp120Neoplasm Proteinsp38 Mitogen-Activated Protein KinasesReceptors, CXCR3Receptors, CXCR4RNA-Binding Proteinssmall inducible cytokine subfamily E, member 1emphysemaendotheliumgp120HIVlung

Identifiers

PMID24318111
PMCPMC3920224
OpenAlexW2135032149

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.