Evidence map›Paper›PMID 26469087›Full record

ArticlePloS one2015

Protective Role of Rho Guanosine Diphosphate Dissociation Inhibitor, Ly-GDI, in Pulmonary Alveolitis.

Chunguang Yan, Ximo Wang, Yanlan Liu, Raja-Elie Abdulnour, Min Wu, Hongwei Gao

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 89% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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 at 4 institutions in 2 countries.

Chunguang YanDepartment of Anesthesiology, Perioperative&Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America; Department of Basic Sciences, University of North Dakota, Grand Forks, North Dakota, United States of America.
Ximo WangDepartment of Surgery, Tianjin Nankai Hospital, Tianjin, China.
Yanlan LiuDepartment of Anesthesiology, Perioperative&Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.
Raja-Elie AbdulnourPulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.
Min WuDepartment of Basic Sciences, University of North Dakota, Grand Forks, North Dakota, United States of America.
Hongwei GaoDepartment of Anesthesiology, Perioperative&Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America; Department of Surgery, Tianjin Nankai Hospital, Tianjin, China.
Harvard University · USTianjin Nankai Hospital · CNBrigham and Women's Hospital · USUniversity of North Dakota · US

Funding

Pilot Projects CoreP30GM103329 · NIGMS · UNIVERSITY OF NORTH DAKOTA · PI GEIGER, JONATHAN DAVID · 2012 to 2016
$5.1M
STAT3 and its Acetylation in Acute Lung InjuryR01HL092905 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI GAO, HONGWEI · 2008 to 2012
$1.8M
NHLBI NIH HHS 5R01HL092905NHLBI NIH HHS R01 HL092905NIGMS NIH HHS P30 GM103329
6 · The paper itself

Abstract

Growing evidences indicate that Ly-GDI, an inhibitory protein of Rho GTPases, plays an essential role in regulating actin cytoskeletal alteration which is indispensible for the process such as phagocytosis. However, the role of Ly-GDI in inflammation remains largely unknown. In the current study, we found that Ly-GDI expression was significantly decreased in the IgG immune complex-injured lungs. To determine if Ly-GDI might regulate the lung inflammatory response, we constructed adenovirus vectors that could mediate ectopic expression of Ly-GDI (Adeno-Ly-GDI). In vivo mouse lung expression of Ly-GDI resulted in a significant attenuation of IgG immune complex-induced lung injury, which was due to the decreased pulmonary permeability and lung inflammatory cells, especially neutrophil accumulation. Upon IgG immune complex deposition, mice with Ly-GDI over-expression in the lungs produced significant less inflammatory mediators (TNF-α, IL-6, MCP-1, and MIP-1α) in bronchoalveolar lavage fluid when compared control mice receiving airway injection of Adeno-GFP. Mechanically, IgG immune complex-induced NF-κB activity was markedly suppressed by Ly-GDI in both alveolar macrophages and lungs as measured by luciferase assay and electrophoretic mobility shift assay. These findings suggest that Ly-GDI is a critical regulator of inflammatory injury after deposition of IgG immune complexes and that it negatively regulates the lung NF-κB activity.

Indexed as

Acute Lung InjuryAnimalsCells, CulturedCytoprotectionGenetic TherapyHEK293 CellsHumansImmunoglobulin GMaleMiceMice, Inbred C57BLMinor Histocompatibility AntigensPneumoniaPulmonary Alveolirho Guanine Nucleotide Dissociation Inhibitor betaArhgdib protein, mouseImmunoglobulin GMinor Histocompatibility Antigensrho Guanine Nucleotide Dissociation Inhibitor beta

Identifiers

PMID26469087
PMCPMC4607448
OpenAlexW2271025711

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.