Evidence map›Paper›PMID 39543165›Full record

ArticleScientific reports2024

Cigarette smoke alters calcium flux to induce PP2A membrane trafficking and endothelial cell permeability.

Abdoulaye J Dabo, Sonya Raghavan, Wendy Ezegbunam, Jincy Thankachen, Oleg Evgrafov, Sue Majka, Patrick Geraghty, Robert F Foronjy

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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.

Abdoulaye J DaboDivision of Pulmonary & Critical Care Medicine, Department of Medicine, State University of New York Downstate Health Sciences University, Brooklyn, NY, USA.
Sonya RaghavanDivision of Pulmonary, and Critical Care Medicine, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Wendy EzegbunamDivision of Pulmonary & Critical Care Medicine, Department of Medicine, State University of New York Downstate Health Sciences University, Brooklyn, NY, USA.
Jincy ThankachenDivision of Pulmonary, and Critical Care Medicine, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Oleg EvgrafovDepartment of Cell Biology, State University of New York Downstate Health Sciences University, Brooklyn, NY, USA.
Sue MajkaDivision of Pulmonary, Critical Care and Sleep Medicine, Department of Immunology and Genomic Medicine, National Jewish Health, Denver, CO, USA.
Patrick GeraghtyDivision of Pulmonary & Critical Care Medicine, Department of Medicine, State University of New York Downstate Health Sciences University, Brooklyn, NY, USA.
Robert F ForonjyDivision of Pulmonary & Critical Care Medicine, Department of Medicine, State University of New York Downstate Health Sciences University, Brooklyn, NY, USA. robert.foronjy@downstate.edu.

Funding

The Role of HuR in HIV related COPDR01HL162590 · NHLBI · SUNY DOWNSTATE MEDICAL CENTER · PI FORONJY, ROBERT F · 2022 to 2025
$2.9M
Alpha-1 Foundation 493373Flight Attendant Medical Research Institute CIA160005Flight Attendant Medical Research Institute CIA160028NHLBI NIH HHS R01 HL162590NIH HHS 5 R01-HL162590-03
6 · The paper itself

Abstract

Alveolar capillary barrier disruption induces local edema and inflammation that impairs pulmonary function and promotes alveolar destruction in COPD. This study aimed to determine how cigarette smoke modulated the serine-threonine phosphatase protein phosphatase 2 A (PP2A) to alter the barrier function of human lung microvascular endothelial cells (HLMVECs). Cigarette smoke exposure lowered overall PP2A activity and enhanced endothelial permeability in HLMVECs. However, directly decreasing PP2A activity with Fostriecin significantly reduced endothelial cell permeability. Protein fractionation studies determined that cigarette smoke diminished cytosolic PP2A activity but increased membrane and cytoskeletal activity. These changes coincided with the translocation of PP2A to the membrane, which reduced occludin phosphorylation in the membrane. Cigarette smoke decreased protein tyrosine phosphatase 1B (PTP1B) activity, a PP2A activator which also counters calcium intracellular influx. The decrease in PTP1B activity correlated with reduced calcium efflux in endothelial cells and these changes in calcium flux regulated PP2A activity. Indeed, culturing endothelial cells in low calcium medium prevented the decrease in cytosolic PP2A activity mediated by cigarette smoke. Together, these findings outline a mechanism whereby cigarette smoke acts via calcium to traffic PP2A from the cytosol to the membrane where it dephosphorylates occludin to increase endothelial cell permeability.

Indexed as

CalciumCell Membrane PermeabilityEndothelial CellsOccludinProtein Phosphatase 2Protein Tyrosine Phosphatase, Non-Receptor Type 1SmokeCell MembraneCells, CulturedCytosolHumansLungPhosphorylationProtein TransportCalciumOccludinProtein Phosphatase 2Protein Tyrosine Phosphatase, Non-Receptor Type 1PTPN1 protein, humanSmokeAnd cigarette smokeChronic obstructive pulmonary diseaseEndotheliumInflammationPermeabilityProtein phosphatase 2A

Identifiers

PMID39543165
PMCPMC11564810

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.