Evidence map›Paper›PMID 30360778›Full record

ArticleCurrent topics in membranes2018

Sphingolipids Signaling in Lamellipodia Formation and Enhancement of Endothelial Barrier Function.

Panfeng Fu, Mark Shaaya, Anantha Harijith, Jeffrey R Jacobson, Andrei Karginov, Viswanathan Natarajan

Open access · greenAbstract read
In one paragraph

Article in Current topics in membranes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

13 citing papers in PubMed, 14 citations in OpenAlex.

  1. ORMDL Proteins Turnover via Proteasome and Autophagy Is Cell-Type Dependent and Tied to Ceramide Homeostasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Review
  3. Article
  4. DOCK4 Regulation of Rho GTPases Mediates Pulmonary Vascular Barrier Function.Arteriosclerosis, thrombosis, and vascular biology · 2022
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Post-translational modifications of S1PR1 and endothelial barrier regulation.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020
    Review
  10. Review
  11. Review
  12. Mobilization of endothelial progenitor cells in sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
    Review
  13. 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

6 authors at 1 institution in 1 country.

Panfeng FuDepartment of Pharmacology, University of Illinois at Chicago, Chicago, IL, United States.
Mark ShaayaDepartment of Pharmacology, University of Illinois at Chicago, Chicago, IL, United States.
Anantha HarijithDepartment of Pediatrics, University of Illinois at Chicago, Chicago, IL, United States.
Jeffrey R JacobsonDepartment of Medicine, University of Illinois at Chicago, Chicago, IL, United States.
Andrei KarginovDepartment of Pharmacology, University of Illinois at Chicago, Chicago, IL, United States.
Viswanathan NatarajanDepartment of Pharmacology, University of Illinois at Chicago, Chicago, IL, United States; Department of Medicine, University of Illinois at Chicago, Chicago, IL, United States. Electronic address: visnatar@uic.edu.
University of Illinois Chicago · US

Funding

TRPC6 Regulation of Lung Endothelial Barrier FunctionP01HL060678 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MALIK, ASRAR B. · 2000 to 2020
$40.1M
Structure-Function Analysis of nmMLCK in EC Barrier ResponsesP01HL126609 · NHLBI · UNIVERSITY OF FLORIDA · PI Joe G. N. Garcia · 2016 to 2026
$24.4M
TRAINING PROGRAM IN LUNG BIOLOGY AND PATHOBIOLOGYT32HL007829 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DOLLY MEHTA · 1995 to 2026
$15.6M
NHLBI NIH HHS P01 HL060678NHLBI NIH HHS P01 HL126609NHLBI NIH HHS T32 HL007829
6 · The paper itself

Abstract

Sphingolipids, first described in the brain in 1884, are important structural components of biological membranes of all eukaryotic cells. In recent years, several lines of evidence support the critical role of sphingolipids such as sphingosine, sphingosine-1-phosphate (S1P), and ceramide as anti- or pro-inflammatory bioactive lipid mediators in a variety of human pathologies including pulmonary and vascular disorders. Among the sphingolipids, S1P is a naturally occurring agonist that exhibits potent barrier enhancing property in the endothelium by signaling via G protein-coupled S1P1 receptor. S1P, S1P analogs, and other barrier enhancing agents such as HGF, oxidized phospholipids, and statins also utilize the S1P/S1P1 signaling pathway to generate membrane protrusions or lamellipodia, which have been implicated in resealing of endothelial gaps and maintenance of barrier integrity. A better understanding of sphingolipids mediated regulation of lamellipodia formation and barrier enhancement of the endothelium will be critical for the development of sphingolipid-based therapies to alleviate pulmonary disorders such as sepsis-, radiation-, and mechanical ventilation-induced acute lung injury.

Indexed as

Signal TransductionAcute Lung InjuryEndothelium, VascularHumansLysophospholipidsPhosphotransferases (Alcohol Group Acceptor)PseudopodiaReactive Oxygen SpeciesSimvastatinSphingolipidsSphingosineSphingosine KinaseLysophospholipidsPhosphotransferases (Alcohol Group Acceptor)Reactive Oxygen SpeciesSimvastatinSphingolipidsSphingosinesphingosine 1-phosphateSphingosine KinaseBarrier restorationEndotheliumLamellipodiaReactive oxygen speciesSphingolipidsSphingosine-1-phosphateSphingosine kinase

Identifiers

PMID30360778
PMCPMC6383653
OpenAlexW2893461606

What OpenQuestion holds

Textmetadata
LicenceTDM
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.