Evidence map›Paper›PMID 21302311›Full record

ArticleJournal of cellular physiology2011

The suppression of myosin light chain (MLC) phosphorylation during the response to lipopolysaccharide (LPS): beneficial or detrimental to endothelial barrier?

Natalia V Bogatcheva, Marina A Zemskova, Christophe Poirier, Tamara Mirzapoiazova, Irina Kolosova, Anne R Bresnick, Alexander D Verin

Abstract read
In one paragraph

Article in Journal of cellular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

27 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Calpain Promotes LPS-induced Lung Endothelial Barrier Dysfunction via Cleavage of Talin.American journal of respiratory cell and molecular biology · 2023
    Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Noncanonical function of long myosin light chain kinase in increasing ER-PM junctions and augmentation of SOCE.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Mediators of inflammation · 2018
    Article
  14. [Role of epidermal growth factor receptor in house dust mite-induced airway epithelial barrier dysfunction].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2017
    Article
  15. Review
  16. Article
  17. Article
  18. Article
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  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

7 authors at 4 institutions in 1 country.

Natalia V BogatchevaVascular Biology Center, Georgia Health Sciences University, Augusta, Georgia 30912, USA. nbogatcheva@georgiahealth.edu
Marina A Zemskova
Christophe Poirier
Tamara Mirzapoiazova
Irina Kolosova
Anne R Bresnick
Alexander D Verin
Augusta University Health · USAlbert Einstein College of Medicine · USJohns Hopkins University · USUniversity of Chicago · US

Funding

Microtubules in lung endothelial cell barrier regulationR01HL067307 · NHLBI · UNIVERSITY OF CHICAGO · PI VERIN, ALEXANDER D · 2001 to 2009
$2.5M
ATP in Lung Endothelial Barrier EnhancementR01HL083327 · NHLBI · UNIVERSITY OF CHICAGO · PI VERIN, ALEXANDER D · 2006 to 2009
$1.5M
ALK/SMAD Signaling in TGF beta-induced EC PermeabilityR01HL080675 · NHLBI · UNIVERSITY OF CHICAGO · PI VERIN, ALEXANDER D · 2005 to 2008
$1.5M
NHLBI NIH HHS HL-067307NHLBI NIH HHS HL-080675NHLBI NIH HHS HL-083327NHLBI NIH HHS R01 HL067307NHLBI NIH HHS R01 HL080675NHLBI NIH HHS R01 HL083327
6 · The paper itself

Abstract

Sepsis-induced vascular leakage is a major underlying cause of the respiratory dysfunction seen in severe sepsis. Here, we studied the role of MLC phosphorylation in LPS-induced endothelial hyperpermeability and assessed how the changes in phospho-MLC distribution affect LPS-induced barrier dysfunction. We demonstrated that the changes in human lung microvascular endothelial permeability are preceded by the increase in intracellular calcium level, and increase in MYPT and MLC phosphorylation. Using the siRNA approach, we showed that both LPS-induced barrier dysfunction and MLC phosphorylation are attenuated by the depletion of the smooth muscle isoform of MLC kinase (MLCK) and Rho kinase 2 (ROCK2). Surprisingly, pharmacological inhibition of both ROCK1 and 2 with Y-27632 exacerbated LPS-induced drop in transendothelial resistance, although significantly decreasing MLC phosphorylation level. We next studied the involvement of protein kinase A (PKA)-dependent pathways in LPS-induced barrier dysfunction. We showed that LPS decreased the level of PKA-dependent phosphorylation in endothelial cells; and the pretreatment with forskolin or PKA activator bnz-cAMP counteracted this effect. Forskolin and bnz-cAMP also attenuated LPS-induced increase in MLC phosphorylation level. As we have shown earlier (Bogatcheva et al., 2009), forskolin and bnz-cAMP provide protection from LPS-induced barrier dysfunction. We compared the effects of bnz-cAMP and Y-27632 on phospho-MLC distribution and observed that while bnz-cAMP increased the association of the phospho-MLC signal with the cortical structures, Y-27632 decreased this association. These data indicate that an overall decrease in MLC phosphorylation could be either beneficial or detrimental to endothelial barrier, depending on the intracellular locale of major phospho-MLC changes.

Indexed as

AmidesCalciumCapillary PermeabilityCells, CulturedColforsinCyclic AMPDextransElectric ImpedanceEndothelial CellsEndotoxinsFluorescein-5-isothiocyanateHumansLungMicrovesselsMyosin-Light-Chain KinaseMyosin-Light-Chain PhosphataseAmidesCalciumColforsinCyclic AMPDextransendotoxin, Escherichia coliEndotoxinsFluorescein-5-isothiocyanatefluorescein isothiocyanate dextranMyosin-Light-Chain KinaseMyosin-Light-Chain PhosphataseMyosin Light ChainsN(6)-benzoyl-cyclic AMPProtein Kinase InhibitorsPyridinesrho-Associated KinasesROCK1 protein, humanROCK2 protein, humanY 27632

Identifiers

PMID21302311
PMCPMC3130083
OpenAlexW2027218800

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.