Evidence map›Paper›PMID 11448997›Full record

ArticleThe Journal of cell biology2001

RhoA is required for monocyte tail retraction during transendothelial migration.

R A Worthylake, S Lemoine, J M Watson, K Burridge

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 197 papers.

0numbers the graph read from it
0cells of the map it votes in
197citing papers in PubMed
12.4field-weighted citation impact, top 1% 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

197 citing papers in PubMed, 494 citations in OpenAlex.

  1. Trial
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  16. Toxins · 2022
    Article
  17. Article
  18. Wound Healing from an Actin Cytoskeletal Perspective.Cold Spring Harbor perspectives in biology · 2022
    Review
  19. Article
  20. Review

137 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

R A WorthylakeDepartment of Cell and Developmental Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. becky_worthylake@med.unc.edu
S Lemoine
J M Watson
K Burridge
University of North Carolina at Chapel Hill · US

Funding

THE ROLE OF RAP1 IN INTEGRIN ACTIVATION AND PLATELET SIGNALINGP01HL045100 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BURRIDGE, KEITH · 1993 to 2007
$13.7M
STRESS, ADRENERGIC AND INFLAMMATORY FACTORS IN 4 DISORDERSP60DE013079 · NIDCR · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI FLOOD, PATRICK MICHAEL · 1999 to 2003
$9.2M
REGULATION OF TRANSENDOTHELIAL MIGRATION BY RHO GTPASESF32CA083301 · NCI · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI WORTHYLAKE, BECKY · 1999 to 2001
$17k
NCI NIH HHS F32 CA083301NCI NIH HHS F32 CA83301-02NHLBI NIH HHS HL45100NHLBI NIH HHS P01 HL045100NIDCR NIH HHS DE13079NIDCR NIH HHS P60 DE013079
6 · The paper itself

Abstract

Transendothelial migration of monocytes is the process by which monocytes leave the circulatory system and extravasate through the endothelial lining of the blood vessel wall and enter the underlying tissue. Transmigration requires coordination of alterations in cell shape and adhesive properties that are mediated by cytoskeletal dynamics. We have analyzed the function of RhoA in the cytoskeletal reorganizations that occur during transmigration. By loading monocytes with C3, an inhibitor of RhoA, we found that RhoA was required for transendothelial migration. We then examined individual steps of transmigration to explore the requirement for RhoA in extravasation. Our studies showed that RhoA was not required for monocyte attachment to the endothelium nor subsequent spreading of the monocyte on the endothelial surface. Time-lapse video microscopy analysis revealed that C3-loaded monocytes also had significant forward crawling movement on the endothelial monolayer and were able to invade between neighboring endothelial cells. However, RhoA was required to retract the tail of the migrating monocyte and complete diapedesis. We also demonstrate that p160ROCK, a serine/threonine kinase effector of RhoA, is both necessary and sufficient for RhoA-mediated tail retraction. Finally, we find that p160ROCK signaling negatively regulates integrin adhesions and that inhibition of RhoA results in an accumulation of beta2 integrin in the unretracted tails.

Indexed as

AmidesCD18 AntigensCell AdhesionCell MovementCells, CulturedChemokine CCL2Coculture TechniquesCytoskeletonDose-Response Relationship, DrugElectroporationEndothelium, VascularEnzyme InhibitorsGlutathione TransferaseHumansInterleukin-1Intracellular Signaling Peptides and ProteinsAmidesCD18 AntigensChemokine CCL2Enzyme InhibitorsGlutathione TransferaseInterleukin-1Intracellular Signaling Peptides and ProteinsMyosinsProtein Serine-Threonine KinasesPyridinesRecombinant Fusion ProteinsrhoA GTP-Binding Proteinrho-Associated KinasesY 27632

Identifiers

PMID11448997
PMCPMC2196864
OpenAlexW2157943033

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.