Evidence map›Paper›PMID 24557763›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2014

Src-mediated caveolin-1 phosphorylation regulates intestinal epithelial restitution by altering Ca(2+) influx after wounding.

Navneeta Rathor, Ran Zhuang, Jian-Ying Wang, James M Donahue, Douglas J Turner, Jaladanki N Rao

Abstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  4. Inhibition of Notch signaling pathway reduces angiogenesis in hypertrophic scar.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2021
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  5. TRPC1-mediated CaPhysiological reports · 2021
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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 2 institutions in 1 country.

Navneeta RathorDepartment of Surgery, Cell Biology Group, University of Maryland School of Medicine, Baltimore, Maryland;
Ran Zhuang
Jian-Ying Wang
James M Donahue
Douglas J Turner
Jaladanki N Rao
University of Maryland, Baltimore · USVeterans Health Administration · US

Funding

Intestinal Mucosal Growth in Health & Surgical DiseasesR01DK057819 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI Jian-Ying Wang · 2000 to 2026
$7.4M
Surgical Studies of Gut PermeabilityR01DK068491 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI Jian-Ying Wang · 2004 to 2026
$7.0M
Mucosal Repair in Gut Surgical DisordersR01DK061972 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI WANG, JIAN-YING · 2002 to 2023
$6.7M
Barrier Dysfunction in Severe Surgical DiseasesI01BX000113 · VA · BALTIMORE VA MEDICAL CENTER · PI TURNER, DOUGLAS J · 2009 to 2024
–
BLRD VA I01 BX000113NIDDK NIH HHS DK-57819NIDDK NIH HHS DK-61972NIDDK NIH HHS DK-68491NIDDK NIH HHS R01 DK057819
6 · The paper itself

Abstract

Early mucosal restitution occurs as a consequence of intestinal epithelial cell (IEC) migration to reseal superficial wounds, but its exact mechanism remains largely unknown. Caveolin-1 (Cav1), a major component associated with caveolar lipid rafts in the plasma membrane, is implicated in many aspects of cellular functions. This study determined if c-Src kinase (Src)-induced Cav1 phosphorylation promotes intestinal epithelial restitution after wounding by activating Cav1-mediated Ca(2+) signaling. Src directly interacted with Cav1, formed Cav1-Src complexes, and phosphorylated Cav1 in IECs. Inhibition of Src activity by its chemical inhibitor PP2 or suppression of the functional caveolin scaffolding domain by caveolin-scaffolding domain peptides prevented Cav1-Src interaction, reduced Cav1 phosphorylation, decreased Ca(2+) influx, and inhibited cell migration after wounding. Disruption of caveolar lipid raft microdomains by methyl-β-cyclodextrin reduced Cav1-mediated Ca(2+) influx and repressed epithelial restitution. Moreover, Src silencing prevented subcellular redistribution of phosphorylated Cav1 in migrating IECs. These results indicate that Src-induced Cav1 phosphorylation stimulates epithelial restitution by increasing Cav1-mediated Ca(2+) signaling after wounding, thus contributing to the maintenance of gut mucosal integrity under various pathological conditions.

Indexed as

Intestinal MucosaCalciumCaveolin 1Cell MovementCells, CulturedCSK Tyrosine-Protein KinaseHumansSignal Transductionsrc-Family KinasesWound HealingCalciumCaveolin 1CSK protein, humanCSK Tyrosine-Protein Kinasesrc-Family Kinasescalcium influxcaveolin-1 scaffolding domain peptidecell migrationcyclopiazonic acidIEC-6 cellsintracellular calciumSrc activity

Identifiers

PMID24557763
PMCPMC3989706
OpenAlexW2000289269

What OpenQuestion holds

Textmetadata
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.