Evidence map›Paper›PMID 26336927›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2015

RhoA enhances store-operated Ca2+ entry and intestinal epithelial restitution by interacting with TRPC1 after wounding.

Hee Kyoung Chung, Navneeta Rathor, Shelley R Wang, Jian-Ying Wang, Jaladanki N Rao

Abstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 20% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Stabilization ofAmerican journal of physiology. Gastrointestinal and liver physiology · 2023
    Article
  3. Article
  4. Polysaccharides fromJournal of ginseng research · 2023
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. TRPC1-mediated CaPhysiological reports · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
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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

5 authors at 1 institution in 1 country.

Hee Kyoung ChungCell Biology Group, Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland; Baltimore Veterans Affairs Medical Center, Baltimore, Maryland.
Navneeta RathorCell Biology Group, Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland; Baltimore Veterans Affairs Medical Center, Baltimore, Maryland.
Shelley R WangCell Biology Group, Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland;
Jian-Ying WangCell Biology Group, Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland; Department of Pathology, University of Maryland School of Medicine, Baltimore, Maryland; and Baltimore Veterans Affairs Medical Center, Baltimore, Maryland.
Jaladanki N RaoCell Biology Group, Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland; Baltimore Veterans Affairs Medical Center, Baltimore, Maryland rjaladanki@smail.umaryland.edu.
University of Maryland, Baltimore · 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
SURGICAL STUDIES ON MUCOSAL HOMEOSTASISI01BX000713 · VA · BALTIMORE VA MEDICAL CENTER · PI WANG, JIAN-YING · 2011 to 2024
–
BLRD VA I01 BX000713NIDDK NIH HHS DK-57819NIDDK NIH HHS DK-61972NIDDK NIH HHS DK-68491NIDDK NIH HHS R01 DK057819NIDDK NIH HHS R01 DK061972NIDDK NIH HHS R01 DK068491
6 · The paper itself

Abstract

Early mucosal restitution occurs as a consequence of epithelial cell migration to resealing of superficial wounds after injury. Our previous studies show that canonical transient receptor potential-1 (TRPC1) functions as a store-operated Ca(2+) channel (SOC) in intestinal epithelial cells (IECs) and plays an important role in early epithelial restitution by increasing Ca(2+) influx. Here we further reported that RhoA, a small GTP-binding protein, interacts with and regulates TRPC1, thus enhancing SOC-mediated Ca(2+) entry (SOCE) and epithelial restitution after wounding. RhoA physically associated with TRPC1 and formed the RhoA/TRPC1 complexes, and this interaction increased in stable TRPC1-transfected IEC-6 cells (IEC-TRPC1). Inactivation of RhoA by treating IEC-TRPC1 cells with exoenzyme C3 transferase (C3) or ectopic expression of dominant negative RhoA (DNMRhoA) reduced RhoA/TRPC1 complexes and inhibited Ca(2+) influx after store depletion, which was paralleled by an inhibition of cell migration over the wounded area. In contrast, ectopic expression of wild-type (WT)-RhoA increased the levels of RhoA/TRPC1 complexes, induced Ca(2+) influx through activation of SOCE, and promoted cell migration after wounding. TRPC1 silencing by transfecting stable WT RhoA-transfected cells with siRNA targeting TRPC1 (siTRPC1) reduced SOCE and repressed epithelial restitution. Moreover, ectopic overexpression of WT-RhoA in polyamine-deficient cells rescued the inhibition of Ca(2+) influx and cell migration induced by polyamine depletion. These findings indicate that RhoA interacts with and activates TRPC1 and thus stimulates rapid epithelial restitution after injury by inducing Ca(2+) signaling.

Indexed as

Calcium SignalingWound HealingAnimalsCell LineCell MovementCell ProliferationEpithelial CellsHumansIntestinal MucosaRatsRe-EpithelializationrhoA GTP-Binding ProteinRNA InterferenceTransfectionTRPC Cation ChannelsrhoA GTP-Binding ProteinRHOA protein, humantransient receptor potential cation channel, subfamily C, member 1TRPC Cation ChannelsCa2+ influxcyclopiazonic acidepithelial restitutionGTP-binding proteinspolyamines

Identifiers

PMID26336927
PMCPMC4628965
OpenAlexW1251238164

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.