Evidence map›Paper›PMID 20631248›Full record

ArticleAmerican journal of physiology. Cell physiology2010

STIM1 translocation to the plasma membrane enhances intestinal epithelial restitution by inducing TRPC1-mediated Ca2+ signaling after wounding.

Jaladanki N Rao, Navneeta Rathor, Tongtong Zou, Lan Liu, Lan Xiao, Ting-Xi Yu, Yu-Hong Cui, Jian-Ying Wang

Abstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2010. 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
2.9field-weighted citation impact, top 9% 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, 47 citations in OpenAlex.

  1. Article
  2. Stabilization ofAmerican journal of physiology. Gastrointestinal and liver physiology · 2023
    Article
  3. Article
  4. Article
  5. TRPC1-mediated CaPhysiological reports · 2021
    Article
  6. Advances in CaExperimental and therapeutic medicine · 2020
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  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

8 authors at 1 institution in 1 country.

Jaladanki N RaoCell Biology Group, Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Navneeta Rathor
Tongtong Zou
Lan Liu
Lan Xiao
Ting-Xi Yu
Yu-Hong Cui
Jian-Ying Wang
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
NIDDK NIH HHS DK-57819NIDDK NIH HHS DK-61972NIDDK NIH HHS DK-68491
6 · The paper itself

Abstract

Early epithelial restitution is an important repair modality in the gut mucosa and occurs as a consequence of epithelial cell migration. Canonical transient receptor potential-1 (TRPC1) functions as a store-operated Ca2+ channel (SOCs) in intestinal epithelial cells (IECs) and regulates intestinal restitution, but the exact upstream signals initiating TRPC1 activation after mucosal injury remain elusive. Stromal interaction molecule 1 (STIM1) is a single membrane-spanning protein and is recently identified as essential components of SOC activation. The current study was performed to determine whether STIM1 plays a role in the regulation of intestinal epithelial restitution by activating TRPC1 channels. STIM1 translocation to the plasma membrane increased after wounding, which was followed by an increase in IEC migration to reseal wounds. Increased STIM1 levels at the plasma membrane by overexpressing EF-hand mutant STIM1 enhanced Ca2+ influx through SOCs and stimulated IEC migration after wounding. STIM1 interacted with TRPC1 and formed STIM1/TRPC1 complex, whereas inactivation of STIM1 by STIM1 silencing decreased SOC-mediated Ca2+ influx and inhibited epithelial restitution. In cells overexpressing EF-hand mutant STIM1, TRPC1 silencing also decreased STIM1/TRPC1 complex, reduced SOC-mediated Ca2+ influx, and repressed cell migration after wounding. Our findings demonstrate that induced STIM1 translocation to the plasma membrane promotes IEC migration after wounding by enhancing TRPC1-mediated Ca2+ signaling and provide new insight into the mechanism of intestinal epithelial restitution.

Indexed as

Calcium SignalingWound HealingAnimalsCalciumCalcium ChannelsCell LineCell MembraneCell MovementDrosophila ProteinsEpithelial CellsIntestinal MucosaMembrane ProteinsProtein TransportRatsStromal Interaction Molecule 1TRPC Cation ChannelsCalciumCalcium ChannelsDrosophila ProteinsMembrane ProteinsStim protein, DrosophilaStromal Interaction Molecule 1transient receptor potential cation channel, subfamily C, member 1TRPC Cation Channels

Identifiers

PMID20631248
PMCPMC2944314
OpenAlexW2147042111

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.