Evidence map›Paper›PMID 27255610›Full record

ReviewThe Journal of investigative dermatology2016

Endoplasmic Reticulum Calcium Regulates Epidermal Barrier Response and Desmosomal Structure.

Anna Celli, Debra Crumrine, Jason M Meyer, Theodora M Mauro

Abstract readReview
In one paragraph

Review in The Journal of investigative dermatology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Endoplasmic Reticulum Dysfunction: An Emerging Mechanism of Vitiligo Pathogenesis.Clinical, cosmetic and investigational dermatology · 2024
    Review
  7. Article
  8. Store-operated calcium channels in skin.Frontiers in physiology · 2022
    Review
  9. Review
  10. Article
  11. Darier Disease - A Multi-organ Condition?Acta dermato-venereologica · 2021
    Review
  12. Article
  13. Article
  14. Article
  15. Skin Barrier and Calcium.Annals of dermatology · 2018
    Review
  16. Article
  17. Article
  18. Article
  19. 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

4 authors.

Anna CelliDermatology Service, Department of Veterans Affairs Medical Center, and Department of Dermatology, University of California, San Francisco, California, USA. Electronic address: Anna.celli2@ucsf.edu.
Debra CrumrineDermatology Service, Department of Veterans Affairs Medical Center, and Department of Dermatology, University of California, San Francisco, California, USA.
Jason M MeyerDermatology Service, Department of Veterans Affairs Medical Center, and Department of Dermatology, University of California, San Francisco, California, USA.
Theodora M MauroDermatology Service, Department of Veterans Affairs Medical Center, and Department of Dermatology, University of California, San Francisco, California, USA.

Funding

Pathogenesis and Therapy of Ichthyosis in Disorders of Lipid MetabolismR01AR061106 · NIAMS · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI MAURO, THEODORA M · 2012 to 2022
$3.3M
ATP2A2-Regulated Keretinocyted Ca2+ Signaling MechanismsR01AR051930 · NIAMS · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI MAURO, THEODORA M · 2006 to 2019
$3.2M
The Lipid and Tight Junction Epidermal Barriers are InterdependentR21AR061583 · NIAMS · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI MAURO, THEODORA M · 2012 to 2013
$358k
NIAMS NIH HHS R01 AR051930NIAMS NIH HHS R01 AR061106NIAMS NIH HHS R21 AR061583
6 · The paper itself

Abstract

Ca(2+) fluxes direct keratinocyte differentiation, cell-to-cell adhesion, migration, and epidermal barrier homeostasis. We previously showed that intracellular Ca(2+) stores constitute a major portion of the calcium gradient especially in the stratum granulosum. Loss of the calcium gradient triggers epidermal barrier homeostatic responses. In this report, using unfixed ex vivo epidermis and human epidermal equivalents we show that endoplasmic reticulum (ER) Ca(2+) is released in response to barrier perturbation, and that this release constitutes the major shift in epidermal Ca(2+) seen after barrier perturbation. We find that ER Ca(2+) release correlates with a transient increase in extracellular Ca(2+). Lastly, we show that ER calcium release resulting from barrier perturbation triggers transient desmosomal remodeling, seen as an increase in extracellular space and a loss of the desmosomal intercellular midline. Topical application of thapsigargin, which inhibits the ER Ca(2+) ATPase activity without compromising barrier integrity, also leads to desmosomal remodeling and loss of the midline structure. These experiments establish the ER Ca(2+) store as a master regulator of the Ca(2+) gradient response to epidermal barrier perturbation, and suggest that ER Ca(2+) homeostasis also modulates normal desmosomal reorganization, both at rest and after acute barrier perturbation.

Indexed as

AnimalsBiopsy, NeedleCalciumCell Membrane PermeabilityDesmosomesEndoplasmic ReticulumEpidermisHomeostasisHumansImmunohistochemistrySkin AbsorptionThapsigarginCalciumThapsigargin

Identifiers

PMID27255610
PMCPMC5070468

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.