Evidence map›Paper›PMID 26365984›Full record

ArticleScientific reports2015

IP3R deficit underlies loss of salivary fluid secretion in Sjögren's Syndrome.

Leyla Y Teos, Yu Zhang, Ana P Cotrim, William Swaim, Jon H Won, Julian Ambrus, Long Shen, Lolita Bebris, Margaret Grisius, Shyh-Ing Jang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Molecular Insights into Oral Manifestations in Sjögren's Disease.International journal of molecular sciences · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. STIMulating Salivary Glands.Function (Oxford, England) · 2025
    Article
  9. Dysregulated CaeLife · 2024
    Article
  10. Review
  11. Dysregulated CabioRxiv : the preprint server for biology · 2024
    Article
  12. Review
  13. Review
  14. Metformin-induced activation of CaJournal of translational autoimmunity · 2023
    Article
  15. Review
  16. Review
  17. Aquaporins in Glandular Secretion.Advances in experimental medicine and biology · 2023
    Article
  18. Article
  19. Review
  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

13 authors at 3 institutions in 1 country.

Leyla Y TeosSjögren's Syndrome and Salivary Gland Dysfunction Unit MPTB, NIDCR, NIH, Bethesda, MD 20892.
Yu ZhangDepartment of Pharmacology and Physiology, University of Rochester, Rochester, NY 14642.
Ana P CotrimSjögren's Syndrome and Salivary Gland Dysfunction Unit MPTB, NIDCR, NIH, Bethesda, MD 20892.
William SwaimSecretory and Physiology Section, MPTB, NIDCR, NIH, Bethesda, MD 20892.
Jon H WonDepartment of Pharmacology and Physiology, University of Rochester, Rochester, NY 14642.
Julian AmbrusDivision of Allergy, Immunology and Rheumatology, Department of Medicine, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, NY 14203.
Long ShenDivision of Allergy, Immunology and Rheumatology, Department of Medicine, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, NY 14203.
Lolita BebrisSjögren's Syndrome and Salivary Gland Dysfunction Unit MPTB, NIDCR, NIH, Bethesda, MD 20892.
Margaret GrisiusSjögren's Syndrome and Salivary Gland Dysfunction Unit MPTB, NIDCR, NIH, Bethesda, MD 20892.
Shyh-Ing JangSjögren's Syndrome and Salivary Gland Dysfunction Unit MPTB, NIDCR, NIH, Bethesda, MD 20892.
David I YuleDepartment of Pharmacology and Physiology, University of Rochester, Rochester, NY 14642.
Indu S AmbudkarSecretory and Physiology Section, MPTB, NIDCR, NIH, Bethesda, MD 20892.
Ilias AlevizosSjögren's Syndrome and Salivary Gland Dysfunction Unit MPTB, NIDCR, NIH, Bethesda, MD 20892.
National Institute of Dental and Craniofacial Research · USUniversity of Rochester · USUniversity at Buffalo, State University of New York · US

Funding

Molecular Mechanisms Regulating Calcium Flux In Salivary GlandsZIADE000438 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI AMBUDKAR, INDU S. · 2009 to 2025
$42.5M
Clinical Investigations of Sjogren's SyndromeZIADE000704 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI WARNER, BLAKE · 2009 to 2025
$22.3M
[Ca2+]i and Secretory Dynamics in Parotid Acinar CellsR01DE014756 · NIDCR · UNIVERSITY OF ROCHESTER · PI David I Yule · 2002 to 2026
$9.9M
Training Program in Oral ScienceT90DE021985 · NIDCR · UNIVERSITY OF ROCHESTER · PI OVITT, CATHERINE, YULE, DAVID I · 2011 to 2021
$5.6M
[Ca2+]i and Secretory Dynamics in Parotid Acinar CellsR56DE014756 · NIDCR · UNIVERSITY OF ROCHESTER · PI YULE, DAVID I · 2007 to 2007
$395k
NIDCR NIH HHS DE014756NIDCR NIH HHS R01 DE014756NIDCR NIH HHS R56 DE014756NIDCR NIH HHS T90 DE021985
6 · The paper itself

Abstract

The autoimmune exocrinopathy, Sjögren's syndrome (SS), is associated with secretory defects in patients, including individuals with mild lymphocytic infiltration and minimal glandular damage. The mechanism(s) underlying the secretory dysfunction is not known. We have used minor salivary gland biopsies from SS patients and healthy individuals to assess acinar cell function in morphologically intact glandular areas. We report that agonist-regulated intracellular Ca(2+) release, critically required for Ca(2+) entry and fluid secretion, is defective in acini from SS patients. Importantly, these acini displayed reduction in IP3R2 and IP3R3, but not AQP5 or STIM1. Similar decreases in IP3R and carbachol (CCh)-stimulated [Ca(2+)]i elevation were detected in acinar cells from lymphotoxin-alpha (LTα) transgenic (TG) mice, a model for (SS). Treatment of salivary glands from healthy individuals with LT α, a cytokine linked to disease progression in SS and IL14α mice, reduced Ca(2+) signaling. Together, our findings reveal novel IP3R deficits in acinar cells that underlie secretory dysfunction in SS patients.

Indexed as

Acinar CellsAnimalsCalciumCalcium SignalingCarbacholCase-Control StudiesCells, CulturedCell SizeDisease Models, AnimalFemaleHumansInositol 1,4,5-Trisphosphate ReceptorsInterleukinsLymphotoxin-alphaMiceMice, Inbred C57BLCalciumCarbacholInositol 1,4,5-Trisphosphate ReceptorsInterleukinsLymphotoxin-alphaTXLNA protein, mouseVesicular Transport Proteins

Identifiers

PMID26365984
PMCPMC4568516
OpenAlexW2188524517

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Registered trials

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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.