Evidence map›Paper›PMID 31111119›Full record

ArticleFASEB bioAdvances2019

TRPC1 expression and function inhibit ER stress and cell death in salivary gland cells.

Pramod Sukumaran, Yuyang Sun, Fredice Quenum Zangbede, Viviane Nascimento da Conceicao, Bibhuti Mishra, Brij B Singh

Open access · goldAbstract read
In one paragraph

Article in FASEB bioAdvances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Metformin-induced activation of CaJournal of translational autoimmunity · 2023
    Article
  3. Article
  4. Article
  5. New Frontiers on ER Stress Modulation: Are TRP Channels the Leading Actors?International journal of molecular sciences · 2022
    Review
  6. Article
  7. Article
  8. Inhibition of CaFrontiers in physiology · 2022
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. 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

6 authors at 2 institutions in 1 country.

Pramod SukumaranDepartment of Periodontics, School of Dentistry, University of Texas Health Science Center, San Antonio, TX 78229.
Yuyang SunDepartment of Periodontics, School of Dentistry, University of Texas Health Science Center, San Antonio, TX 78229.
Fredice Quenum ZangbedeDepartment of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58201.
Viviane Nascimento da ConceicaoDepartment of Periodontics, School of Dentistry, University of Texas Health Science Center, San Antonio, TX 78229.
Bibhuti MishraDepartment of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58201.
Brij B SinghDepartment of Periodontics, School of Dentistry, University of Texas Health Science Center, San Antonio, TX 78229.
The University of Texas Health Science Center at San Antonio · USUniversity of North Dakota · US

Funding

Yersina perstis interactions with macrophagesP20GM113123 · NIGMS · UNIVERSITY OF NORTH DAKOTA · PI BRADLEY, DAVID S. · 2016 to 2025
$19.9M
TRPC1, Calcium, and Saliva SecretionR01DE017102 · NIDCR · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Brij B Singh · 2006 to 2026
$7.5M
Epigenetic regulations in Sjogern's syndromeR01DE022765 · NIDCR · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI SINGH, BRIJ B · 2017 to 2021
$1.8M
Galectins as novel alarmins in salivary gland inflammationR21DE024300 · NIDCR · UNIVERSITY OF NORTH DAKOTA · PI MISHRA, BIBHUTI BHUSAN, SINGH, BRIJ B · 2015 to 2016
$382k
NIDCR NIH HHS R01 DE017102NIDCR NIH HHS R01 DE022765NIDCR NIH HHS R21 DE024300NIGMS NIH HHS P20 GM113123
6 · The paper itself

Abstract

Disturbances in endoplasmic reticulum (ER) Ca2+ homeostasis have been associated with many diseases including loss of salivary glands. Although significant progress has been accomplished which led to the increase in our understanding of the cellular responses to ER stress, the factors/ion channels that could inhibit ER stress are not yet identified. Here we show that TRPC1 (transient receptor potential canonical 1) is involved in regulating Ca2+ homeostasis and loss of TRPC1 decreased ER Ca2+ levels, inhibited the unfolded protein response (UPR), that induced loss of salivary gland cells. We provide further evidence that ER stress inducing agents (Tunicamycin and Brefeldin A) disrupts Ca2+ homeostasis by directly inhibiting TRPC1-mediated Ca2+ entry, which led to ER stress in salivary gland cells. Moreover, induction of ER stress lead to an increase in CHOP expression, which decreased TRPC1 expression and subsequently attenuated autophagy along with increased apoptosis. Importantly, TRPC1-/- mice showed increased ER stress, increased immune cell infiltration, loss of Ca2+ homeostasis, decreased saliva secretion, and decreased salivary gland survival. Finally, restoration of TRPC1 not only maintained Ca2+ homeostasis, but inhibited ER stress that induced cell survival. Overall these results suggest a significant role of TRPC1 Ca2+ channels in ER stress and homeostatic function/survival of salivary gland cells.

Indexed as

ER stressSalivary GlandSOCETRPC1Tunicamycin

Identifiers

PMID31111119
PMCPMC6524637
OpenAlexW2945683847

What OpenQuestion holds

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LicenceCC BY
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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.