Evidence map›Paper›PMID 18815229›Full record

ArticleAmerican journal of physiology. Cell physiology2008

Electrogenic NBCe1 (SLC4A4), but not electroneutral NBCn1 (SLC4A7), cotransporter undergoes cholinergic-stimulated endocytosis in salivary ParC5 cells.

Clint Perry, David O Quissell, Mary E Reyland, Irina I Grichtchenko

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.7field-weighted citation impact, top 36% 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

15 citing papers in PubMed, 18 citations in OpenAlex.

  1. Potential Theranostic Roles of SLC4 Molecules in Human Diseases.International journal of molecular sciences · 2023
    Review
  2. Understanding the Physiological Role of Electroneutral NaPharmaceuticals (Basel, Switzerland) · 2022
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Cation-coupled bicarbonate transporters.Comprehensive Physiology · 2014
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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 at 1 institution in 1 country.

Clint PerryUniv. of Colorado and Denver Health Sciences Center, Dept. of Physiology and Biophysics, Mail Stop 8307, P.O. Box 6511, Aurora, CO 80045, USA.
David O Quissell
Mary E Reyland
Irina I Grichtchenko
University of Colorado Anschutz Medical Campus · US

Funding

Regulation of Salivary Cell Apoptosis by Protein Kinase CR01DE015648 · NIDCR · UNIVERSITY OF COLORADO DENVER · PI REYLAND, MARY ELAINE · 2004 to 2019
$5.6M
NIDCR NIH HHS DE-015648NIDCR NIH HHS R01 DE015648
6 · The paper itself

Abstract

Cholinergic agonists are major stimuli for fluid secretion in parotid acinar cells. Saliva bicarbonate is essential for maintaining oral health. Electrogenic and electroneutral Na(+)-HCO(3)(-) cotransporters (NBCe1 and NBCn1) are abundant in parotid glands. We previously reported that angiotensin regulates NBCe1 by endocytosis in Xenopus oocytes. Here, we studied cholinergic regulation of NBCe1 and NBCn1 membrane trafficking by confocal fluorescent microscopy and surface biotinylation in parotid epithelial cells. NBCe1 and NBCn1 colocalized with E-cadherin monoclonal antibody at the basolateral membrane (BLM) in polarized ParC5 cells. Inhibition of constitutive recycling with the carboxylic ionophore monensin or the calmodulin antagonist W-13 caused NBCe1 to accumulate in early endosomes with a parallel loss from the BLM, suggesting that NBCe1 is constitutively endocytosed. Carbachol and PMA likewise caused redistribution of NBCe1 from BLM to early endosomes. The PKC inhibitor, GF-109203X, blocked this redistribution, indicating a role for PKC. In contrast, BLM NBCn1 was not downregulated in parotid acinar cells treated with constitutive recycling inhibitors, cholinergic stimulators, or PMA. We likewise demonstrate striking differences in regulation of membrane trafficking of NBCe1 vs. NBCn1 in resting and stimulated cells. We speculate that endocytosis of NBCe1, which coincides with the transition to a steady-state phase of stimulated fluid secretion, could be a part of acinar cell adjustment to a continuous secretory response. Stable association of NBCn1 at the membrane may facilitate constitutive uptake of HCO(3)(-) across the BLM, thus supporting HCO(3)(-) luminal secretion and/or maintaining acid-base homeostasis in stimulated cells.

Indexed as

AnimalsBicarbonatesBiotinylationCalmodulinCarbacholCell LineCell MembraneCell PolarityCholinergic AgonistsEndocytosisEndosomesGene Transfer TechniquesHydrogen-Ion ConcentrationIndolesMaleimidesMicroscopy, ConfocalBicarbonatesbisindolylmaleimide ICalmodulinCarbacholCholinergic AgonistsIndolesMaleimidesMonensinN-(4-aminobutyl)-5-chloro-2-naphthalenesulfonamideProtein Kinase CProtein Kinase InhibitorsReceptors, MuscarinicSlc4a4 protein, ratSlc4a7 protein, ratSodium-Bicarbonate SymportersSulfonamidesTetradecanoylphorbol Acetate

Identifiers

PMID18815229
PMCPMC2584990
OpenAlexW2120065189

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.