Evidence map›Paper›PMID 21148289›Full record

ArticleMolecular biology of the cell2011

Phenotypic changes in mouse pancreatic stellate cell Ca2+ signaling events following activation in culture and in a disease model of pancreatitis.

Jong Hak Won, Yu Zhang, Baoan Ji, Craig D Logsdon, David I Yule

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 12% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. The role of CaCell calcium · 2023
    Review
  8. Article
  9. Article
  10. Frontiers in pharmacology · 2022
    Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Plasma Membrane CaCancers · 2020
    Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review
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

5 authors at 2 institutions in 1 country.

Jong Hak WonDepartment of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY 14642, USA.
Yu Zhang
Baoan Ji
Craig D Logsdon
David I Yule
University of Rochester Medical Center · USThe University of Texas MD Anderson Cancer Center · US

Funding

[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
PANCREATIC SECRETION--G PROTEIN MEDIATED CA++ SIGNALINGR01DK054568 · NIDDK · UNIVERSITY OF ROCHESTER · PI YULE, DAVID I · 1998 to 2012
$3.1M
NIDCR NIH HHS R01 DE014756NIDCR NIH HHS R01-DE14756NIDCR NIH HHS T90 DE021985NIDDK NIH HHS R01 DK054568NIDDK NIH HHS R01-DK05468
6 · The paper itself

Abstract

The specific characteristics of intracellular Ca 2+ signaling and the downstream consequences of these events were investigated in mouse pancreatic stellate cells (PSC) in culture and in situ using multiphoton microscopy in pancreatic lobules. PSC undergo a phenotypic transformation from a quiescent state to a myofibroblast-like phenotype in culture. This is believed to parallel the induction of an activated state observed in pancreatic disease such as chronic pancreatitis and pancreatic cancer. By day 7 in culture, the complement of cell surface receptors coupled to intracellular Ca 2+ signaling was shown to be markedly altered. Specifically, protease-activated receptors (PAR) 1 and 2, responsive to thrombin and trypsin, respectively, and platelet-derived growth factor (PDGF) receptors were expressed only in activated PSC (aPSC). PAR-1, ATP, and PDGF receptor activation resulted in prominent nuclear Ca 2+ signals. Nuclear Ca 2+ signals and aPSC proliferation were abolished by expression of parvalbumin targeted to the nucleus. In pancreatic lobules, PSC responded to agonists consistent with the presence of only quiescent PSC. aPSC were observed following induction of experimental pancreatitis. In contrast, in a mouse model of pancreatic disease harboring elevated K-Ras activity in acinar cells, aPSC were present under control conditions and their number greatly increased following induction of pancreatitis. These data are consistent with nuclear Ca 2+ signaling generated by agents such as trypsin and thrombin, likely present in the pancreas in disease states, resulting in proliferation of "primed" aPSC to contribute to the severity of pancreatic disease.

Indexed as

Calcium SignalingPhenotypeAnimalsCell Culture TechniquesCell ProliferationCells, CulturedMicePancreatic Stellate CellsPancreatitisReceptor, PAR-1Receptor, PAR-2Receptors, Cell SurfaceReceptor, PAR-1Receptor, PAR-2Receptors, Cell Surface

Identifiers

PMID21148289
PMCPMC3031471
OpenAlexW2138975466

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.