ArticleOpen biology2016
Nitric oxide signals are interlinked with calcium signals in normal pancreatic stellate cells upon oxidative stress and inflammation.
Article in Open biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Experimental Acute Pancreatitis Models: History, Current Status, and Role in Translational Research.Frontiers in physiology · 2020Pooled it
- Pancreatic stellate cells: Key players in pancreatic health and diseases (Review).Molecular medicine reports · 2024Review
- Fibroblast subtypes in pancreatic cancer and pancreatitis: from mechanisms to therapeutic strategies.Cellular oncology (Dordrecht, Netherlands) · 2024Review
- The role of CaCell calcium · 2023Review
- Watching Living Cells in Action in the Exocrine Pancreas: The Palade Prize Lecture.Function (Oxford, England) · 2023Review
- Driver Mutations of Pancreatic Cancer Affect CaFunction (Oxford, England) · 2023Article
- The 2022 George E Palade Medal Lecture: Toxic CaPancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2023Review
- Precision Medicine in Pancreatitis: The Future of Acute Pancreatitis Care.Function (Oxford, England) · 2023Review
- Activation of pancreatic stellate cells attenuates intracellular CaCell death & disease · 2022Article
- Acute Pancreatitis: Diagnosis and Treatment.Drugs · 2022Review
- SARS-CoV-2 S Protein Subunit 1 Elicits CaFunction (Oxford, England) · 2022Article
- Pancreatic stellate cells - rising stars in pancreatic pathologies.Physiological research · 2021Review
- Repositioning of duloxetine to target pancreatic stellate cells.Oncology letters · 2021Article
- Calcium Signaling in Pancreatic Immune CellsFunction (Oxford, England) · 2021Article
- Article
- Electron paramagnetic resonance spectroscopy reveals alterations in the redox state of endogenous copper and iron complexes in photodynamic stress-induced ischemic mouse liver.Redox biology · 2020Article
- Synthesis of crocetin derivatives and their potent inhibition in multiple tumor cells proliferation and inflammatory property of macrophage.BMC complementary medicine and therapies · 2020Article
- Molecular Mechanism of Pancreatic Stellate Cells Activation in Chronic Pancreatitis and Pancreatic Cancer.Journal of Cancer · 2020Review
- Protonation of Piezo1 Impairs Cell-Matrix Interactions of Pancreatic Stellate Cells.Frontiers in physiology · 2020Article
- Signaling in the Physiology and Pathophysiology of Pancreatic Stellate Cells -Frontiers in physiology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The mammalian diffuse stellate cell system comprises retinoid-storing cells capable of remarkable transformations from a quiescent to an activated myofibroblast-like phenotype. Activated pancreatic stellate cells (PSCs) attract attention owing to the pivotal role they play in development of tissue fibrosis in chronic pancreatitis and pancreatic cancer. However, little is known about the actual role of PSCs in the normal pancreas. These enigmatic cells have recently been shown to respond to physiological stimuli in a manner that is markedly different from their neighbouring pancreatic acinar cells (PACs). Here, we demonstrate the capacity of PSCs to generate nitric oxide (NO), a free radical messenger mediating, for example, inflammation and vasodilatation. We show that production of cytosolic NO in PSCs is unambiguously related to cytosolic Ca(2+) signals. Only stimuli that evoke Ca(2+) signals in the PSCs elicit consequent NO generation. We provide fresh evidence for the striking difference between signalling pathways in PSCs and adjacent PACs, because PSCs, in contrast to PACs, generate substantial Ca(2+)-mediated and NOS-dependent NO signals. We also show that inhibition of NO generation protects both PSCs and PACs from necrosis. Our results highlight the interplay between Ca(2+) and NO signalling pathways in cell-cell communication, and also identify a potential therapeutic target for anti-inflammatory therapies.
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What OpenQuestion holds
Registered trials
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.