ArticleThe Journal of clinical investigation2011
CGRP induction in cystic fibrosis airways alters the submucosal gland progenitor cell niche in mice.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers.
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
27 citing papers in PubMed, 43 citations in OpenAlex.
- Structural and cellular mechanisms of mucus plugging in the larger airways.Chinese medical journal pulmonary and critical care medicine · 2026Review
- Sensory nerves drive migration of dental pulp stem cells via the CGRP-Ramp1 axis in pulp repair.Cellular and molecular life sciences : CMLS · 2024Article
- Calcitonin Gene-Related Peptide Level in Cystic Fibrosis Patients.Life (Basel, Switzerland) · 2024Article
- CGRP physiology, pharmacology, and therapeutic targets: migraine and beyond.Physiological reviews · 2023Review
- Basic Science Perspective on Engineering and Modeling the Large Airways.Advances in experimental medicine and biology · 2023Article
- Article
- Lung Regeneration: Cells, Models, and Mechanisms.Cold Spring Harbor perspectives in biology · 2022Review
- CGRP: A New Endogenous Cell Stemness Maintenance Molecule.Oxidative medicine and cellular longevity · 2022Review
- Molecular crosstalk in tracheal development and its recurrence in adult tissue regeneration.Developmental dynamics : an official publication of the American Association of Anatomists · 2021Review
- Mammalian Neuropeptides as Modulators of Microbial Infections: Their Dual Role in Defense versus Virulence and Pathogenesis.International journal of molecular sciences · 2021Review
- Airway stem cells sense hypoxia and differentiate into protective solitary neuroendocrine cells.Science (New York, N.Y.) · 2021Article
- Neuropeptides in asthma, chronic obstructive pulmonary disease and cystic fibrosis.Respiratory research · 2018Review
- Submucosal Gland Myoepithelial Cells Are Reserve Stem Cells That Can Regenerate Mouse Tracheal Epithelium.Cell stem cell · 2018Article
- Depletion of Airway Submucosal Glands and TP63American journal of respiratory and critical care medicine · 2018Article
- Multipotent Myoepithelial Progenitor Cells Are Born Early during Airway Submucosal Gland Development.American journal of respiratory cell and molecular biology · 2017Article
- Transplantation of Airway Epithelial Stem/Progenitor Cells: A Future for Cell-Based Therapy.American journal of respiratory cell and molecular biology · 2017Article
- Wnt Signaling Regulates Airway Epithelial Stem Cells in Adult Murine Submucosal Glands.Stem cells (Dayton, Ohio) · 2016Article
- A novel function of calcitonin gene-related peptide in body fluid Cl- homeostasis.Proceedings. Biological sciences · 2016Article
- Glandular Proteome Identifies Antiprotease Cystatin C as a Critical Modulator of Airway Hydration and Clearance.American journal of respiratory cell and molecular biology · 2016Article
- Article
Corrections and comments
- Erratum issued
Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
In cystic fibrosis (CF), a lack of functional CF transmembrane conductance regulator (CFTR) chloride channels causes defective secretion by submucosal glands (SMGs), leading to persistent bacterial infection that damages airways and necessitates tissue repair. SMGs are also important niches for slow-cycling progenitor cells (SCPCs) in the proximal airways, which may be involved in disease-related airway repair. Here, we report that calcitonin gene-related peptide (CGRP) activates CFTR-dependent SMG secretions and that this signaling pathway is hyperactivated in CF human, pig, ferret, and mouse SMGs. Since CGRP-expressing neuroendocrine cells reside in bronchiolar SCPC niches, we hypothesized that the glandular SCPC niche may be dysfunctional in CF. Consistent with this hypothesis, CFTR-deficient mice failed to maintain glandular SCPCs following airway injury. In wild-type mice, CGRP levels increased following airway injury and functioned as an injury-induced mitogen that stimulated SMG progenitor cell proliferation in vivo and altered the proliferative potential of airway progenitors in vitro. Components of the receptor for CGRP (RAMP1 and CLR) were expressed in a very small subset of SCPCs, suggesting that CGRP indirectly stimulates SCPC proliferation in a non-cell-autonomous manner. These findings demonstrate that CGRP-dependent pathways for CFTR activation are abnormally upregulated in CF SMGs and that this sustained mitogenic signal alters properties of the SMG progenitor cell niche in CF airways. This discovery may have important implications for injury/repair mechanisms in the CF airway.
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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.