ArticlePloS one2013
An IP3R3- and NPY-expressing microvillous cell mediates tissue homeostasis and regeneration in the mouse olfactory epithelium.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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.
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Who cites it
27 citing papers in PubMed, 35 citations in OpenAlex.
- Olfactory epithelium regeneration and homeostasis: cellular and molecular mechanisms and novel methodological advances.Cell regeneration (London, England) · 2026Review
- Olfactory immunity: defending the neural-mucosal barrier.Journal of immunology (Baltimore, Md. : 1950) · 2026Review
- Chemosensory tobacco product toxicology part 1: sensory mechanisms.Toxicological sciences : an official journal of the Society of Toxicology · 2025Review
- A nasal cell atlas reveals heterogeneity of tuft cells and their role in directing olfactory stem cell proliferation.Science immunology · 2024Article
- Constitutive and evoked release of ATP in adult mouse olfactory epithelium.Open life sciences · 2024Article
- Sex steroid hormone synthesis, metabolism, and the effects on the mammalian olfactory system.Cell and tissue research · 2023Review
- The nervous system during COVID-19: Caught in the crossfire.Immunological reviews · 2022Review
- Chitinase-Like Protein Ym2 (Chil4) Regulates Regeneration of the Olfactory Epithelium via Interaction with Inflammation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Modulation of olfactory signal detection in the olfactory epithelium: focus on the internal and external environment, and the emerging role of the immune system.Cell and tissue research · 2021Review
- Inhibition of focal adhesion kinase increases adult olfactory stem cell self-renewal and neuroregeneration through ciliary neurotrophic factor.Stem cell research · 2020Article
- Increased Retinoic Acid Catabolism in Olfactory Sensory Neurons Activates Dormant Tissue-Specific Stem Cells and Accelerates Age-Related Metaplasia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- TRPM5-expressing Microvillous Cells Regulate Region-specific Cell Proliferation and Apoptosis During Chemical Exposure.Neuroscience · 2020Article
- Alzheimer's Disease: What Can We Learn From the Peripheral Olfactory System?Frontiers in neuroscience · 2020Review
- Purinergic Signaling in the Vertebrate Olfactory System.Frontiers in cellular neuroscience · 2019Review
- Chemical Exposure-Induced Changes in the Expression of Neurotrophins and Their Receptors in the Main Olfactory System of Mice Lacking TRPM5-Expressing Microvillous Cells.International journal of molecular sciences · 2018Article
- Deconstructing Olfactory Stem Cell Trajectories at Single-Cell Resolution.Cell stem cell · 2017Article
- Stem and progenitor cells of the mammalian olfactory epithelium: Taking poietic license.The Journal of comparative neurology · 2017Review
- Functional Reintegration of Sensory Neurons and Transitional Dendritic Reduction of Mitral/Tufted Cells during Injury-Induced Recovery of the LarvalFrontiers in cellular neuroscience · 2017Article
- Effects of Neuropeptide Y on Stem Cells and Their Potential Applications in Disease Therapy.Stem cells international · 2017Review
- Ascl3 transcription factor marks a distinct progenitor lineage for non-neuronal support cells in the olfactory epithelium.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Calcium-dependent release of neurotrophic factors plays an important role in the maintenance of neurons, yet the release mechanisms are understudied. The inositol triphosphate (IP3) receptor is a calcium release channel that has a physiological role in cell growth, development, sensory perception, neuronal signaling and secretion. In the olfactory system, the IP3 receptor subtype 3 (IP3R3) is expressed exclusively in a microvillous cell subtype that is the predominant cell expressing neurotrophic factor neuropeptide Y (NPY). We hypothesized that IP3R3-expressing microvillous cells secrete sufficient NPY needed for both the continual maintenance of the neuronal population and for neuroregeneration following injury. We addressed this question by assessing the release of NPY and the regenerative capabilities of wild type, IP3R3(+/-), and IP3R3(-/-) mice. Injury, simulated using extracellular ATP, induced IP3 receptor-mediated NPY release in wild-type mice. ATP-evoked NPY release was impaired in IP3R3(-/-) mice, suggesting that IP3R3 contributes to NPY release following injury. Under normal physiological conditions, both IP3R3(-/-) mice and explants from these mice had fewer progenitor cells that proliferate and differentiate into immature neurons. Although the number of mature neurons and the in vivo rate of proliferation were not altered, the proliferative response to the olfactotoxicant satratoxin G and olfactory bulb ablation injury was compromised in the olfactory epithelium of IP3R3(-/-) mice. The reductions in both NPY release and number of progenitor cells in IP3R3(-/-) mice point to a role of the IP3R3 in tissue homeostasis and neuroregeneration. Collectively, these data suggest that IP3R3 expressing microvillous cells are actively responsive to injury and promote recovery.
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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.