Stem and progenitor cells of the mammalian olfactory epithelium: Taking poietic license
Schwob JE., Jang W., Holbrook EH., Lin B., Herrick DB., Peterson JN.
Narrative Review, published in J Comp Neurol (2017) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Narrative Review
- Journal
- J Comp Neurol (2017)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 27560601
- PMCID
- PMC5805156
- DOI
- 10.1002/cne.24105
- Citations
- 209
Abstract (original English)
The capacity of the olfactory epithelium (OE) for lifelong neurogenesis and regeneration depends on the persistence of neurocompetent stem cells, which self-renew as well as generating all of the cell types found within the nasal epithelium. This Review focuses on the types of stem and progenitor cells in the epithelium and their regulation. Both horizontal basal cells (HBCs) and some among the population of globose basal cells (GBCs) are stem cells, but the two types plays vastly different roles. The GBC population includes the basal cells that proliferate in the uninjured OE and is heterogeneous with respect to transcription factor expression. From upstream in the hierarchy to downstream, GBCs encompass 1) Sox2 + /Pax6 + stem-like cells that are totipotent and self-renew over the long term, 2) Ascl1 + transit-amplifying progenitors with a limited capacity for expansive proliferation, and 3) Neurog1 + /NeuroD1 + immediate precursor cells that make neurons directly. In contrast, the normally quiescent HBCs are activated to multipotency and proliferate when sustentacular cells are killed, but not when only OSNs die, indicating that HBCs are reserve stem cells that respond to severe epithelial injury. The master regulator of HBC activation is the ΔN isoform of the transcription factor p63; eliminating ΔNp63 unleashes HBC multipotency. Notch signaling, via Jagged1 ligand on Sus ce
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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