| http://purl.uniprot.org/citations/32224228 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/32224228 | http://www.w3.org/2000/01/rdf-schema#comment | "The mammalian main olfactory epithelium (MOE) is exposed to a wide spectrum of external chemicals during respiration and relies on adaptive plasticity to maintain its structural and functional integrity. We previously reported that the chemo-responsive and cholinergic transient receptor potential channel M5 (TRPM5)-expressing-microvillous cells (MCs) in the MOE are required for maintaining odor-evoked electrophysiological responses and olfactory-guided behavior during two-week exposure to an inhaled chemical mixture. Here, we investigated the underlying factors by assessing the potential modulatory effects of TRPM5-MCs on MOE morphology and cell proliferation and apoptosis, which are important for MOE maintenance. In the posterior MOE of TRPM5-GFP mice, we found that two-week chemical exposure induced a significant increase in Ki67-expressing proliferating basal stem cells without a significant reduction in the thickness of the whole epithelium or mature olfactory sensory neuron (OSN) layer. This adaptive increase in stem cell proliferation was missing in chemical-exposed transcription factor Skn-1a knockout (Skn-1a-/-) mice lacking TRPM5-MCs. In addition, a greater number of isolated OSNs from chemical-exposed Skn-1a-/- mice displayed unhealthily high levels of resting intracellular Ca2+. Intriguingly, in the anterior MOE where we found a higher density of TRPM5-MCs, chemical-exposed TRPM5-GFP mice exhibited a time-dependent increase in apoptosis and a loss of mature OSNs without a significant increase in proliferation or neurogenesis to compensate for OSN loss. Together, our data suggest that TRPM5-MC-dependent region-specific upregulation of cell proliferation in the majority of the MOE during chemical exposure contributes to the adaptive maintenance of OSNs and olfactory function."xsd:string |
| http://purl.uniprot.org/citations/32224228 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.neuroscience.2020.03.029"xsd:string |
| http://purl.uniprot.org/citations/32224228 | http://purl.uniprot.org/core/author | "Fu Z."xsd:string |
| http://purl.uniprot.org/citations/32224228 | http://purl.uniprot.org/core/author | "Lin W."xsd:string |
| http://purl.uniprot.org/citations/32224228 | http://purl.uniprot.org/core/author | "Ogura T."xsd:string |
| http://purl.uniprot.org/citations/32224228 | http://purl.uniprot.org/core/author | "Lemons K."xsd:string |
| http://purl.uniprot.org/citations/32224228 | http://purl.uniprot.org/core/date | "2020"xsd:gYear |
| http://purl.uniprot.org/citations/32224228 | http://purl.uniprot.org/core/name | "Neuroscience"xsd:string |
| http://purl.uniprot.org/citations/32224228 | http://purl.uniprot.org/core/pages | "171-190"xsd:string |
| http://purl.uniprot.org/citations/32224228 | http://purl.uniprot.org/core/title | "TRPM5-expressing Microvillous Cells Regulate Region-specific Cell Proliferation and Apoptosis During Chemical Exposure."xsd:string |
| http://purl.uniprot.org/citations/32224228 | http://purl.uniprot.org/core/volume | "434"xsd:string |
| http://purl.uniprot.org/citations/32224228 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/32224228 |
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