Evidence map›Paper›PMID 27003941›Full record

ArticleNeurotoxicity research2016

Cigarette Smoke Delays Regeneration of the Olfactory Epithelium in Mice.

Rumi Ueha, Satoshi Ueha, Takashi Sakamoto, Kaori Kanaya, Keigo Suzukawa, Hironobu Nishijima, Shu Kikuta, Kenji Kondo, Kouji Matsushima, Tatsuya Yamasoba

Abstract read
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Article in Neurotoxicity research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.2field-weighted citation impact, top 15% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 30 citations in OpenAlex.

  1. Trial
  2. Review
  3. Chemosensory tobacco product toxicology part 1: sensory mechanisms.Toxicological sciences : an official journal of the Society of Toxicology · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Rumi UehaDepartment of Otolaryngology, The University of Tokyo, 7-3-1 Hongo Bunkyo-ku, Tokyo, 113-8655, Japan. ruu1025@yahoo.co.jp.
Satoshi UehaDepartment of Molecular Preventive Medicine, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo Bunkyo-ku, Tokyo, 113-0033, Japan.
Takashi SakamotoDepartment of Otolaryngology, The University of Tokyo, 7-3-1 Hongo Bunkyo-ku, Tokyo, 113-8655, Japan.
Kaori KanayaDepartment of Otolaryngology, Tokyo Metropolitan Bokutoh Hospital, 4-23-15 Kotobashi Sumida-ku, Tokyo, 130-8575, Japan.
Keigo SuzukawaDepartment of Otolaryngology, Tokyo Metropolitan Bokutoh Hospital, 4-23-15 Kotobashi Sumida-ku, Tokyo, 130-8575, Japan.
Hironobu NishijimaDepartment of Otolaryngology, The University of Tokyo, 7-3-1 Hongo Bunkyo-ku, Tokyo, 113-8655, Japan.
Shu KikutaDepartment of Otolaryngology, The University of Tokyo, 7-3-1 Hongo Bunkyo-ku, Tokyo, 113-8655, Japan.
Kenji KondoDepartment of Otolaryngology, The University of Tokyo, 7-3-1 Hongo Bunkyo-ku, Tokyo, 113-8655, Japan.
Kouji MatsushimaDepartment of Molecular Preventive Medicine, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo Bunkyo-ku, Tokyo, 113-0033, Japan.
Tatsuya YamasobaDepartment of Otolaryngology, The University of Tokyo, 7-3-1 Hongo Bunkyo-ku, Tokyo, 113-8655, Japan.
The University of Tokyo · JPTokyo Metropolitan Bokutoh Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The olfactory system is a unique part of the mammalian nervous system due to its capacity for neurogenesis and the replacement of degenerating receptor neurons. Cigarette smoking is a major cause of olfactory dysfunction. However, the mechanisms by which cigarette smoke impairs the regenerative olfactory receptor neurons (ORNs) remain unclear. Here, we investigated the influence of cigarette smoke on ORN regeneration following methimazole-induced ORN injury. Administration of methimazole caused detachment of the olfactory epithelium from the basement membrane and induced olfactory dysfunction, thus enabling us to analyze the process of ORN regeneration. We found that intranasal administration of cigarette smoke solution (CSS) suppressed the recovery of ORNs and olfaction following ORN injury. Defective ORN recovery in CSS-treated mice was not associated with any change in the number of SOX2(+) ORN progenitor cells in the basal layer of the OE, but was associated with impaired recovery of GAP43(+) immature ORNs. In the nasal mucosa, mRNA expression levels of neurotrophic factors such as brain-derived neurotrophic factor, neurotrophin-3, neurotrophin-5, glial cell-derived neurotrophic factor, and insulin-like growth factor-1 (IGF-1) were increased following OE injury, whereas CSS administration decreased the ORN injury-induced IGF-1 expression. Administration of recombinant human IGF-1 prevented the CSS-induced suppression of ORN recovery following injury. These results suggest that CSS impairs regeneration of ORNs by suppressing the development of immature ORNs from ORN progenitors, at least partly by reducing IGF-1 in the nasal mucosa.

Indexed as

Nerve RegenerationNicotianaSmokeAdministration, IntranasalAnimalsDisease Models, AnimalInsulin-Like Growth Factor IMaleMethimazoleMice, Inbred C57BLNeural Stem CellsNeuroprotective AgentsOlfaction DisordersOlfactory MucosaOlfactory Receptor NeuronsRecombinant ProteinsIGF1 protein, humaninsulin-like growth factor-1, mouseInsulin-Like Growth Factor IMethimazoleNeuroprotective AgentsRecombinant ProteinsRNA, MessengerSmokeCigarette smoke solutionInsulin-like growth factor-1Olfactory epitheliumOlfactory receptor neuronRegeneration

Identifiers

PMID27003941
OpenAlexW2304839922

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.