Evidence map›Paper›PMID 27540365›Full record

ArticleFrontiers in physiology2016

Olfactory Receptors Modulate Physiological Processes in Human Airway Smooth Muscle Cells.

Benjamin Kalbe, Jürgen Knobloch, Viola M Schulz, Christine Wecker, Marian Schlimm, Paul Scholz, Fabian Jansen, Erich Stoelben, Stathis Philippou, Erich Hecker and 4 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Article
  3. Asthma endotypes and theratypes.Chinese medical journal pulmonary and critical care medicine · 2026
    Review
  4. Article
  5. Review
  6. Olfactory receptors and human diseases.Cell and tissue research · 2025
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Exposure to TiONanomaterials (Basel, Switzerland) · 2021
    Article
  19. Article
  20. Article
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

14 authors at 4 institutions in 1 country.

Benjamin KalbeDepartment of Cell Physiology, Ruhr-University Bochum Bochum, Germany.
Jürgen KnoblochDepartment of Internal Medicine III for Pneumology, Allergology, Sleep- and Respiratory Medicine, University Hospital Bergmannsheil Bochum, Germany.
Viola M SchulzDepartment of Cell Physiology, Ruhr-University Bochum Bochum, Germany.
Christine WeckerDepartment of Cell Physiology, Ruhr-University Bochum Bochum, Germany.
Marian SchlimmDepartment of Cell Physiology, Ruhr-University Bochum Bochum, Germany.
Paul ScholzDepartment of Cell Physiology, Ruhr-University Bochum Bochum, Germany.
Fabian JansenDepartment of Cell Physiology, Ruhr-University Bochum Bochum, Germany.
Erich StoelbenDepartment of Thoracic Surgery, Lungenklinik Merheim, Kliniken der Stadt Köln Cologne, Germany.
Stathis PhilippouDepartment of Pathology and Cytology, Augusta-Kranken-Anstalt Bochum, Germany.
Erich HeckerThoraxzentrum Ruhrgebiet, Department of Thoracic Surgery, Evangelisches Krankenhaus Herne Herne, Germany.
Hermann LübbertDepartment of Animal Physiology, Ruhr-University Bochum Bochum, Germany.
Andrea KochDepartment of Internal Medicine III for Pneumology, Allergology, Sleep- and Respiratory Medicine, University Hospital Bergmannsheil Bochum, Germany.
Hanns HattDepartment of Cell Physiology, Ruhr-University Bochum Bochum, Germany.
Sabrina OsterlohDepartment of Cell Physiology, Ruhr-University Bochum Bochum, Germany.
Ruhr University Bochum · DEBG University Hospital Bergmannsheil Bochum · DEAugusta-Kranken-Anstalt · DEKliniken der Stadt Köln · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pathophysiological mechanisms in human airway smooth muscle cells (HASMCs) significantly contribute to the progression of chronic inflammatory airway diseases with limited therapeutic options, such as severe asthma and COPD. These abnormalities include the contractility and hyperproduction of inflammatory proteins. To develop therapeutic strategies, key pathological mechanisms, and putative clinical targets need to be identified. In the present study, we demonstrated that the human olfactory receptors (ORs) OR1D2 and OR2AG1 are expressed at the RNA and protein levels in HASMCs. Using fluorometric calcium imaging, specific agonists for OR2AG1 and OR1D2 were identified to trigger transient Ca(2+) increases in HASMCs via a cAMP-dependent signal transduction cascade. Furthermore, the activation of OR2AG1 via amyl butyrate inhibited the histamine-induced contraction of HASMCs, whereas the stimulation of OR1D2 with bourgeonal led to an increase in cell contractility. In addition, OR1D2 activation induced the secretion of IL-8 and GM-CSF. Both effects were inhibited by the specific OR1D2 antagonist undecanal. We herein provide the first evidence to show that ORs are functionally expressed in HASMCs and regulate pathophysiological processes. Therefore, ORs might be new therapeutic targets for these diseases, and blocking ORs could be an auspicious strategy for the treatment of early-stage chronic inflammatory lung diseases.

Indexed as

contractioncytokinesolfactory receptorsignalingsmooth muscle cells

Identifiers

PMID27540365
PMCPMC4972829
OpenAlexW2491447331

What OpenQuestion holds

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LicenceCC BY
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.