Evidence map›Paper›PMID 27791986›Full record

ArticleOncotarget2016

Human airway smooth muscle cell proliferation from asthmatics is negatively regulated by semaphorin3A.

Hesam Movassagh, Nazanin Tatari, Lianyu Shan, Latifa Koussih, Duaa Alsubait, Mahdi Khattabi, Naresh S Redhu, Michael Roth, Michael Tamm, Jamila Chakir and 1 more

Abstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. LAPTM5 potentiates airway remodeling by regulating MAPKs-mediated airway smooth muscle cells' dysfunction.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
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  4. Review
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  13. Gpr97 Exacerbates AKI by Mediating Sema3A Signaling.Journal of the American Society of Nephrology : JASN · 2018
    Article
  14. Article
  15. Review
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

11 authors.

Hesam MovassaghDepartment of Immunology, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
Nazanin TatariDepartment of Immunology, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
Lianyu ShanDepartment of Immunology, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
Latifa KoussihDepartment of Immunology, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
Duaa AlsubaitDepartment of Immunology, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
Mahdi KhattabiDepartment of Immunology, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
Naresh S RedhuDepartment of Immunology, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
Michael RothDepartment of Biomedicine, Pneumology & Pulmonary Cell Research, University Hospital Basel and University of Basel, Basel, Switzerland.
Michael TammDepartment of Biomedicine, Pneumology & Pulmonary Cell Research, University Hospital Basel and University of Basel, Basel, Switzerland.
Jamila ChakirCentre de Recherche de l'Institut Universitaire de Cardiologie et de Pneumologie du Quebec, Universite´ Laval, Quebec City, Canada.
Abdelilah S GounniDepartment of Immunology, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Airway smooth muscle (ASM) hyperplasia is a key feature of airway remodeling in development of lung diseases such as asthma. Anomalous proliferation of ASM cells directly contributes to ASM hyperplasia. However, the molecular mechanisms controlling ASM cell proliferation are not completely understood. Semaphorins are versatile regulators of various cellular processes including cell growth and proliferation. The role of semaphorins in ASM cell proliferation has remained to be addressed. Here, we report that semaphorin 3A (Sema3A) receptor, neuropilin 1 (Nrp1), is expressed on human ASM cells (HASMC) isolated from healthy and asthmatic donors and treatment of these cells with exogenous Sema3A inhibits growth factor-induced proliferation. Sema3A inhibitory effect on HASMC proliferation is associated with decreased tyrosine phosphorylation of PDGFR, downregulation of Rac1 activation, STAT3 and GSK-3β phosphorylation. Bronchial sections from severe asthmatics displayed immunoreactivity of Nrp1, suggestive of functional contribution of Sema3A-Nrp1 axis in airway remodeling. Together, our data suggest Sema3A-Nrp1 signaling as a novel regulatory pathway of ASM hyperplasia.

Indexed as

Airway RemodelingCell ProliferationAdultAsthmaBronchiCase-Control StudiesCell LineFemaleGlycogen Synthase Kinase 3 betaHumansHyperplasiaMaleMuscle, SmoothMyocytes, Smooth MuscleNeuropilin-1PhosphorylationGlycogen Synthase Kinase 3 betaGSK3B protein, humanNeuropilin-1rac1 GTP-Binding ProteinRAC1 protein, humanReceptors, Platelet-Derived Growth FactorSEMA3A protein, humanSemaphorin-3ASTAT3 protein, humanSTAT3 Transcription Factorairway remodelingasthmaneuropilin 1Pathology Sectionplatelet-derived growth factorsemaphorin 3A

Identifiers

PMID27791986
PMCPMC5348316

What Socratic holds

Textmetadata
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 Socratic graph.