Literature DB >> 20451038

Airway smooth muscle remodeling is a dynamic process in severe long-standing asthma.

Muhannad Hassan1, Taisuke Jo, Paul-André Risse, Barbara Tolloczko, Catherine Lemière, Ronald Olivenstein, Qutayba Hamid, James G Martin.   

Abstract

BACKGROUND: The origin of the excess airway smooth muscle in asthma and when in the course of the disease it is acquired are uncertain.
OBJECTIVES: We examined the relative sensitivities of 2 markers of proliferation, proliferating cell nuclear antigen (PCNA) and Ki 67, in airway smooth muscle in vivo and in vitro. We then studied whether muscle remodeling is a dynamic process in asthma by quantifying proliferation rate and area. Finally we examined heparin-binding epidermal growth factor as a biomarker of remodeling.
METHODS: We obtained bronchoscopic biopsies from subjects with moderate or severe asthma and healthy controls (n = 9/group). For in vitro studies, airway smooth muscle cells were cultured from tracheas of transplant donors. The proliferation rate was quantified from PCNA and Ki 67, co-localized to smooth muscle-specific alpha-actin cells in vivo. Muscle area was assessed morphometrically. We examined the expression of heparin-binding epidermal growth factor on tissues by in situ hybridization and by immunohistochemistry and in cells in culture by RT-PCR.
RESULTS: Proliferating cell nuclear antigen and Ki 67 were highly correlated, but PCNA was a significantly more sensitive marker both in vivo and in vitro. Muscle area was 3.4-fold greater and the fraction of PCNA(+) nuclei in muscle was 5-fold greater in severe asthma than in healthy subjects. Heparin-binding epidermal growth factor was upregulated in proliferating muscle cells in culture and in airway smooth muscle in severe asthmatic tissues.
CONCLUSION: Proliferating cell nuclear antigen is a highly sensitive marker of proliferation and heparin-binding epidermal growth factor is a potential biomarker during active remodeling of ASM in severe asthma. Copyright 2010 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.

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Year:  2010        PMID: 20451038     DOI: 10.1016/j.jaci.2010.02.031

Source DB:  PubMed          Journal:  J Allergy Clin Immunol        ISSN: 0091-6749            Impact factor:   10.793


  38 in total

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2.  Drug Repurposing: The Anthelmintics Niclosamide and Nitazoxanide Are Potent TMEM16A Antagonists That Fully Bronchodilate Airways.

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3.  Synergistic interaction between PPAR ligands and salbutamol on human bronchial smooth muscle cell proliferation.

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5.  Plasminogen-stimulated airway smooth muscle cell proliferation is mediated by urokinase and annexin A2, involving plasmin-activated cell signalling.

Authors:  A G Stewart; Y C Xia; T Harris; S Royce; J A Hamilton; M Schuliga
Journal:  Br J Pharmacol       Date:  2013-12       Impact factor: 8.739

6.  YKL-40 mediates airway remodeling in asthma via activating FAK and MAPK signaling pathway.

Authors:  Yu Sun; Zhaoquan Shi; Bing Liu; Xian'Gui Li; Ge Li; Feng Yang; Hao Tang
Journal:  Cell Cycle       Date:  2020-04-14       Impact factor: 4.534

7.  Effect of TRPV1 channel on proliferation and apoptosis of airway smooth muscle cells of rats.

Authors:  Li-Min Zhao; Hong-Yan Kuang; Luo-Xian Zhang; Ji-Zhen Wu; Xian-Liang Chen; Xiao-Yu Zhang; Li-Jun Ma
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8.  Pulmonary remodeling in asthma.

Authors:  Phil Lieberman
Journal:  F1000 Med Rep       Date:  2010-10-12

9.  Fibulin-1 is increased in asthma--a novel mediator of airway remodeling?

Authors:  Justine Y Lau; Brian G Oliver; Melissa Baraket; Emma L Beckett; Nicole G Hansbro; Lyn M Moir; Steve D Wilton; Carolyn Williams; Paul S Foster; Philip M Hansbro; Judith L Black; Janette K Burgess
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Review 10.  Airway smooth muscle in asthma: just a target for bronchodilation?

Authors:  Judith L Black; Reynold A Panettieri; Audreesh Banerjee; Patrick Berger
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