Gene expression profiling of laser microdissected airway smooth muscle tissue in asthma and atopy

Yick, Ching Yong; Zwinderman, Aeilko H.; Kunst, Peter W.A.; Grünberg, Katrien; Mauad, Thaís; Chowdhury, Saheli; Bel, Elisabeth H.; Baas, Frank; Lutter, René; Sterk, Peter J.

doi:10.1111/all.12452

Cited by 39 publications

(34 citation statements)

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“…Gene expression profiling captures phenotypes of patients in relation to frequent exacerbations (50) and sensitivity to inhaled steroids (51), thereby discovering novel biological pathways in COPD. Similar findings have recently been published among children with severe asthma when using gene expression profiles of peripheral blood leukocytes (52) and in adults with asthma on the basis of transcriptomics of epithelial cells or laser-dissected airway smooth muscle (53,54). The next step will be to apply similar methodology to broader population samples.…”

Section: The Datasupporting

confidence: 62%

Systems Biology and Clinical Practice in Respiratory Medicine. The Twain Shall Meet

Thamrin

Frey

Kaminsky

et al. 2016

Am J Respir Crit Care Med

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Respiratory diseases are highly complex, being driven by host-environment interactions and manifested by inflammatory, structural, and functional abnormalities that vary over time. Traditional reductionist approaches have contributed vastly to our knowledge of biological systems in health and disease to date; however, they are insufficient to provide an understanding of the behavior of the system as a whole. In this Pulmonary Perspective, we discuss systems biology approaches, especially but not limited to the study of the lung as a complex system. Such integrative approaches take into account the large number of dynamic subunits and their interactions found in biological systems. Borrowing methods from physics and mathematics, it is possible to study the collective behavior of these systems over time and in a multidimensional manner. We first examine the physiological basis for complexity in the respiratory system and its implications for disease. We then expand on the potential applications of systems biology methods to study complex systems, within the context of diagnosis and monitoring of respiratory diseases including asthma, chronic obstructive pulmonary disease (COPD), and critical illness. We summarize the significant advances made in recent years using systems approaches for disease phenotyping, applied to data ranging from the molecular to clinical level, obtained from large-scale asthma and COPD networks. We describe new studies using temporal complexity patterns to characterize asthma and COPD and predict exacerbations as well as predict adverse outcomes in critical care. We highlight new methods that are emerging with this approach and discuss remaining questions that merit greater attention in the field.

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Section: The Datasupporting

confidence: 62%

Systems Biology and Clinical Practice in Respiratory Medicine. The Twain Shall Meet

Thamrin

Frey

Kaminsky

et al. 2016

Am J Respir Crit Care Med

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“…Previous studies have identified transcriptional changes related to airway hyperresponsiveness (14)(15)(16). However, cell types other than smooth muscle (e.g., immune and epithelial cells) may have driven both transcriptional changes and airway hyperresponsiveness in these prior studies.…”

Section: Introductionmentioning

confidence: 92%

CF airway smooth muscle transcriptome reveals a role for PYK2

Cook¹,

Adam

Zarei

et al. 2017

JCI Insight

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“…It would also be important to show that the inflammatory environment around the ASM indeed contains IgE, interleukins, and other inflammatory mediators. Additional studies on ASM microdissected directly from asthmatic airways (Yick et al 2013(Yick et al , 2014) may better determine the gene expression changes in asthmatic ASM that occurs in the "asthmatic environment". To date, there still has been no clear consensus on whether the ASM from asthmatic subjects is any more contractile than non-asthmatic subjects.…”

Section: Discussionmentioning

confidence: 99%

“…Two recent studies using RNA-seq have identified changes in the expression of genes not directly related to ASM contractile function in asthmatic versus non-asthmatic tissue (Yick et al 2013(Yick et al , 2014. In their first paper, they micro-dissected ASM from asthmatics and found 174 genes differentially expressed when compared with the controls.…”

Section: Proteins Unrelated To Contractile Functionmentioning

confidence: 99%

Gene expression in asthmatic airway smooth muscle: a mixed bag

Pascoe

Swyngedouw

Seow

et al. 2015

Can. J. Physiol. Pharmacol.

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It has long been known that airway smooth muscle (ASM) contraction contributes significantly to the reversible airflow obstruction that defines asthma. It has also been postulated that phenotypic changes in ASM contribute to the airway hyperresponsiveness (AHR) that is a characteristic feature of asthma. Although there is agreement that the mass of ASM surrounding the airways is significantly increased in asthmatic compared with non-asthmatic airways, it is still uncertain whether there are quantitative or qualitative changes in the level of expression of the genes and proteins involved in the canonical contractile pathway in ASM that could account for AHR. This review will summarize past attempts at quantifying gene expression changes in the ASM of asthmatic lungs as well as non-asthmatic ASM cells stimulated with various inflammatory cytokines. The lack of consistent findings in asthmatic samples coupled with the relative concordance of results from stimulated ASM cells suggests that changes to the contractility of ASM tissues in asthma may be dependent on the presence of an inflammatory environment surrounding the ASM layer. Removal of the ASM from this environment could explain why hypercontractility is rarely seen ex vivo.Key words: asthma, airway smooth muscle, gene expression, protein expression, cytokines. Résumé :On sait depuis longtemps que la contraction du muscle lisse respiratoire (MLR) contribue de manière significative à l'obstruction réversible du débit d'air qui définit l'asthme. Il a aussi été postulé que des changements phénotypiques dans le MLR contribue à l'hyperréactivité bronchique (HRB) qui caractérise l'asthme. Même si l'on s'accorde sur le fait que la masse de MLR qui entoure les voies respiratoires est significativement plus importante en situation d'asthme comparativement à l'absence d'asthme, on ne sait pas encore avec certitude si des changements quantitatifs ou qualitatifs du niveau d'expression de gènes et de protéines impliqués dans les voies standards de régulation de la contraction chez le MLR pourraient expliquer l'HRB. Cet article de revue résumera les tentatives passées de quantification de changements d'expression génique dans des cellules de MLR de poumons asthmatiques et non asthmatiques, stimulées à l'aide de différentes cytokines inflammatoires. L'absence de données cohérentes issues d'échantillons asthmatiques, couplée à la concordance relative des résultats obtenus à partir de cellules de MLR stimulées suggère que les changements de contractilité du MLR dans l'asthme peuvent être dépendants de la présence d'un environnement inflammatoire autour de la couche de MLR. Le fait de retirer le MLR de son environnement pourrait expliquer pourquoi l'hyper-contractilité est rarement observée ex vivo. [Traduit par la Rédaction] Mots-clés : asthme, muscle lisse respiratoire, expression génique, expression protéique, cytokines.

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Gene expression profiling of laser microdissected airway smooth muscle tissue in asthma and atopy

Abstract: Airway smooth muscle from asthma patients can be distinguished from that of atopic and nonatopic control subjects by a specific gene expression profile, which is associated with airway hyper-responsiveness.

Cited by 39 publications

References 39 publications

Systems Biology and Clinical Practice in Respiratory Medicine. The Twain Shall Meet

Systems Biology and Clinical Practice in Respiratory Medicine. The Twain Shall Meet

CF airway smooth muscle transcriptome reveals a role for PYK2

Gene expression in asthmatic airway smooth muscle: a mixed bag

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