Microfibrillar-associated protein 4 modulates airway smooth muscle cell phenotype in experimental asthma

BackgroundRecently, several proteins of the extracellular matrix have been characterised as active contributors to allergic airway disease. Microfibrillar-associated protein 4 (MFAP4) is an extracellular matrix protein abundant in the lung, whose biological functions remain poorly understood. In the...

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Published inThorax Vol. 70; no. 9; pp. 862 - 872
Main Authors Pilecki, Bartosz, Schlosser, Anders, Wulf-Johansson, Helle, Trian, Thomas, Moeller, Jesper B, Marcussen, Niels, Aguilar-Pimentel, Juan A, de Angelis, Martin Hrabe, Vestbo, Jorgen, Berger, Patrick, Holmskov, Uffe, Sorensen, Grith L
Format Journal Article
LanguageEnglish
Published England BMJ Publishing Group LTD 01.09.2015
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Abstract BackgroundRecently, several proteins of the extracellular matrix have been characterised as active contributors to allergic airway disease. Microfibrillar-associated protein 4 (MFAP4) is an extracellular matrix protein abundant in the lung, whose biological functions remain poorly understood. In the current study we investigated the role of MFAP4 in experimental allergic asthma.MethodsMFAP4-deficient mice were subjected to alum/ovalbumin and house dust mite induced models of allergic airway disease. In addition, human healthy and asthmatic primary bronchial smooth muscle cell cultures were used to evaluate MFAP4-dependent airway smooth muscle responses.ResultsMFAP4 deficiency attenuated classical hallmarks of asthma, such as eosinophilic inflammation, eotaxin production, airway remodelling and hyperresponsiveness. In wild-type mice, serum MFAP4 was increased after disease development and correlated with local eotaxin levels. MFAP4 was expressed in human bronchial smooth muscle cells and its expression was upregulated in asthmatic cells. Regarding the underlying mechanism, we showed that MFAP4 interacted with integrin αvβ5 and promoted asthmatic bronchial smooth muscle cell proliferation and CCL11 release dependent on phosphatidyloinositol-3-kinase but not extracellular signal-regulated kinase pathway.ConclusionsMFAP4 promoted the development of asthmatic airway disease in vivo and pro-asthmatic functions of bronchial smooth muscle cells in vitro. Collectively, our results identify MFAP4 as a novel contributor to experimental asthma, acting through modulation of airway smooth muscle cells.
AbstractList Recently, several proteins of the extracellular matrix have been characterised as active contributors to allergic airway disease. Microfibrillar-associated protein 4 (MFAP4) is an extracellular matrix protein abundant in the lung, whose biological functions remain poorly understood. In the current study we investigated the role of MFAP4 in experimental allergic asthma. MFAP4-deficient mice were subjected to alum/ovalbumin and house dust mite induced models of allergic airway disease. In addition, human healthy and asthmatic primary bronchial smooth muscle cell cultures were used to evaluate MFAP4-dependent airway smooth muscle responses. MFAP4 deficiency attenuated classical hallmarks of asthma, such as eosinophilic inflammation, eotaxin production, airway remodelling and hyperresponsiveness. In wild-type mice, serum MFAP4 was increased after disease development and correlated with local eotaxin levels. MFAP4 was expressed in human bronchial smooth muscle cells and its expression was upregulated in asthmatic cells. Regarding the underlying mechanism, we showed that MFAP4 interacted with integrin αvβ5 and promoted asthmatic bronchial smooth muscle cell proliferation and CCL11 release dependent on phosphatidyloinositol-3-kinase but not extracellular signal-regulated kinase pathway. MFAP4 promoted the development of asthmatic airway disease in vivo and pro-asthmatic functions of bronchial smooth muscle cells in vitro. Collectively, our results identify MFAP4 as a novel contributor to experimental asthma, acting through modulation of airway smooth muscle cells.
Background Recently, several proteins of the extracellular matrix have been characterised as active contributors to allergic airway disease. Microfibrillar-associated protein 4 (MFAP4) is an extracellular matrix protein abundant in the lung, whose biological functions remain poorly understood. In the current study we investigated the role of MFAP4 in experimental allergic asthma. Methods MFAP4-deficient mice were subjected to alum/ovalbumin and house dust mite induced models of allergic airway disease. In addition, human healthy and asthmatic primary bronchial smooth muscle cell cultures were used to evaluate MFAP4-dependent airway smooth muscle responses. Results MFAP4 deficiency attenuated classical hallmarks of asthma, such as eosinophilic inflammation, eotaxin production, airway remodelling and hyperresponsiveness. In wild-type mice, serum MFAP4 was increased after disease development and correlated with local eotaxin levels. MFAP4 was expressed in human bronchial smooth muscle cells and its expression was upregulated in asthmatic cells. Regarding the underlying mechanism, we showed that MFAP4 interacted with integrin αvβ5 and promoted asthmatic bronchial smooth muscle cell proliferation and CCL11 release dependent on phosphatidyloinositol-3-kinase but not extracellular signal-regulated kinase pathway. Conclusions MFAP4 promoted the development of asthmatic airway disease in vivo and pro-asthmatic functions of bronchial smooth muscle cells in vitro. Collectively, our results identify MFAP4 as a novel contributor to experimental asthma, acting through modulation of airway smooth muscle cells.
BackgroundRecently, several proteins of the extracellular matrix have been characterised as active contributors to allergic airway disease. Microfibrillar-associated protein 4 (MFAP4) is an extracellular matrix protein abundant in the lung, whose biological functions remain poorly understood. In the current study we investigated the role of MFAP4 in experimental allergic asthma.MethodsMFAP4-deficient mice were subjected to alum/ovalbumin and house dust mite induced models of allergic airway disease. In addition, human healthy and asthmatic primary bronchial smooth muscle cell cultures were used to evaluate MFAP4-dependent airway smooth muscle responses.ResultsMFAP4 deficiency attenuated classical hallmarks of asthma, such as eosinophilic inflammation, eotaxin production, airway remodelling and hyperresponsiveness. In wild-type mice, serum MFAP4 was increased after disease development and correlated with local eotaxin levels. MFAP4 was expressed in human bronchial smooth muscle cells and its expression was upregulated in asthmatic cells. Regarding the underlying mechanism, we showed that MFAP4 interacted with integrin αvβ5 and promoted asthmatic bronchial smooth muscle cell proliferation and CCL11 release dependent on phosphatidyloinositol-3-kinase but not extracellular signal-regulated kinase pathway.ConclusionsMFAP4 promoted the development of asthmatic airway disease in vivo and pro-asthmatic functions of bronchial smooth muscle cells in vitro. Collectively, our results identify MFAP4 as a novel contributor to experimental asthma, acting through modulation of airway smooth muscle cells.
Author Trian, Thomas
Marcussen, Niels
Pilecki, Bartosz
Schlosser, Anders
Moeller, Jesper B
Aguilar-Pimentel, Juan A
Berger, Patrick
Wulf-Johansson, Helle
Holmskov, Uffe
Sorensen, Grith L
Vestbo, Jorgen
de Angelis, Martin Hrabe
Author_xml – sequence: 1
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  surname: Pilecki
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  organization: Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark
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  givenname: Anders
  surname: Schlosser
  fullname: Schlosser, Anders
  email: glsorensen@health.sdu.dk
  organization: Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark
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  givenname: Helle
  surname: Wulf-Johansson
  fullname: Wulf-Johansson, Helle
  email: glsorensen@health.sdu.dk
  organization: Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark
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  givenname: Thomas
  surname: Trian
  fullname: Trian, Thomas
  email: glsorensen@health.sdu.dk
  organization: Department of Pharmacology, Bordeaux University, Cardio-thoracic Research Centre, U, Bordeaux, France
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  givenname: Jesper B
  surname: Moeller
  fullname: Moeller, Jesper B
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  organization: Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark
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  givenname: Niels
  surname: Marcussen
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  email: glsorensen@health.sdu.dk
  organization: Department of Pathology, Odense University Hospital, Odense, Denmark
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  givenname: Juan A
  surname: Aguilar-Pimentel
  fullname: Aguilar-Pimentel, Juan A
  email: glsorensen@health.sdu.dk
  organization: Department of Dermatology and Allergology am Biederstein, University Hospital Klinikum rechts der Isar, Technical University Munich, Munich, Germany
– sequence: 8
  givenname: Martin Hrabe
  surname: de Angelis
  fullname: de Angelis, Martin Hrabe
  email: glsorensen@health.sdu.dk
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  surname: Vestbo
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  givenname: Patrick
  surname: Berger
  fullname: Berger, Patrick
  email: glsorensen@health.sdu.dk
  organization: Department of Lung Function Testing, Department of Thoracic Chirurgy, Department of Anatomy and Pathology, CHU Bordeaux Teaching Hospital, Pessac, France
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  givenname: Uffe
  surname: Holmskov
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  email: glsorensen@health.sdu.dk
  organization: Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark
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  givenname: Grith L
  surname: Sorensen
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  email: glsorensen@health.sdu.dk
  organization: Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark
BackLink https://www.ncbi.nlm.nih.gov/pubmed/26038533$$D View this record in MEDLINE/PubMed
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Snippet BackgroundRecently, several proteins of the extracellular matrix have been characterised as active contributors to allergic airway disease....
Recently, several proteins of the extracellular matrix have been characterised as active contributors to allergic airway disease. Microfibrillar-associated...
Background Recently, several proteins of the extracellular matrix have been characterised as active contributors to allergic airway disease....
BACKGROUNDRecently, several proteins of the extracellular matrix have been characterised as active contributors to allergic airway disease....
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StartPage 862
SubjectTerms Animals
Antibodies
Asthma
Asthma - metabolism
Blotting, Western
Carrier Proteins - metabolism
Cell Adhesion
Cell adhesion & migration
Cell Culture Techniques
Cell Proliferation
Cytokines
Disease Models, Animal
Extracellular Matrix Proteins - metabolism
Female
Glycoproteins - metabolism
Humans
Kinases
Lung - metabolism
Mice
Myocytes, Smooth Muscle - metabolism
Penicillin
Phenotype
Proteins
Real-Time Polymerase Chain Reaction
Signal transduction
Smooth muscle
Title Microfibrillar-associated protein 4 modulates airway smooth muscle cell phenotype in experimental asthma
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https://www.ncbi.nlm.nih.gov/pubmed/26038533
https://www.proquest.com/docview/1781826133
https://search.proquest.com/docview/1704349187
Volume 70
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