MFAP4 Promotes Vascular Smooth Muscle Migration, Proliferation and Accelerates Neointima Formation

OBJECTIVE—Arterial injury stimulates remodeling responses that, when excessive, lead to stenosis. These responses are influenced by integrin signaling in vascular smooth muscle cells (VSMCs). Microfibrillar-associated protein 4 (MFAP4) is an integrin ligand localized to extracellular matrix fibers i...

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Published inArteriosclerosis, thrombosis, and vascular biology Vol. 36; no. 1; pp. 122 - 133
Main Authors Schlosser, Anders, Pilecki, Bartosz, Hemstra, Line E, Kejling, Karin, Kristmannsdottir, Gudlaug B, Wulf-Johansson, Helle, Moeller, Jesper B, Füchtbauer, Ernst-Martin, Nielsen, Ole, Kirketerp-Møller, Katrine, Dubey, Lalit K, Hansen, Pernille B.L, Stubbe, Jane, Wrede, Christoph, Hegermann, Jan, Ochs, Matthias, Rathkolb, Birgit, Schrewe, Anja, Bekeredjian, Raffi, Wolf, Eckhard, Gailus-Durner, Valérie, Fuchs, Helmut, Hrabě de Angelis, Martin, Lindholt, Jes S, Holmskov, Uffe, Sorensen, Grith L
Format Journal Article
LanguageEnglish
Published United States American Heart Association, Inc 01.01.2016
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Abstract OBJECTIVE—Arterial injury stimulates remodeling responses that, when excessive, lead to stenosis. These responses are influenced by integrin signaling in vascular smooth muscle cells (VSMCs). Microfibrillar-associated protein 4 (MFAP4) is an integrin ligand localized to extracellular matrix fibers in the vascular wall. The role of MFAP4 in vascular biology is unknown. We aimed to test the hypothesis that MFAP4 would enhance integrin-dependent VSMC activation. APPROACH AND RESULTS—We produced Mfap4-deficient (Mfap4) mice and performed carotid artery ligation to explore the role of MFAP4 in vascular biology in vivo. Furthermore, we investigated the effects of MFAP4 in neointimal formation ex vivo and in primary VSMC and monocyte cultures in vitro. When challenged with carotid artery ligation, Mfap4 mice exhibited delayed neointimal formation, accompanied by early reduction in the number of proliferating medial and neointimal cells, as well as infiltrating leukocytes. Delayed neointimal formation was associated with decreased cross-sectional area of ligated Mfap4 carotid arteries resulting in lumen narrowing 28 days after ligation. MFAP4 blockade prohibited the formation of neointimal hyperplasia ex vivo. Moreover, we demonstrated that MFAP4 is a ligand for integrin αVβ3 and mediates VSMC phosphorylation of focal adhesion kinase, migration, and proliferation in vitro. MFAP4-dependent VSMC activation was reversible by treatment with MFAP4-blocking antibodies and inhibitors of focal adhesion kinase and downstream kinases. In addition, we showed that MFAP4 promotes monocyte chemotaxis in integrin αVβ3–dependent manner. CONCLUSIONS—MFAP4 regulates integrin αVβ3–induced VSMC proliferation and migration, as well as monocyte chemotaxis, and accelerates neointimal hyperplasia after vascular injury.
AbstractList Arterial injury stimulates remodeling responses that, when excessive, lead to stenosis. These responses are influenced by integrin signaling in vascular smooth muscle cells (VSMCs). Microfibrillar-associated protein 4 (MFAP4) is an integrin ligand localized to extracellular matrix fibers in the vascular wall. The role of MFAP4 in vascular biology is unknown. We aimed to test the hypothesis that MFAP4 would enhance integrin-dependent VSMC activation. We produced Mfap4-deficient (Mfap4(-/-)) mice and performed carotid artery ligation to explore the role of MFAP4 in vascular biology in vivo. Furthermore, we investigated the effects of MFAP4 in neointimal formation ex vivo and in primary VSMC and monocyte cultures in vitro. When challenged with carotid artery ligation, Mfap4(-/-) mice exhibited delayed neointimal formation, accompanied by early reduction in the number of proliferating medial and neointimal cells, as well as infiltrating leukocytes. Delayed neointimal formation was associated with decreased cross-sectional area of ligated Mfap4(-/-) carotid arteries resulting in lumen narrowing 28 days after ligation. MFAP4 blockade prohibited the formation of neointimal hyperplasia ex vivo. Moreover, we demonstrated that MFAP4 is a ligand for integrin αVβ3 and mediates VSMC phosphorylation of focal adhesion kinase, migration, and proliferation in vitro. MFAP4-dependent VSMC activation was reversible by treatment with MFAP4-blocking antibodies and inhibitors of focal adhesion kinase and downstream kinases. In addition, we showed that MFAP4 promotes monocyte chemotaxis in integrin αVβ3-dependent manner. MFAP4 regulates integrin αVβ3-induced VSMC proliferation and migration, as well as monocyte chemotaxis, and accelerates neointimal hyperplasia after vascular injury.
OBJECTIVEArterial injury stimulates remodeling responses that, when excessive, lead to stenosis. These responses are influenced by integrin signaling in vascular smooth muscle cells (VSMCs). Microfibrillar-associated protein 4 (MFAP4) is an integrin ligand localized to extracellular matrix fibers in the vascular wall. The role of MFAP4 in vascular biology is unknown. We aimed to test the hypothesis that MFAP4 would enhance integrin-dependent VSMC activation.APPROACH AND RESULTSWe produced Mfap4-deficient (Mfap4(-/-)) mice and performed carotid artery ligation to explore the role of MFAP4 in vascular biology in vivo. Furthermore, we investigated the effects of MFAP4 in neointimal formation ex vivo and in primary VSMC and monocyte cultures in vitro. When challenged with carotid artery ligation, Mfap4(-/-) mice exhibited delayed neointimal formation, accompanied by early reduction in the number of proliferating medial and neointimal cells, as well as infiltrating leukocytes. Delayed neointimal formation was associated with decreased cross-sectional area of ligated Mfap4(-/-) carotid arteries resulting in lumen narrowing 28 days after ligation. MFAP4 blockade prohibited the formation of neointimal hyperplasia ex vivo. Moreover, we demonstrated that MFAP4 is a ligand for integrin αVβ3 and mediates VSMC phosphorylation of focal adhesion kinase, migration, and proliferation in vitro. MFAP4-dependent VSMC activation was reversible by treatment with MFAP4-blocking antibodies and inhibitors of focal adhesion kinase and downstream kinases. In addition, we showed that MFAP4 promotes monocyte chemotaxis in integrin αVβ3-dependent manner.CONCLUSIONSMFAP4 regulates integrin αVβ3-induced VSMC proliferation and migration, as well as monocyte chemotaxis, and accelerates neointimal hyperplasia after vascular injury.
OBJECTIVE—Arterial injury stimulates remodeling responses that, when excessive, lead to stenosis. These responses are influenced by integrin signaling in vascular smooth muscle cells (VSMCs). Microfibrillar-associated protein 4 (MFAP4) is an integrin ligand localized to extracellular matrix fibers in the vascular wall. The role of MFAP4 in vascular biology is unknown. We aimed to test the hypothesis that MFAP4 would enhance integrin-dependent VSMC activation. APPROACH AND RESULTS—We produced Mfap4-deficient (Mfap4) mice and performed carotid artery ligation to explore the role of MFAP4 in vascular biology in vivo. Furthermore, we investigated the effects of MFAP4 in neointimal formation ex vivo and in primary VSMC and monocyte cultures in vitro. When challenged with carotid artery ligation, Mfap4 mice exhibited delayed neointimal formation, accompanied by early reduction in the number of proliferating medial and neointimal cells, as well as infiltrating leukocytes. Delayed neointimal formation was associated with decreased cross-sectional area of ligated Mfap4 carotid arteries resulting in lumen narrowing 28 days after ligation. MFAP4 blockade prohibited the formation of neointimal hyperplasia ex vivo. Moreover, we demonstrated that MFAP4 is a ligand for integrin αVβ3 and mediates VSMC phosphorylation of focal adhesion kinase, migration, and proliferation in vitro. MFAP4-dependent VSMC activation was reversible by treatment with MFAP4-blocking antibodies and inhibitors of focal adhesion kinase and downstream kinases. In addition, we showed that MFAP4 promotes monocyte chemotaxis in integrin αVβ3–dependent manner. CONCLUSIONS—MFAP4 regulates integrin αVβ3–induced VSMC proliferation and migration, as well as monocyte chemotaxis, and accelerates neointimal hyperplasia after vascular injury.
Author Kristmannsdottir, Gudlaug B
Bekeredjian, Raffi
Nielsen, Ole
Hansen, Pernille B.L
Füchtbauer, Ernst-Martin
Stubbe, Jane
Schlosser, Anders
Pilecki, Bartosz
Moeller, Jesper B
Kejling, Karin
Wulf-Johansson, Helle
Holmskov, Uffe
Sorensen, Grith L
Hemstra, Line E
Dubey, Lalit K
Rathkolb, Birgit
Wrede, Christoph
Kirketerp-Møller, Katrine
Hrabě de Angelis, Martin
Lindholt, Jes S
Schrewe, Anja
Fuchs, Helmut
Ochs, Matthias
Wolf, Eckhard
Gailus-Durner, Valérie
Hegermann, Jan
AuthorAffiliation From the Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark (A.S., B.P., L.E.H., K.K., G.B.K., H.W.-J., J.B.M., K.K.-M., L.K.D., P.B.L.H., J.S., U.H, G.L.S.); Department of Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark (E.-M.F.); Department of Pathology, Odense University Hospital, Odense, Denmark (O.N.); Institute of Functional and Applied Anatomy, Hannover Medical School, Hannover, Germany (C.W., J.H., M.O.); Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Member of the German Center for Lung Research (DZL), Hannover, Germany (C.W., J.H., M.O.); REBIRTH Cluster of Excellence, Hannover, Germany (C.W., J.H., M.O.); German Mouse Clinic, Institute of Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, Munich, Germany (B.R., A.S., V.G.-D., H.F., M.H.d.A.); Institute of Molecular Animal Breeding and Biotechnology, Gene Center, Ludwig-Maximilians-University Münch
AuthorAffiliation_xml – name: From the Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark (A.S., B.P., L.E.H., K.K., G.B.K., H.W.-J., J.B.M., K.K.-M., L.K.D., P.B.L.H., J.S., U.H, G.L.S.); Department of Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark (E.-M.F.); Department of Pathology, Odense University Hospital, Odense, Denmark (O.N.); Institute of Functional and Applied Anatomy, Hannover Medical School, Hannover, Germany (C.W., J.H., M.O.); Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Member of the German Center for Lung Research (DZL), Hannover, Germany (C.W., J.H., M.O.); REBIRTH Cluster of Excellence, Hannover, Germany (C.W., J.H., M.O.); German Mouse Clinic, Institute of Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, Munich, Germany (B.R., A.S., V.G.-D., H.F., M.H.d.A.); Institute of Molecular Animal Breeding and Biotechnology, Gene Center, Ludwig-Maximilians-University München, Munich, Germany (B.R, E.W.); Division of Cardiology, Department of Medicine III, University of Heidelberg, Heidelberg, Germany (A.S., R.B.); Chair of Experimental Genetics, Center of Life and Food Sciences Weihenstephan, Technische Universität München, Freising-Weihenstephan, Munich, Germany (M.H.d.A.); Cardiovascular Research Unit, Viborg Hospital, Viborg, Denmark (J.S.L.); and Department of Cardiothoracic and Vascular Surgery, Center of Individualized Medicine in Arterial Diseases (CIMA), Odense University Hospital, Odense, Denmark (J.S.L.)
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  fullname: Schlosser, Anders
  organization: From the Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark (A.S., B.P., L.E.H., K.K., G.B.K., H.W.-J., J.B.M., K.K.-M., L.K.D., P.B.L.H., J.S., U.H, G.L.S.); Department of Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark (E.-M.F.); Department of Pathology, Odense University Hospital, Odense, Denmark (O.N.); Institute of Functional and Applied Anatomy, Hannover Medical School, Hannover, Germany (C.W., J.H., M.O.); Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Member of the German Center for Lung Research (DZL), Hannover, Germany (C.W., J.H., M.O.); REBIRTH Cluster of Excellence, Hannover, Germany (C.W., J.H., M.O.); German Mouse Clinic, Institute of Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, Munich, Germany (B.R., A.S., V.G.-D., H.F., M.H.d.A.); Institute of Molecular Animal Breeding and Biotechnology, Gene Center, Ludwig-Maximilians-University München, Munich, Germany (B.R, E.W.); Division of Cardiology, Department of Medicine III, University of Heidelberg, Heidelberg, Germany (A.S., R.B.); Chair of Experimental Genetics, Center of Life and Food Sciences Weihenstephan, Technische Universität München, Freising-Weihenstephan, Munich, Germany (M.H.d.A.); Cardiovascular Research Unit, Viborg Hospital, Viborg, Denmark (J.S.L.); and Department of Cardiothoracic and Vascular Surgery, Center of Individualized Medicine in Arterial Diseases (CIMA), Odense University Hospital, Odense, Denmark (J.S.L.)
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/26564819$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright 2016 American Heart Association, Inc.
2015 American Heart Association, Inc.
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Issue 1
Keywords mouse
extracellular matrix proteins
integrin alphaVbeta3
muscle
hyperplasia
carotid stenosis
vascular
MFAP4 protein
smooth
Language English
License 2015 American Heart Association, Inc.
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  text: 2016-January
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PublicationTitle Arteriosclerosis, thrombosis, and vascular biology
PublicationTitleAlternate Arterioscler Thromb Vasc Biol
PublicationYear 2016
Publisher American Heart Association, Inc
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Snippet OBJECTIVE—Arterial injury stimulates remodeling responses that, when excessive, lead to stenosis. These responses are influenced by integrin signaling in...
Arterial injury stimulates remodeling responses that, when excessive, lead to stenosis. These responses are influenced by integrin signaling in vascular smooth...
OBJECTIVEArterial injury stimulates remodeling responses that, when excessive, lead to stenosis. These responses are influenced by integrin signaling in...
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SubjectTerms Animals
Apoptosis
Carotid Arteries - metabolism
Carotid Arteries - pathology
Carotid Artery Diseases - genetics
Carotid Artery Diseases - metabolism
Carotid Artery Diseases - pathology
Carrier Proteins - genetics
Carrier Proteins - metabolism
Cell Movement - drug effects
Cell Proliferation - drug effects
Cells, Cultured
Chemotaxis, Leukocyte
Disease Models, Animal
Extracellular Matrix Proteins - deficiency
Extracellular Matrix Proteins - genetics
Extracellular Matrix Proteins - metabolism
Focal Adhesion Kinase 1 - antagonists & inhibitors
Focal Adhesion Kinase 1 - metabolism
Genotype
Glycoproteins - deficiency
Glycoproteins - genetics
Glycoproteins - metabolism
Humans
Hyperplasia
Integrin alphaVbeta3 - metabolism
Ligands
Male
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Knockout
Monocytes - metabolism
Muscle, Smooth, Vascular - drug effects
Muscle, Smooth, Vascular - metabolism
Muscle, Smooth, Vascular - pathology
Myocytes, Smooth Muscle - drug effects
Myocytes, Smooth Muscle - metabolism
Myocytes, Smooth Muscle - pathology
Neointima
Phenotype
Phosphorylation
Protein Kinase Inhibitors - pharmacology
Signal Transduction
Time Factors
Vascular Remodeling
Title MFAP4 Promotes Vascular Smooth Muscle Migration, Proliferation and Accelerates Neointima Formation
URI https://www.ncbi.nlm.nih.gov/pubmed/26564819
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