Interferon-Beta, a Decisive Factor in Angiogenesis and Arteriogenesis
In this review we discuss the current literature on the effects of type I interferons (IFN) and their downstream effectors on vascular growth in experimental models in vitro and in vivo. In addition to its well-documented role in angiogenesis, that is, the growth of new capillaries from existing ves...
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Veröffentlicht in: | Journal of interferon & cytokine research 2015-06, Vol.35 (6), p.411-420 |
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description | In this review we discuss the current literature on the effects of type I interferons (IFN) and their downstream effectors on vascular growth in experimental models in vitro and in vivo. In addition to its well-documented role in angiogenesis, that is, the growth of new capillaries from existing vessels, we will also describe emerging evidence and mechanisms by which type I IFN may inhibit arteriogenesis, that is, the expansive remodeling of existing collateral arteries. Crucial in both processes is the common role of circulating monocytes, which are known to act as pivotal cellular modulators in revascularization through secreted chemokines, proteases, and growth factors. These secreted molecules, which are all modulated by IFN signaling, act via degradation of the extracellular matrix and by stimulating the proliferation of vascular smooth muscle cells and endothelial cells. Thus, next to the antiviral and immunomodulatory activities of type I IFNs, a potent role of IFN-β as modulator of revascularization is now emerging and may be considered a potential clinical target for the stimulation of angiogenesis and arteriogenesis in ill-perfused tissues. |
doi_str_mv | 10.1089/jir.2014.0184 |
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In addition to its well-documented role in angiogenesis, that is, the growth of new capillaries from existing vessels, we will also describe emerging evidence and mechanisms by which type I IFN may inhibit arteriogenesis, that is, the expansive remodeling of existing collateral arteries. Crucial in both processes is the common role of circulating monocytes, which are known to act as pivotal cellular modulators in revascularization through secreted chemokines, proteases, and growth factors. These secreted molecules, which are all modulated by IFN signaling, act via degradation of the extracellular matrix and by stimulating the proliferation of vascular smooth muscle cells and endothelial cells. Thus, next to the antiviral and immunomodulatory activities of type I IFNs, a potent role of IFN-β as modulator of revascularization is now emerging and may be considered a potential clinical target for the stimulation of angiogenesis and arteriogenesis in ill-perfused tissues.</description><identifier>ISSN: 1079-9907</identifier><identifier>EISSN: 1557-7465</identifier><identifier>DOI: 10.1089/jir.2014.0184</identifier><identifier>PMID: 25714660</identifier><language>eng</language><publisher>United States: Mary Ann Liebert, Inc</publisher><subject>Animals ; Aortic Valve Stenosis - immunology ; Aortic Valve Stenosis - metabolism ; Aortic Valve Stenosis - pathology ; Arteries - cytology ; Arteries - drug effects ; Arteries - immunology ; Cell Proliferation - drug effects ; Endothelial Cells - cytology ; Endothelial Cells - drug effects ; Endothelial Cells - immunology ; Extracellular Matrix - drug effects ; Extracellular Matrix - immunology ; Extracellular Matrix - metabolism ; Humans ; Intercellular Signaling Peptides and Proteins - genetics ; Intercellular Signaling Peptides and Proteins - immunology ; Intercellular Signaling Peptides and Proteins - pharmacology ; Interferon-beta - genetics ; Interferon-beta - immunology ; Interferon-beta - pharmacology ; Monocytes - cytology ; Monocytes - drug effects ; Monocytes - immunology ; Morphogenesis - drug effects ; Muscle, Smooth, Vascular - cytology ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - immunology ; Myocardial Ischemia - immunology ; Myocardial Ischemia - metabolism ; Myocardial Ischemia - pathology ; Myocytes, Smooth Muscle - cytology ; Myocytes, Smooth Muscle - drug effects ; Myocytes, Smooth Muscle - immunology ; Neovascularization, Physiologic - drug effects</subject><ispartof>Journal of interferon & cytokine research, 2015-06, Vol.35 (6), p.411-420</ispartof><rights>(©) Copyright 2015, Mary Ann Liebert, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c420t-a23d529dbccd7a595db0dc329d63f42c4e860bd944975764140833417a433c553</citedby><cites>FETCH-LOGICAL-c420t-a23d529dbccd7a595db0dc329d63f42c4e860bd944975764140833417a433c553</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25714660$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yıldırım, Cansu</creatorcontrib><creatorcontrib>Nieuwenhuis, Sylvia</creatorcontrib><creatorcontrib>Teunissen, Paul F</creatorcontrib><creatorcontrib>Horrevoets, Anton J G</creatorcontrib><creatorcontrib>van Royen, Niels</creatorcontrib><creatorcontrib>van der Pouw Kraan, Tineke C T M</creatorcontrib><title>Interferon-Beta, a Decisive Factor in Angiogenesis and Arteriogenesis</title><title>Journal of interferon & cytokine research</title><addtitle>J Interferon Cytokine Res</addtitle><description>In this review we discuss the current literature on the effects of type I interferons (IFN) and their downstream effectors on vascular growth in experimental models in vitro and in vivo. 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In addition to its well-documented role in angiogenesis, that is, the growth of new capillaries from existing vessels, we will also describe emerging evidence and mechanisms by which type I IFN may inhibit arteriogenesis, that is, the expansive remodeling of existing collateral arteries. Crucial in both processes is the common role of circulating monocytes, which are known to act as pivotal cellular modulators in revascularization through secreted chemokines, proteases, and growth factors. These secreted molecules, which are all modulated by IFN signaling, act via degradation of the extracellular matrix and by stimulating the proliferation of vascular smooth muscle cells and endothelial cells. 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subjects | Animals Aortic Valve Stenosis - immunology Aortic Valve Stenosis - metabolism Aortic Valve Stenosis - pathology Arteries - cytology Arteries - drug effects Arteries - immunology Cell Proliferation - drug effects Endothelial Cells - cytology Endothelial Cells - drug effects Endothelial Cells - immunology Extracellular Matrix - drug effects Extracellular Matrix - immunology Extracellular Matrix - metabolism Humans Intercellular Signaling Peptides and Proteins - genetics Intercellular Signaling Peptides and Proteins - immunology Intercellular Signaling Peptides and Proteins - pharmacology Interferon-beta - genetics Interferon-beta - immunology Interferon-beta - pharmacology Monocytes - cytology Monocytes - drug effects Monocytes - immunology Morphogenesis - drug effects Muscle, Smooth, Vascular - cytology Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - immunology Myocardial Ischemia - immunology Myocardial Ischemia - metabolism Myocardial Ischemia - pathology Myocytes, Smooth Muscle - cytology Myocytes, Smooth Muscle - drug effects Myocytes, Smooth Muscle - immunology Neovascularization, Physiologic - drug effects |
title | Interferon-Beta, a Decisive Factor in Angiogenesis and Arteriogenesis |
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