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          Institute: MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut)     Collection: Yearbook 2016     Display Documents



ID: 723920.0, MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut) / Yearbook 2016
Complement C1q-induced activation of beta-catenin signalling causes hypertensive arterial remodelling
Authors:Sumida, T.; Naito, A. T.; Nomura, S.; Nakagawa, A.; Higo, T.; Hashimoto, A.; Okada, K.; Sakai, T.; Ito, M.; Yamaguchi, T.; Oka, T.; Akazawa, H.; Lee, J. K.; Minamino, T.; Offermanns, S.; Noda, T.; Botto, M.; Kobayashi, Y.; Morita, H.; Manabe, I.; Nagai, T.; Shiojima, I.; Komuro, I.
Date of Publication (YYYY-MM-DD):2015
Title of Journal:Nat Commun
Volume:6
Start Page:6241
Audience:Not Specified
Abstract / Description:Hypertension induces structural remodelling of arteries, which leads to arteriosclerosis and end-organ damage. Hyperplasia of vascular smooth muscle cells (VSMCs) and infiltration of immune cells are the hallmark of hypertensive arterial remodelling. However, the precise molecular mechanisms of arterial remodelling remain elusive. We have recently reported that complement C1q activates beta-catenin signalling independent of Wnts. Here, we show a critical role of complement C1-induced activation of beta-catenin signalling in hypertensive arterial remodelling. Activation of beta-catenin and proliferation of VSMCs were observed after blood-pressure elevation, which were prevented by genetic and chemical inhibition of beta-catenin signalling. Macrophage depletion and C1qa gene deletion attenuated the hypertension-induced beta-catenin signalling, proliferation of VSMCs and pathological arterial remodelling. Our findings unveil the link between complement C1 and arterial remodelling and suggest that C1-induced activation of beta-catenin signalling becomes a novel therapeutic target to prevent arteriosclerosis in patients with hypertension.
External Publication Status:published
Document Type:Article
Communicated by:n.n.
Affiliations:MPI für physiologische und klinische Forschung
External Affiliations:1] Department of Cardiovascular Medicine, The University of Tokyo Graduate School of Medicine, Tokyo 113-8655, Japan [2] CREST, Japan Science and Technology Agency, Tokyo 102-0075, Japan [3] Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan. Department of Cardiovascular Medicine, The University of Tokyo Graduate School of Medicine, Tokyo 113-8655, Japan. Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan. 1] CREST, Japan Science and Technology Agency, Tokyo 102-0075, Japan [2] Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan. Department of Cardiovascular Biology and Medicine, Niigata University Graduate School of Medical and Dental Sciences, Niigata 951-8510, Japan. Department of Pharmacology, Max-Planck-Institute for Heart and Lung Research, Bad Nauheim D-61231, Germany. Department of Cell Biology, The Cancer Institute, Japanese Foundation for Cancer Research, Tokyo 135-8550, Japan. Centre for Complement and Inflammation Research, Department of Medicine, Imperial College London, London SW7 2AZ, UK. Department of Cardiovascular Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan. 1] CREST, Japan Science and Technology Agency, Tokyo 102-0075, Japan [2] Department of Medicine II, Kansai Medical University, Osaka 573-1191, Japan.
Identifiers:ISSN:2041-1723 (Electronic) 2041-1723 (Linking) %R 10.1038/ncomms7241
URL:http://www.ncbi.nlm.nih.gov/pubmed/25716000
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