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Smooth muscle cell recruitment to lymphatic vessels requires PDGFB and impacts vessel size but not identity
Karolinska Inst, Div Vasc Biol, Dept Med Biochem & Biophys, Scheeles Vag 2, SE-17177 Stockholm, Sweden..
Karolinska Inst, Div Vasc Biol, Dept Med Biochem & Biophys, Scheeles Vag 2, SE-17177 Stockholm, Sweden..
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology.ORCID iD: 0000-0002-3436-3278
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2017 (English)In: Development, ISSN 0950-1991, E-ISSN 1477-9129, Vol. 144, no 19, p. 3590-3601Article in journal (Refereed) Published
Abstract [en]

Tissue fluid drains through blind-ended lymphatic capillaries, via smooth muscle cell (SMC)-covered collecting vessels into venous circulation. Both defective SMC recruitment to collecting vessels and ectopic recruitment to lymphatic capillaries are thought to contribute to vessel failure, leading to lymphedema. However, mechanisms controlling lymphatic SMC recruitment and its role in vessel maturation are unknown. Here, we demonstrate that platelet-derived growth factor B (PDGFB) regulates lymphatic SMC recruitment in multiple vascular beds. PDGFB is selectively expressed by lymphatic endothelial cells (LECs) of collecting vessels. LEC-specific deletion of Pdgfb prevented SMC recruitment causing dilation and failure of pulsatile contraction of collecting vessels. However, vessel remodelling and identity were unaffected. Unexpectedly, Pdgfb overexpression in LECs did not induce SMC recruitment to capillaries. This was explained by the demonstrated requirement of PDGFB extracellular matrix (ECM) retention for lymphatic SMC recruitment, and the low presence of PDGFB-binding ECM components around lymphatic capillaries. These results demonstrate the requirement of LEC-autonomous PDGFB expression and retention for SMC recruitment to lymphatic vessels, and suggest an ECM-controlled checkpoint that prevents SMC investment of capillaries, which is a common feature in lymphedematous skin.

Place, publisher, year, edition, pages
COMPANY OF BIOLOGISTS LTD , 2017. Vol. 144, no 19, p. 3590-3601
Keywords [en]
Lymphatic vasculature, PDGFB, Contraction, Lymphedema, Morphogenesis, Smooth muscle cell
National Category
Developmental Biology
Identifiers
URN: urn:nbn:se:uu:diva-337076DOI: 10.1242/dev.147967ISI: 000412120700018PubMedID: 28851707OAI: oai:DiVA.org:uu-337076DiVA, id: diva2:1179389
Funder
Swedish Research Council, 521-2011-3044Swedish Research Council, 2015-00550Swedish Research Council, 542-2014-3535Swedish Cancer Society, CAN 2014/855Swedish Cancer Society, CAN 2015/0735Knut and Alice Wallenberg Foundation, 2015.0030EU, European Research Council, AdG 294556 BbbarrierEU, European Research Council, ERC-2014-CoG-646849Available from: 2018-02-01 Created: 2018-02-01 Last updated: 2018-04-25Bibliographically approved

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Mäe, Maarja AndaloussiZhang, YangOrtsäter, HenrikBetsholtz, ChristerMäkinen, Taija

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