ArticleArteriosclerosis, thrombosis, and vascular biology2016
Deletion of Hyaluronan Synthase 3 Inhibits Neointimal Hyperplasia in Mice.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- Hyaluronan in cardiac disease: implications for the extracellular matrix beyond collagen.American journal of physiology. Heart and circulatory physiology · 2026Review
- ITIH5-mediated fibroblast/macrophage crosstalk exacerbates cardiac remodelling after myocardial infarction.Journal of translational medicine · 2025Article
- Hyaluronan synthase 3 deficiency lowers the incidence of ruptures of abdominal aortic aneurysms by reducing monocyte infiltration.Frontiers in immunology · 2025Article
- Matrix stiffness, endothelial dysfunction and atherosclerosis.Molecular biology reports · 2023Review
- Aggrecan and Hyaluronan: The Infamous Cartilage Polyelectrolytes - Then and Now.Advances in experimental medicine and biology · 2023Article
- SMC-Derived Hyaluronan Modulates Vascular SMC Phenotype in Murine Atherosclerosis.Circulation research · 2021Article
- Angiostatic cues from the matrix: Endothelial cell autophagy meets hyaluronan biology.The Journal of biological chemistry · 2020Review
- Matrix Remodeling and Hyaluronan Production by Myofibroblasts and Cancer-Associated Fibroblasts in 3D Collagen Matrices.Gels (Basel, Switzerland) · 2020Article
- Dissecting the role of hyaluronan synthases in the tumor microenvironment.The FEBS journal · 2019Review
- Hyaluronan biology: A complex balancing act of structure, function, location and context.Matrix biology : journal of the International Society for Matrix Biology · 2019Review
- Cervical hyaluronan biology in pregnancy, parturition and preterm birth.Matrix biology : journal of the International Society for Matrix Biology · 2019Review
- The CD44-HA axis and inflammation in atherosclerosis: A temporal perspective.Matrix biology : journal of the International Society for Matrix Biology · 2019Review
- 4-Methylumbelliferone improves the thermogenic capacity of brown adipose tissue.Nature metabolism · 2019Article
- Vascular smooth muscle-MAPK14 is required for neointimal hyperplasia by suppressing VSMC differentiation and inducing proliferation and inflammation.Redox biology · 2019Article
- Knockout of hyaluronan synthase 1, but not 3, impairs formation of the retrocalcaneal bursa.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2018Article
- Hyaluronan synthase 3 promotes plaque inflammation and atheroprogression.Matrix biology : journal of the International Society for Matrix Biology · 2018Article
- Versican is differentially regulated in the adventitial and medial layers of human vein grafts.PloS one · 2018Article
- Provisional matrix: A role for versican and hyaluronan.Matrix biology : journal of the International Society for Matrix Biology · 2017Review
- Selective expression of TSPAN2 in vascular smooth muscle is independently regulated by TGF-β1/SMAD and myocardin/serum response factor.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Vascular Smooth Muscle Cells.Arteriosclerosis, thrombosis, and vascular biology · 2016Review
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Authors and funding
16 authors at 1 institution in 3 countries.
Funding
Abstract
objectiveHyaluronan (HA) is a polymeric glucosaminoglycan that forms a provisional extracellular matrix in diseased vessels. HA is synthesized by 3 different HA synthases (HAS1, HAS2, and HAS3). Aim of this study was to unravel the role of the HAS3 isoenzyme during experimental neointimal hyperplasia. APPROACH AND
resultsNeointimal hyperplasia was induced in Has3-deficient mice by ligation of the carotid artery. HA in the media of Has3-deficient mice was decreased 28 days after ligation, and neointimal hyperplasia was strongly inhibited. However, medial and luminal areas were unaffected. Cell density, proliferation, and apoptosis were not altered, suggesting a proportional decrease of both, the number of cells and extracellular matrix. In addition, endothelial function as determined by acetylcholine-induced relaxation of aortic rings, immunoblotting of endothelial nitric oxide synthase, and arterial blood pressure were not affected. Furthermore, the oxidative stress response was not affected as determined in total protein extracts from aortae. Transcriptome analysis comparing control versus ligated carotid arteries hinted toward a mitigated differential regulation of various signaling pathways in Has3-deficient mice in response to ligation that were related to vascular smooth muscle cell (VSMC) migration, including focal adhesions, integrins, mitogen-activated protein kinase, and phosphatidylinositol signaling system. Lentiviral overexpression of HAS3 in VSMC supported the migratory phenotype of VSMC in response to platelet-derived growth factor BB in vitro. Accordingly, knockdown of HAS3 reduced the migratory response to platelet-derived growth factor BB and in addition decreased the expression of PDGF-B mRNA.
conclusionsHAS3-mediated HA synthesis after vessel injury supports seminal signaling pathways in activation of VSMC, increases platelet-derived growth factor BB-mediated migration, and in turn enhances neointimal hyperplasia in vivo.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.