ArticleTissue engineering. Part A2010
Expression of versican isoform V3 in the absence of ascorbate improves elastogenesis in engineered vascular constructs.
Article in Tissue engineering. Part A, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 32 citations in OpenAlex.
- Elastogenesis in Focus: Navigating Elastic Fibers Synthesis for Advanced Dermal Biomaterial Formulation.Advanced healthcare materials · 2024Review
- V3: an enigmatic isoform of the proteoglycan versican.American journal of physiology. Cell physiology · 2023Review
- Deletion of type VIII collagen reduces blood pressure, increases carotid artery functional distensibility and promotes elastin deposition.Matrix biology plus · 2021Article
- Innovative Human Three-Dimensional Tissue-Engineered Models as an Alternative to Animal Testing.Bioengineering (Basel, Switzerland) · 2020Review
- Whole exome sequencing in patients with Williams-Beuren syndrome followed by disease modeling in mice points to four novel pathways that may modify stenosis risk.Human molecular genetics · 2020Article
- Functional Vascular Tissue Engineering Inspired by Matricellular Proteins.Frontiers in cardiovascular medicine · 2019Review
- G1 Domain of Versican Regulates Hyaluronan Organization and the Phenotype of Cultured Human Dermal Fibroblasts.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2016Article
- Expression of V3 Versican by Rat Arterial Smooth Muscle Cells Promotes Differentiated and Anti-inflammatory Phenotypes.The Journal of biological chemistry · 2015Article
- Computational model of the in vivo development of a tissue engineered vein from an implanted polymeric construct.Journal of biomechanics · 2014Article
- Expression of versican V3 by arterial smooth muscle cells alters tumor growth factor β (TGFβ)-, epidermal growth factor (EGF)-, and nuclear factor κB (NFκB)-dependent signaling pathways, creating a microenvironment that resists monocyte adhesion.The Journal of biological chemistry · 2014Article
- Biological and engineering design considerations for vascular tissue engineered blood vessels (TEBVs).Current opinion in chemical engineering · 2014Article
- Advances in biomimetic regeneration of elastic matrix structures.Drug delivery and translational research · 2012Article
- Tissue engineering and regenerative strategies to replicate biocomplexity of vascular elastic matrix assembly.Tissue engineering. Part B, Reviews · 2012Review
- Induced elastic matrix deposition within three-dimensional collagen scaffolds.Tissue engineering. Part A · 2011Article
- Substantial expression of mature elastin in arterial constructs.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
A promising method to fabricate tissue-engineered blood vessels is to have cells synthesize the supportive extracellular matrix scaffold of the tissue-engineered blood vessel; however, a shortcoming of this method has been limited elastogenesis. Previously, we found that arterial smooth muscle cells (ASMCs) produced significant quantities of elastin when transduced with splice variant 3 of the proteoglycan versican (V3). In this study, we assessed whether elastogenesis and the structural properties of entirely cell-derived engineered vascular constructs could be improved by the incorporation of V3-transduced rat ASMCs. After 18 weeks of culture, V3 constructs had more tropoelastin, more elastin crosslinks, higher burst strengths, greater elasticity, and thicker collagen fiber bundles compared with empty-vector controls. The expression of elastin and elastin-associated proteins was increased in V3 and control ASMC monolayer cultures when ascorbic acid, which promotes collagen synthesis and inhibits elastogenesis, was removed from the medium. Engineered vascular constructs with ascorbate withdrawn for 14 weeks, after an initial 4-week exposure to ascorbate, exhibited increased elastin, desmosine content, elasticity, and burst strength compared with constructs exposed continuously to ascorbate. Our results show that V3 coupled with limited exposure to ascorbate promotes elastogenesis and improves the structural and functional properties of engineered vascular constructs.
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Registered trials
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