CCN1 promotes the differentiation of endothelial progenitor cells and reendothelialization in the early phase after vascular injury
Abstract
Endothelial progenitor cells (EPCs) contribute to the process of reendothelialization and prevent neointimal formation after vascular injury. The present study was designed to investigate whether the cysteine-rich 61 (CYR61, CCN1), an important matricellular component of local vascular microenvironment, has effect on EPCs differentiation and reendothelialization in response to vascular injury in rat. Following balloon injury, CCN1 was rapidly induced and dynamically changed at vascular lesions. Overexpression of CCN1 by adenovirus (Ad-CCN1) accelerated reendothelialization and inhibited neointimal formation in the early phase (day 14) after vascular injury (p < 0.05), while no effect was shown on day 21. Ad-CCN1 treatment increased the adhering EPCs on the surface of injured vessels on day 7, and the ratio of GFP- and vWF-positive area to the total luminal length on day 14 was 2.3-fold higher in the Ad-CCN1-EPC-transplanted group than in controls. Consistent with these findings, CCN1-stimulated EPC differentiation in vitro and 20 genes were found differentially expressed during CCN1-induced EPC differentiation, including Id1, Vegf-b, Vegf-c, Kdr, Igf-1, Ereg, Tgf, Mdk, Ptn, Timp2, etc. Among them, negative transcriptional regulator Id1 was associated with CCN1 effect on EPC differentiation. Our data suggest that CCN1, from the microenvironment of injured vessels, enhances reendothelialization via a direct action on EPC differentiation, revealing a possible new mechanism underlying the process of vascular repair.
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CCN1 can recruit CD34+ endothelial progenitor cells to the endothelial monolayer and promote their differentiation.
“Overexpression of CCN1 from an adenoviral vector accelerates re-endothelialization after balloon injury, possibly because CCN1 can recruit CD34+ endothelial progenitor cells to the endothelial monolayer and promote their differentiation [88,138].”
From CCN1/CYR61: the very model of a modern matricellular protein (2011) · cites this paper as [138]
Overexpression of CCN1 from an adenoviral vector accelerates re-endothelialization after balloon injury.
“Overexpression of CCN1 from an adenoviral vector accelerates re-endothelialization after balloon injury, possibly because CCN1 can recruit CD34+ endothelial progenitor cells to the endothelial monolayer and promote their differentiation [88,138].”
From CCN1/CYR61: the very model of a modern matricellular protein (2011) · cites this paper as [138]
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CCN1/CYR61: the very model of a modern matricellular protein
Lau, L. F. (2011) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-011-0778-3 · Cited by 338 · see citing works
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- Authors
- Yu, Y., Gao, Y., Qin, J., Kuang, C.-Y., Song, M.-B., Yu, S.-Y., Cui, B., Chen, J.-F., & Huang, L.
- Affiliations
- Army Medical University (CN)
- Corresponding author
- Huang, Lan
- Venue
- Basic Research in Cardiology
- Published
- 2010-09-10
- Volume
- 105
- Issue
- 6
- Pages
- 713-724
- ISSN
- 0003-9217 (ISSN-L)
- 0300-8428
- 1435-1803
- OpenAlex
- W2075148755
- Cited by
- 44
- References
- 44
- Citations by year
- 2026: 1 · 2023: 2 · 2022: 3 · 2021: 2 · 2020: 1 · 2019: 4 · 2018: 3 · 2017: 3 · 2016: 2 · 2015: 4 · 2014: 8 · 2013: 3 · 2012: 3
- FWCI
- 1.43
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Basic Research in Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Connective Tissue Growth Factor Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Keywords
- CYR61, endothelial progenitor cells, re-endothelialization, vascular injury, neointima formation, balloon injury, Id1, EPC differentiation, vascular repair, matricellular proteins, gene expression profiling, adenoviral gene transfer
- MeSH terms
- Animals, Cell Adhesion, Cell Differentiation, Cells, Cultured, Disease Models, Animal, Gene Expression Regulation, Male, RNA, Messenger, Stem Cells, Time Factors, Transduction, Genetic, Rats, Sprague-Dawley, Carotid Artery Injuries, Stem Cell Transplantation, Endothelial Cells, Cell Proliferation, Rats, Inhibitor of Differentiation Protein 1, Cysteine-Rich Protein 61
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