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Cited by 52Connective Tissue Growth Factor ResearchCardiovascular, Neuropeptides, and Oxidative Stress ResearchSignaling Pathways in Disease

Stretch-inducible Expression of the Angiogenic Factor CCN1 in Vascular Smooth Muscle Cells Is Mediated by Egr-1

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Grote, Karsten, Bavendiek, Udo, Grothusen, Christina, Flach, Inna, Hilfiker-Kleiner, Denise, Drexler, Helmut, Schieffer, Bernhard·2004·Journal of Biological Chemistry
DOI 10.1074/jbc.m406532200
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Abstract

CCN1 is an angiogenic factor that promotes cell adhesion, proliferation, and differentiation. CCN1-deficient mice suffer embryonic death because of vascular defects, demonstrating that CCN1 is required for vessel development. Because mechanical stretch may act as a trigger for vessel development, we investigated the impact of mechanical stretch on the regulatory mechanism of CCN1 expression. Mechanical stretch rapidly enhances CCN1 expression and release in vascular smooth muscle cells (VSMC) in vitro and CCN1 expression in murine aortic segments in vivo. Transfection experiments of VSMC with deletion constructs of the CCN1 promoter revealed the regulatory region responsible for the stretch-induced CCN1 expression in the approximately 200-bp promoter region upstream of the TATA-box containing potential binding sites for early growth response-1 (Egr-1), nuclear factor of activated T-cells and cAMP response element binding protein. Decoy oligonucleotides to Egr-1, but not to nuclear factor of activated T-cells or cAMP response element binding protein, abolished the stretch-induced transcription of CCN1. In addition, mutagenesis of the Egr-1 binding site within the CCN1 promoter completely blunted the stretch-induced activation of the promoter. Furthermore, mechanical stretch induced the expression and DNA-binding activity of Egr-1 in VSMC as demonstrated by Western blot and electromobility shift assay. Moreover, a pressure overload-dependent de novo synthesis of Egr-1 was observed after aortic banding. These findings indicate that mechanical stretch leads to enhanced expression of CCN1 via the mechanosensitive transcription factor Egr-1, suggesting a central role for mechanical stretch in the regulation of CCN1-dependent pro-angiogenic potency.

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  • Egr-1 is involved in stretch-induced activation of CCN1 in vascular smooth muscle cells.

    “The transcription factor Egr-1, although not sensitive to cytoskeletal remodeling, is also involved in stretch-induced activation of CCN1 in vascular smooth muscle cells [42].”

    From CCN1/CYR61: the very model of a modern matricellular protein (2011) · cites this paper as [42]

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Authors
Grote, K., Bavendiek, U., Grothusen, C., Flach, I., Hilfiker-Kleiner, D., Drexler, H., & Schieffer, B.
Affiliations
Medizinische Hochschule Hannover (DE)
Corresponding author
Grote, Karsten
ORCID
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2004-12
Volume
279
Issue
53
Pages
55675-55681
ISSN
0021-9258 (ISSN-L)
DOI
10.1074/jbc.m406532200
OpenAlex
W2012047843
Cited by
52
References
32
Citations by year
2026: 1 · 2024: 1 · 2023: 2 · 2022: 1 · 2021: 1 · 2020: 1 · 2019: 2 · 2018: 3 · 2017: 1 · 2016: 2 · 2015: 3 · 2014: 2 · 2013: 1
FWCI
1.42
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Biological Chemistry (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Connective Tissue Growth Factor Research
  • Health Sciences › Medicine › Surgery › Cardiovascular, Neuropeptides, and Oxidative Stress Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Keywords
CYR61, angiogenic factors, mechanical stretch, vascular smooth muscle cells, EGR1, transcriptional regulation, pressure overload, aortic banding, angiogenesis, NFAT, CREB
MeSH terms
Animals, Aorta, Cell Nucleus, Cells, Cultured, DNA-Binding Proteins, Immunohistochemistry, Luciferases, Mice, Inbred C57BL, Muscle, Smooth, Vascular, Muscles, Neovascularization, Pathologic, Oligonucleotides, Pressure, Promoter Regions, Genetic, Time Factors, Transcription Factors, Transfection, Blotting, Western, Up-Regulation, Gene Deletion, Cyclic AMP Response Element-Binding Protein, Immediate-Early Proteins, DNA, Complementary, Reverse Transcriptase Polymerase Chain Reaction, Myocytes, Smooth Muscle, Mice, Early Growth Response Protein 1, Cysteine-Rich Protein 61

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