Interleukin-18/WNT1-inducible signaling pathway protein-1 signaling mediates human saphenous vein smooth muscle cell proliferation
Open accessAbstract
We demonstrate for the first time that the pro-inflammatory cytokine interleukin (IL)-18 stimulates rapid and significant proliferation of SMC derived from human saphenous vein (VSMC), but not coronary artery. IL-18 also stimulates VSMC growth. Further investigations revealed that IL-18-induced VSMC proliferation was Wnt inducible secreted protein-1 (WISP1) dependent. In addition to inducing its own expression via phosphatidylinositol 3-kinase/Akt-dependent IKK/NF-κB activation, IL-18 stimulated glycogen synthase kinase 3β phosphorylation and degradation, β-catenin nuclear translocation and stabilization, T-cell factor-lymphoid enhancer binding factor (TCF-LEF) activation, and WISP1 induction. Moreover, WISP1 induced its own expression, and that of survivin and multiple matrix metalloproteinases via β-catenin/TCF-LEF interaction. WISP1 also activated AP-1, but not NF-κB, and induced matrix metalloproteinase (MMP)9 transcription in part via AP-1. Interestingly, WISP1 failed to regulate tissue inhibitors of matrix metalloproteinases (TIMP) expression. These novel findings indicate that IL-18 induces a series of signaling events that result in WISP1-mediated VSMC proliferation, survival and MMP induction that are key components of vein graft stenosis and this may be amplified by IL-18 and WISP1 autoregulation and cross-regulation.
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WISP1 promotes cytoprotection in multiple cell types through pathways that require PI 3-K and Akt and, in microglia, involve mTOR and PRAS40.
“WISP1 promotes cytoprotection in multiple cell types through pathways that not only require phosphatidylinositol-3-kinase (PI 3-K) and protein kinase B (Akt) [7, 8, 10, 11, 20, 21], but also utilize pathways in microglia that involve the mammalian target of rapamycin (mTOR) and the proline rich Akt substrate 40 kDa (PRAS40) [13].”
From Tuberous Sclerosis Protein 2 (TSC2) Modulates CCN4 Cytoprotection During Apoptotic Amyloid Toxicity in Microglia (2013) · cites this paper as [21]
The Results section on WISP1-induced VSMC proliferation (page unavailable) shows that blocking PI3K or Akt attenuated proliferation, and the Discussion (page unavailable) reports induction of the pro-survival proteins survivin and Bcl-2 in these cells. The paper does not establish that cytoprotection across multiple cell types requires PI3K and Akt. The microglial mTOR/PRAS40 clause is attached to a different citation, not this paper. (LLM, conf=0.85)
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- Authors
- Reddy, V. S., Valente, A. J., Delafontaine, P., & Chandrasekar, B.
- Affiliations
- The University of Texas at San Antonio Health Science Center (US)
- Tulane University (US)
- Corresponding author
- Chandrasekar, Bysani
- Venue
- Journal of Cellular Physiology
- Publisher
- Wiley
- Published
- 2011-09-23
- Volume
- 226
- Issue
- 12
- Pages
- 3303-3315
- ISSN
- 0021-9541 (ISSN-L)
- PMC
- PMC3111842
- OpenAlex
- W2149929597
- Cited by
- 68
- References
- 49
- Citations by year
- 2026: 2 · 2024: 2 · 2023: 1 · 2022: 4 · 2021: 2 · 2020: 2 · 2019: 8 · 2018: 5 · 2017: 3 · 2016: 6 · 2015: 9 · 2014: 7 · 2013: 6 · 2012: 11
- FWCI
- 3.12
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Cellular Physiology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Veterans Affairs (I01 BX000246)
- Office of Research and Development
- Biomedical Laboratory Research and Development, VA Office of Research and Development
- National Institutes of Health
- National Heart, Lung, and Blood Institute (R01HL086787, HL-86787, HL 70241, HL-80682, R01HL080682, R01HL070241)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Keywords
- IL-18, WISP1, vascular smooth muscle cell proliferation, saphenous vein, vein graft stenosis, Wnt signaling, glycogen synthase kinase-3β, NF-κB, Akt signaling, MMP-9, AP-1, survivin, tissue inhibitors of metalloproteinases, autoregulation
- MeSH terms
- Glycogen Synthase Kinase 3 beta, Cells, Cultured, Coronary Vessels, Humans, Hyperplasia, Muscle, Smooth, Vascular, Mutation, Phosphorylation, Proto-Oncogene Proteins, Recombinant Proteins, Saphenous Vein, Time Factors, Transcription, Genetic, Transfection, Signal Transduction, Gene Expression Regulation, Enzymologic, NF-kappa B, Transcription Factor AP-1, Inflammation Mediators, Interleukin-18, Matrix Metalloproteinase 9, Active Transport, Cell Nucleus, Myocytes, Smooth Muscle, Glycogen Synthase Kinase 3, Intracellular Signaling Peptides and Proteins, Cell Proliferation, Proto-Oncogene Proteins c-akt, beta Catenin, I-kappa B Kinase, Lymphoid Enhancer-Binding Factor 1, CCN Intercellular Signaling Proteins, Protein Stability, Phosphatidylinositol 3-Kinase
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