Anti-Atherogenic Effects of Vaspin on Human Aortic Smooth Muscle Cell/Macrophage Responses and Hyperlipidemic Mouse Plaque Phenotype
Open accessAbstract
Vaspin (visceral adipose tissue-derived serine protease inhibitor) was recently identified as a novel adipocytokine with insulin-sensitizing effects. Serum vaspin levels are reported either increased or decreased in patients with coronary artery disease. Our translational research was performed to evaluate the expression of vaspin in human coronary atherosclerotic lesions, and its effects on atherogenic responses in human macrophages and human aortic smooth muscle cells (HASMC), as well as aortic atherosclerotic lesion development in spontaneously hyperlipidemic Apoe−/− mice, an animal model of atherosclerosis. Vaspin was expressed at high levels in macrophages/vascular smooth muscle cells (VSMCs) within human coronary atheromatous plaques. Vaspin significantly suppressed inflammatory phenotypes with nuclear factor κB down-regulation in human macrophages. Vaspin significantly suppressed oxidized low-density lipoprotein-induced foam cell formation with CD36 and acyl-coenzyme A: cholesterol acyltransferase-1 down-regulation and ATP-binding cassette transporters A1 and G1, and scavenger receptor class B type 1 up-regulation in human macrophages. Vaspin significantly suppressed angiotensin II-induced migration and proliferation with ERK1/2 and JNK down-regulation, and increased collagen production with phosphoinositide 3-kinase and Akt up-regulation in HASMCs. Chronic infusion of vaspin into Apoe−/− mice significantly suppressed the development of aortic atherosclerotic lesions, with significant reductions of intraplaque inflammation and the macrophage/VSMC ratio, a marker of plaque instability. Our study indicates that vaspin prevents atherosclerotic plaque formation and instability, and may serve as a novel therapeutic target in atherosclerotic cardiovascular diseases.
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Vaspin can suppress vascular cell proliferation and migration by reducing JNK and ERK1/2 pathways and increasing collagen via PI3K/Akt pathways.
“It can also suppress vascular cell proliferation and migration by reducing the c-Jun N-terminal kinase (JNK) and ERK1/2 pathways and increasing collagen via the PI3K/Akt pathways [54].”
From Adipokines, Myokines, and Hepatokines: Crosstalk and Metabolic Repercussions (2021) · cites this paper as [54]
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Rôle des adipocytokines dans l'obésité, l'insulino-résistance et leurs conséquences sur la fertilité
Bongrani, A. (2022) · theses.fr (ABES) · doi:10.70675/1b281dcdz1f16z4985z95f8z0706a492c996
- Authors
- Sato, K., Shirai, R., Yamaguchi, M., Yamashita, T., Shibata, K., Okano, T., Mori, Y., Matsuyama, T.-A., Ishibashi-Ueda, H., Hirano, T., & Watanabe, T.
- Affiliations
- Tokyo University of Pharmacy and Life Sciences (JP)
- SHOWA Medical University (JP)
- Department of Pathology, National Cerebral and Cardiovascular Center, Osaka 565-8565, Japan
- Corresponding author
- Watanabe, Takuya
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2018-06-11
- Volume
- 19
- Issue
- 6
- Pages
- 1732
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC6032338
- OpenAlex
- W2805709638
- Cited by
- 36
- References
- 54
- Citations by year
- 2026: 2 · 2025: 3 · 2023: 2 · 2022: 8 · 2021: 8 · 2020: 8 · 2019: 4 · 2018: 1
- FWCI
- 2.26
- Type
- journal article
- Language
- en
- Open access
- gold
- dx.doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Japan Society for the Promotion of Science (16K08943, 25860418, 17J02716, 17K08993)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- vaspin, atherosclerosis, atherogenesis, macrophages, vascular smooth muscle cells, NF-κB, foam cell formation, oxidized LDL, scavenger receptors, angiotensin II, ERK1/2, JNK, phosphatidylinositol 3-kinase/Akt signaling, plaque vulnerability, ApoE-deficient mice, coronary plaque, adipokines, anti-atherogenic therapy
- MeSH terms
- Animals, Aorta, Apolipoproteins E, Cell Movement, Extracellular Matrix, Foam Cells, Humans, Hyperlipidemias, Inflammation, Macrophages, Models, Biological, Phenotype, Signal Transduction, Serpins, Apoptosis, Myocytes, Smooth Muscle, Cell Proliferation, Atherosclerosis, Mice, Plaque, Atherosclerotic
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