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Interleukin-32 plays an essential role in human calcified aortic valve cells Volume 29, numéro 1, March 2018

Illustrations

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Auteurs
1 Division of Cardiovascular Surgery, Taichung Veterans General Hospital, Taiwan
2 Graduate Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan
3 Division of Allergy, Immunology & Rheumatology, Changhua Christian Hospital, Changhua, Taiwan
4 Department of Nursing, College of Medicine & Nursing, Hungkuang University, Taichung, Taiwan
5 Institute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan
6 Department of Pediatrics, Lotung Poh-Ai Hospital, I-Lan, Taiwan
7 Division of Immunology and Rheumatology, Department of Internal Medicine, China Medical University Hospital, Taichung, Taiwan
8 School of Medicine, College of Medicine, China Medical University, Taichung, Taiwan
9 Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan
10 Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, Taiwan
* Correspondence: YY Wu
  • Mots-clés : interleukin 32, MAPK, NF-κB, STAT3, calcific aortic valve disease
  • DOI : 10.1684/ecn.2018.0407
  • Page(s) : 36-47
  • Année de parution : 2018

Interleukin-32 (IL-32) is an inflammatory cytokine produced mainly by T, natural killer, and epithelial cells. Previous studies on IL-32 have primarily investigated its proinflammatory properties. The IL-32 also has been described as an activator of the p38 mitogen-activated protein kinase (MAPK) and NF-κB, and induces several cytokines. In this study, we hypothesized that the inflammatory regulators NF-κB, MAP kinase, STAT1, and STAT3 are associated with the expression of the IL-32 protein in human calcified aortic valve cells. This study comprised aortic valve sclerotic patients and control group patients without calcified aortic valve. Increased IL-32 expression in calcified aortic valvular tissue was shown by immunohistochemical staining and western blotting. There was an increase in NF-κB p65 level, p-ERK, p-JNK, and p-p38 MAPK activation underlying IL-32 expression in the study. The level of p-STAT3 but not p-STAT1 was found to be increased in calcified aortic valve tissue. In cultured primary human aortic valve interstitial cells, inhibition of NF-κB or MAPK kinase pathways results in a decrease of IL-32 expression. Treatment of recombinant IL-32 induced the levels of TNF-α, IL-6, IL-1β, and IL-8. Our findings demonstrate that IL-32 may be an important pro-inflammatory molecule involved in calcific aortic valve disease.