Interleukin-32 plays an essential role in human calcified aortic valve cells View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2018-03

AUTHORS

Chung-Lin Tsai, Ying-Ming Chiu, Yi-Ju Lee, Chin-Tung Hsieh, Dong-Chen Shieh, Gregory J. Tsay, Da-Tian Bau, Yi-Ying Wu

ABSTRACT

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. More... »

PAGES

36-47

Identifiers

URI

http://scigraph.springernature.com/pub.10.1684/ecn.2018.0407

DOI

http://dx.doi.org/10.1684/ecn.2018.0407

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1103946050

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29748157


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