@Article{ecn.2018.0407,
AUTHOR = {Chung-Lin Tsai, Ying-Ming Chiu, Yi-Ju Lee, Chin-Tung Hsieh, Dong-Chen Shieh, Gregory J. Tsay, Da-Tian Bau, Yi-Ying Wu},
TITLE = {Interleukin-32 plays an essential role in human calcified aortic valve cells},
JOURNAL = {European Cytokine Network},
VOLUME = {29},
YEAR = {2018},
NUMBER = {1},
PAGES = {36--47},
URL = {http://www.techscience.com/ECN/v29n1/65410},
ISSN = {1952-4005},
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.},
DOI = {10.1684/ecn.2018.0407}
}