Open Access
ARTICLE
Decreased serum HMGB1 associated with M2 macrophage polarization and patients with calcific aortic valve disease
DONG ZHAO, QIANG JI*, SHIJIE ZHU, KAI ZHU, CHUNSHENG WANG*
Department of Cardiac Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
* Address correspondence to: Qiang Ji, ; Chunsheng Wang,
BIOCELL 2020, 44(3), 315-321. https://doi.org/10.32604/biocell.2020.09169
Received 28 November 2019; Accepted 28 April 2020; Issue published 22 September 2020
Abstract
Except for the standard aortic valve replacement, no effective medical treatment is available to prevent or delay
calcific aortic valve disease (CAVD) progression. Recently, macrophages and high-mobility group box 1 (HMGB1) are the
most intriguing candidates in various inflammatory disorders. However, the association between serum HMGB1, CAVD,
and macrophage polarization remains unclear. Therefore, we examined whether the level of serum HMGB1 is clinically
associated with aortic valve calcification and whether HMGB1 treatment can promote macrophage differentiation toward
M1 or M2 phenotype. This experimental study included 19 CAVD patients and 20 healthy controls whose serum HMGB1
levels were examined by ELISA assay. THP-1 macrophage polarization system was established to test the polarization
capability of HMGB1 treatment. The results showed that serum levels of HMGB1 were significantly reduced in
patients with CAVD. HMGB1 treatment promoted M2 macrophage polarization but not M1 phenotype with
increased IL-10 expression and reduced inducible nitric oxide synthase (iNOS) expression. Our findings suggest that
serum HMGB1 is negatively associated with the development of aortic valve calcification, and HMGB1 treatment may
facilitate M2 macrophage polarization for reducing aortic valve calcification.
Keywords
Cite This Article
ZHAO, D., JI, Q., ZHU, S., ZHU, K., WANG, C. (2020). Decreased serum HMGB1 associated with M2 macrophage polarization and patients with calcific aortic valve disease.
BIOCELL, 44(3), 315–321. https://doi.org/10.32604/biocell.2020.09169
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