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The regulatory role of ProBDNF in monocyte function: Implications in Stanford type‐A aortic dissection disease
Author(s) -
Shen WeiYun,
Luo Cong,
Reinaldo Hurtado Plinio,
HurtadoPerez Ernesto,
Luo RuYi,
Hu ZhaoLan,
Li Hui,
Xu JunMei,
Zhou XinFu,
Dai RuPing
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.201901905rr
Subject(s) - proinflammatory cytokine , cd14 , downregulation and upregulation , cx3cr1 , tumor necrosis factor alpha , medicine , monocyte , brain derived neurotrophic factor , tlr4 , cd68 , cd16 , immunology , neurotrophic factors , chemokine , inflammation , receptor , biology , chemokine receptor , immunohistochemistry , immune system , biochemistry , cd3 , cd8 , gene
Brain‐derived neurotrophic factor precursor (proBDNF) has been reported to strengthen the dysfunction of monocytes/macrophages in animal studies. However, it is still unknown the roles of proBDNF in the dysfunction of monocytes in the inflammatory diseases in humans. In the present study, we showed that proBDNF and pan neurotrophic receptor p75 were significantly upregulated in monocytes from healthy donors (HD) after lipopolysaccharide treatment. Exogenous proBDNF treatment upregulated CD40 and proinflammatory cytokines expression in monocytes including interleukin (IL)‐1β, IL‐6, and tumor necrosis factor (TNF)‐α. In Stanford type‐A acute aortic dissection (AAD) patients, proBDNF was upregulated in CD14 + CD163 + CX3CR1 + M2‐ but not CD14 + CD68 + CCR2 + M1‐like monocytes. In addition, sera from AAD patients activated gene expression of proinflammatory cytokines in cultured PBMCs from HD, which was attenuated by proBDNF monoclonal antibody (Ab‐proB) treatment. These findings suggested that upregulation of proBDNF in M2‐like monocytes may contribute to the proinflammatory response in the AAD.