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      Platelet-neutrophil interaction aggravates vascular inflammation and promotes the progression of atherosclerosis by activating the TLR4/NF-κB pathway.

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          Abstract

          Platelet-neutrophil interaction is well known for its role in inflammatory diseases; however, its biological role in atherosclerosis (AS) progression remains unclear. Human peripheral blood neutrophils were obtained to compare toll-like receptor 4 (TLR4), tumor necrosis factor α (TNF-α), interleukin (IL)-1β and myeloid-related proteins 8/14 (Mrp8/14) levels in 22 AS patients with those in 18 healthy controls using quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). Meanwhile, mouse marrow neutrophils subjected to different treatment were collected for the ELISA assay, cell apoptosis, and Western blot analysis. Normal diet or high-fat diet ApoE-/- mice with or without administration of Mrp8/14 antagonist paquinimod were used for plasma collection to measure total cholesterol, triglycerides, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol, TNF-α, IL-1β, Mrp8/14, TLR4, and nuclear factor (NF)-κB p65 levels. The results showed that Mrp8/14 and TLR4-mediated inflammatory pathway was activated in neutrophils of AS patients. In vitro experiments demonstrated that platelet-neutrophil interaction promoted the Mrp8/14 release and inhibited neutrophil apoptosis via P-selectin. Furthermore, platelet-neutrophil interaction upregulated TLR4/myeloid differentiation factor 88/NF-κB pathway. Conversely, Mrp8/14/TLR4/NF-κB interference alleviated AS progression. In conclusion, Mrp8/14/TLR4/NF-κB activated by platelet-neutrophil interaction is an important inflammatory signaling pathway for AS pathogenesis.

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          Author and article information

          Journal
          J. Cell. Biochem.
          Journal of cellular biochemistry
          Wiley
          1097-4644
          0730-2312
          April 2019
          : 120
          : 4
          Affiliations
          [1 ] Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
          [2 ] Department of Echocardiography, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
          [3 ] Department of Cardiology, Fuwai Hospital of the Chinese Academy of Medical Sciences, Beijing, China.
          [4 ] Cadre Ward, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
          [5 ] Department of Acupuncture, The Second Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang, China.
          Article
          10.1002/jcb.27844
          30302814
          7431542c-ed14-4c4b-9b62-782d31e721c6
          History

          toll-like receptor 4 (TLR4),platelet,neutrophil,inflammation,atherosclerosis (AS)

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