Down-regulation of A20 mRNA expression in peripheral blood mononuclear cells from MDS patients

Hematology. 2024 Dec;29(1):2330851. doi: 10.1080/16078454.2024.2330851. Epub 2024 Mar 21.

Abstract

Myelodysplastic syndrome (MDS) is characterized by activated inflammatory signaling and affects prognosis. Targeting inflammatory signaling may provide a way to treat the disease. We were curious whether there were changes in A20 in peripheral blood mononuclear cells (PBMC) of MDS patients. Therefore, we conducted a study with 60 clinical samples, including 30 MDS patients and 30 healthy controls. All patients with MDS were diagnosed and classified according to the criteria of the 2016 World Health Organization. The study was performed in accordance with the guidelines of the Declaration of Helsinki. Using Quantitative Real-Time RT-PCR, we discovered that A20 mRNA expression in PBMC of the MDS group was significantly lower than that in the control group (P < 0.001). Additionally, using Luminex Liquid Suspension Chip, we observed elevated plasma levels of pro-inflammatory IL-8 and TNF-α in the MDS group compared to the healthy control group (P < 0.001). We did not find a significant correlation between A20 mRNA and clinical characteristics (age, sex, concentration of hemoglobin, neutrophils count, platelets count, percent of blasts, and WHO classification) of the patients, nor between A20 mRNA and plasma cytokines (data not shown). Our study found down-regulated of A20 and increased levels of pro-inflammatory cytokines in the peripheral blood of MDS patients, providing further evidence for the activation of inflammatory signals in MDS.

Keywords: A20; IL-8; Myelodysplastic syndrome; TNF-α‌; inflammatory signaling; mRNA; peripheral blood mononuclear cells; plasma cytokines‌.

MeSH terms

  • Cytokines / genetics
  • Down-Regulation
  • Humans
  • Leukocytes, Mononuclear* / metabolism
  • Myelodysplastic Syndromes* / genetics
  • Myelodysplastic Syndromes* / metabolism
  • RNA, Messenger / genetics
  • Tumor Necrosis Factor alpha-Induced Protein 3 / genetics

Substances

  • Cytokines
  • RNA, Messenger
  • TNFAIP3 protein, human
  • Tumor Necrosis Factor alpha-Induced Protein 3