PMID- 37125077
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230502
IS  - 2405-5808 (Electronic)
IS  - 2405-5808 (Linking)
VI  - 34
DP  - 2023 Jul
TI  - Complement dependent TNFalpha production in neutrophil-like HL60 cells.
PG  - 101465
LID - 10.1016/j.bbrep.2023.101465 [doi]
LID - 101465
AB  - Neutrophils develop in the bone marrow (BM) from hematopoietic stem cells (HSCs) 
      through a series of progenitor cells and mature neutrophils play a critical role 
      in the human immune system. Previous studies revealed that tumor necrosis factor 
      alpha (TNFalpha) produced by immature neutrophils contributes to HSCs development and 
      vascular regeneration in the BM niche. However, the precise mechanism of TNFalpha 
      production in immature neutrophils remains unclear. This study aims to assess the 
      relationship between complement C3 activation and TNFalpha production from immature 
      neutrophils. We investigated the regulatory mechanism of TNFalpha production by 
      complement components in neutrophil-like HL60 cells. Flow cytometric analysis 
      showed that C3a receptor (C3aR) and C3bi receptor (CR3, Mac-1, CD11b/CD18, 
      integrin alphaMbeta2) are expressed on the surface of neutrophil-like HL60 cells. We 
      found that zymosan-treated human serum leads to TNFalpha production in 
      neutrophil-like HL60 cells, but not in human polymorphonuclear cells (PMNs). A 
      C3-convertase inhibitor, compstatin suppresses TNFalpha production. These data 
      suggest that the TNFalpha production is mediated by complement C3 activation. 
      Furthermore, the TNFalpha production is enhanced by Ca(2+) elevating agents, 
      thapsigargin (TG), but is suppressed by treatment with Ca(2+) chelators, EGTA, or 
      BAPTA-AM. In addition, the soluble TNFalpha production is suppressed by treatment 
      with immobilized-fibrinogen or -fibronectin. Thus, the TNFalpha production is 
      enhanced by intracellular Ca(2+) elevation and is negatively regulated by the 
      interaction between the neutrophil-like HL60 cells and fibrinogen or fibronectin.
CI  - (c) 2023 The Authors.
FAU - Tabata, Hiroyuki
AU  - Tabata H
AD  - Division of Biochemistry, Faculty of Pharmaceutical Sciences, Himeji Dokkyo 
      University, Himeji, Hyogo, 670-8524, Japan.
FAU - Morita, Hiroyuki
AU  - Morita H
AD  - Division of Biochemistry, Faculty of Pharmaceutical Sciences, Himeji Dokkyo 
      University, Himeji, Hyogo, 670-8524, Japan.
FAU - Kouyama, Kenichi
AU  - Kouyama K
AD  - Division of Biochemistry, Faculty of Pharmaceutical Sciences, Himeji Dokkyo 
      University, Himeji, Hyogo, 670-8524, Japan.
FAU - Tohyama, Yumi
AU  - Tohyama Y
AD  - Division of Biochemistry, Faculty of Pharmaceutical Sciences, Himeji Dokkyo 
      University, Himeji, Hyogo, 670-8524, Japan.
LA  - eng
PT  - Journal Article
DEP - 20230414
PL  - Netherlands
TA  - Biochem Biophys Rep
JT  - Biochemistry and biophysics reports
JID - 101660999
PMC - PMC10130347
OTO - NOTNLM
OT  - Calcium
OT  - Complement
OT  - Integrin
OT  - Neutrophil
OT  - TNFalpha
COIS- The authors declare that they have no known competing financial interests or 
      personal relationships that could have appeared to influence the work reported in 
      this paper.
EDAT- 2023/05/01 06:42
MHDA- 2023/05/01 06:43
PMCR- 2023/04/14
CRDT- 2023/05/01 03:54
PHST- 2022/11/26 00:00 [received]
PHST- 2023/03/12 00:00 [revised]
PHST- 2023/04/03 00:00 [accepted]
PHST- 2023/05/01 06:43 [medline]
PHST- 2023/05/01 06:42 [pubmed]
PHST- 2023/05/01 03:54 [entrez]
PHST- 2023/04/14 00:00 [pmc-release]
AID - S2405-5808(23)00046-8 [pii]
AID - 101465 [pii]
AID - 10.1016/j.bbrep.2023.101465 [doi]
PST - epublish
SO  - Biochem Biophys Rep. 2023 Apr 14;34:101465. doi: 10.1016/j.bbrep.2023.101465. 
      eCollection 2023 Jul.