Effects of ATP on expression of inflammatory factors in endothelial progenitor cells induced by LPS and the mechanisms.
10.11817/j.issn.1672-7347.2018.12.004
- Author:
Bolin XIAO
1
,
2
,
3
;
Meifang CHEN
1
,
4
;
Mei YANG
1
,
4
;
Zhilin XIAO
1
,
4
Author Information
1. Department of Geriatric Cardiology
2. National Center for Clinical Research of Geriatric Diseases, Xiangya Hospital, Central South University, Changsha 410008
3. School of Stomatology, Lanzhou University, Lanzhou 710000, China.
4. National Center for Clinical Research of Geriatric Diseases, Xiangya Hospital, Central South University, Changsha 410008, China.
- Publication Type:Journal Article
- MeSH:
Adenosine Triphosphate;
pharmacology;
Endothelial Progenitor Cells;
drug effects;
Gene Expression Regulation;
drug effects;
Humans;
Leukocytes, Mononuclear;
cytology;
Lipopolysaccharide Receptors;
genetics;
Lipopolysaccharides;
pharmacology;
Myeloid Differentiation Factor 88;
genetics;
NF-kappa B;
metabolism;
Signal Transduction;
drug effects;
Toll-Like Receptor 4;
genetics
- From:
Journal of Central South University(Medical Sciences)
2018;43(12):1301-1308
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the effects of adenosine triphosphate (ATP) on expression of inflammatory factors induced by lipopolysaccharide (LPS) in endothelial progenitor cells (EPCs), and to elucidate the possible mechanisms.
Methods: Mononuclear cells were isolated from human umbilical cord blood by density gradient centrifugation, RT-PCR was performed to detect the expression of inflammatory factors induced by LPS (1 mg/mL) in EPCs, the effect of low concentration (5 μmol/L) of ATP on expression of IL-1β, MCP-1 and ICAM-1, and the effect of different concentrations (5, 50 μmol/L) of ATP on the expression of Toll-like receptor (TLR) 4, myeloid differentiation primary response protein 88 (MyD88) and CD14. Western blot was performed to detect expression of TLR4 regulated proteins MyD88 and CD14 or to detect the low concentration (1, 5 μmol/L) of ATP on the expression of TLR4, MyD88 and CD14 and the NF-κB signaling pathway.
Results: EPCs highly expressed TLR4, and its ligand LPS (1 mg/mL) significantly upregulated mRNA expression of IL-1β, MCP-1 and ICAM-1 and protein expression of MyD88 and CD14 in a time-dependent manner (P<0.01), accompanied by activation of ERK and NF-κB signal pathway. ATP at low concentration (5 μmol/L) significantly inhibited LPS-induced mRNA expression of IL-1β, MCP-1 and ICAM-1(P<0.05), downregulated the LPS-induced protein expression of TLR4, MyD88 and CD14 in EPCs (P<0.05), and suppressed LPS-induced activation of NF-κB signaling pathway (P<0.05).
Conclusion: ATP at low concentration may suppress LPS-induced expression of inflammatory factors in EPCs through negative regulation of the TLR4 signaling pathway.
