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[Effect of Gas6 in silica-induced inflammation on differentiated human acute monocytic leukemia (THP-1) macrophages]
1Department of Occupational an Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Abstract:
Objective: To investigate the modulation role of Gas6 in silica-induced inflammatory effect on human macrophages. Methods: Differentiated THP-1 macrophages were exposed to different concentrations of silica for 6 h and 24 h. Additionally, silica-activated macrophages were treated with different concentrations of recombine human Gas6 and Gas6 antibody respectively. Cell viabilities were determined by CCK-8 kit. Expression levels of Gas6 and inflammatory cytokines (TNF-α, IL-1β and IL-6) were measured by ELISA assay kits. Results: Silica particles induced clear dose-dependent decreases of cell viability and Gas6 expression at both 6 h and 24 h. The cell viability of 24 h is lower than 6 h at the same concentration of silica (P<0.05). Furthermore, silica activated macrophages treated with Gas6 antibody induced significant decreases of Gas6 both at 6 h and 24 h (P<0.05). After pretreated with various concentrations of Gas6 antibody, silica induced higher expressions of inflammatory cytokines (TNF-α, IL-1β, IL-6) in dose-dependent manners at two time points. Addition of exoge-nous Gas6 significantly suppressed silica-induced inflammatory cytokines concentrations mentioned above in the cell culture supernatants in clear dose-dependent manners. Conclusion: Exogenous Gas6 could inhibit the secre-tion of inflammatory cytokines in macrophages, while the block of Gas6 might enhance this inflammation.
Insights
Growth arrest-specific 6 (Gas6) protein inhibits silica-induced inflammation in human macrophages. Blocking Gas6 exacerbates this inflammation, highlighting Gas6
Area of Science:
- Immunology
- Cell Biology
- Toxicology
Background:
- Silica exposure can trigger inflammatory responses in macrophages.
- The role of Growth arrest-specific 6 (Gas6) in silica-induced inflammation is not fully understood.
Purpose of the Study:
- To investigate the modulatory role of Gas6 in silica-induced inflammatory effects on human macrophages.
- To determine how Gas6 influences inflammatory cytokine production.
Main Methods:
- Human THP-1 macrophages were exposed to silica particles.
- Cells were treated with recombinant human Gas6 or Gas6 antibody.
- Cell viability, Gas6 expression, and inflammatory cytokines (TNF-α, IL-1β, IL-6) were measured.
Main Results:
- Silica exposure decreased cell viability and Gas6 expression in a dose-dependent manner.
- Blocking Gas6 with an antibody enhanced silica-induced inflammatory cytokine production.
- Exogenous Gas6 significantly suppressed silica-induced inflammatory cytokine secretion.
Conclusions:
- Gas6 plays an inhibitory role in silica-induced macrophage inflammation.
- Exogenous Gas6 can suppress inflammatory cytokine secretion, while Gas6 blockade enhances inflammation.
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