MLN4924 Dose-dependently Represses LPS-induced Proinflammatory Cytokine Production in Neutrophils
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- 英文论文题名：MLN4924 Dose-dependently Represses LPS-induced Proinflammatory Cytokine Production in Neutrophils
- 论文作者：Jin Jiayang ; Zhang Jiyan
- 英文论文作者：Jin Jiayang ; Zhang Jiyan ; Institute of Basic Medical Sciences
- 年：2016
- 作者机构：Institute of Basic Medical Sciences;
- 英文论文关键词：Neddylation ; neutrophils ; cytokine
- 会议召开时间：2016-11-04
- 会议录名称：第十一届全国免疫学学术大会摘要汇编
- 英文会议录名称：Abstracts of 2016 CSI Congress on Immunology
- 语种：英文
- 分类号：R392
- 学会代码：IGMD
- 会议名称：第十一届全国免疫学学术大会
- 会议地点：中国安徽合肥
- 主办单位：中国免疫学会
- 学会名称：中国免疫学会
- 页数：1
- 文件大小：270k
- 原文格式：D
- 会议级别：全国
摘要
Neddylation, analogous to ubiquitination, is a newly post-translational modification, which is also essential for the activity and stability of target proteins. It has been reported that neddylation inhibition by a pharmacological agent MLN4924 potently suppresses lipopolysaccharide(LPS)-induced proinflammatory cytokine(such as TNF-a and IL-6) production by preventing the degradation of inhibitor of k B(Ik B) proteins in macrophage cells. However, the role of neddylation in neutrophils remains unknown. Here, we report that MLN4924 treatment, in a dose-dependent manner, led to the accumulation of P-Ik Ba due to impaired Ik Ba degradation in neutrophils as well as reduced production of TNF-a, IL-6, and IL-1b in response to LPS. The viability of neutrophils was only marginally affected under the same conditions. Together, our findings suggest that neddylation inhibition suppresses neutrophil functions through, at least partially, repressing nuclear factor-k B(NF-k B) pathway.
Neddylation, analogous to ubiquitination, is a newly post-translational modification, which is also essential for the activity and stability of target proteins. It has been reported that neddylation inhibition by a pharmacological agent MLN4924 potently suppresses lipopolysaccharide(LPS)-induced proinflammatory cytokine(such as TNF-a and IL-6) production by preventing the degradation of inhibitor of k B(Ik B) proteins in macrophage cells. However, the role of neddylation in neutrophils remains unknown. Here, we report that MLN4924 treatment, in a dose-dependent manner, led to the accumulation of P-Ik Ba due to impaired Ik Ba degradation in neutrophils as well as reduced production of TNF-a, IL-6, and IL-1b in response to LPS. The viability of neutrophils was only marginally affected under the same conditions. Together, our findings suggest that neddylation inhibition suppresses neutrophil functions through, at least partially, repressing nuclear factor-k B(NF-k B) pathway.
Neddylation, analogous to ubiquitination, is a newly post-translational modification, which is also essential for the activity and stability of target proteins. It has been reported that neddylation inhibition by a pharmacological agent MLN4924 potently suppresses lipopolysaccharide(LPS)-induced proinflammatory cytokine(such as TNF-a and IL-6) production by preventing the degradation of inhibitor of k B(Ik B) proteins in macrophage cells. However, the role of neddylation in neutrophils remains unknown. Here, we report that MLN4924 treatment, in a dose-dependent manner, led to the accumulation of P-Ik Ba due to impaired Ik Ba degradation in neutrophils as well as reduced production of TNF-a, IL-6, and IL-1b in response to LPS. The viability of neutrophils was only marginally affected under the same conditions. Together, our findings suggest that neddylation inhibition suppresses neutrophil functions through, at least partially, repressing nuclear factor-k B(NF-k B) pathway.
引文