Immunomodulatory Activity of Ganoderma atrum Polysaccharide on Purified T Lymphocytes through Ca2+/CaN and Mitogen-Activated Protein Kinase Pathway Based on RNA Sequencing

被引:60
作者
Xiang, Quan-Dan [1 ]
Yu, Qiang [1 ]
Wang, Hui [2 ,3 ]
Zhao, Ming-Ming [1 ]
Liu, Shi-Yu [1 ]
Nie, Shao-Ping [1 ]
Xie, Ming-Yong [1 ]
机构
[1] Nanchang Univ, State Key Lab Food Sci & Technol, Nanchang 330047, Jiangxi, Peoples R China
[2] Nanchang Univ, Inst Life Sci, Nanchang 330031, Jiangxi, Peoples R China
[3] Nanchang Univ, Coll Life Sci, Nanchang 330031, Jiangxi, Peoples R China
基金
中国国家自然科学基金;
关键词
Ganoderma atrum polysaccharide; purified T lymphocytes; RNA-seq; Ca2+/CaN pathway; MAPK pathway; TUMOR-BEARING MICE; IMMUNE-RESPONSES; MAP KINASES; CALCINEURIN; SEQ; TRANSCRIPTOME; CALCIUM; CELLS; DIFFERENTIATION; EXPRESSION;
D O I
10.1021/acs.jafc.7b01763
中图分类号
S [农业科学];
学科分类号
09 ;
摘要
Our previous study has demonstrated that Ganoderma atrum polysaccharide (PSG-1) has immunomodulatory activity on spleen lymphocytes. However, how PSG-1 exerts its effect on purified lymphocytes is still obscure. Thus, this study aimed to investigate the immunomodulatory activity of PSG-1 on purified T lymphocytes and further elucidate the underlying mechanism based on RNA sequencing (RNA-seq). Our results showed that PSG-1 promoted T lymphocytes proliferation and increased the production of IL-2, IFN-gamma, and IL-12. Meanwhile, RNA-seq analysis found 394 differentially expressed genes. KEGG pathway analysis identified 20 significant canonical pathways and seven biological functions. Furthermore, PSG-1 elevated intracellular Ca2+ concentration and calcineurin (CaN) activity and raised the p-ERK, p-JNK, and p-p38 expression levels. T lymphocytes proliferation and the production of IL-2, IFN-gamma, and IL-12 were decreased by the inhibitors of calcium channel and mitogen-activated protein kinases (MAPKs). These results indicated that PSG-1 possesses immunomodulatory activity on purified T lymphocytes, in which Ca2+/CaN and MAPK pathways play essential roles.
引用
收藏
页码:5306 / 5315
页数:10
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