The mTOR-RUNX1 pathway regulates DC-SIGN expression in renal tubular epithelial cells

被引：7

作者：

Zhou, Siyuan ^{[1
,2
]}

Zhang, Liya ^{[3
]}

Feng, Danying ^{[1
]}

Luo, Maocai ^{[1
]}

Xie, Rongli ^{[4
]}

Yang, Kaige ^{[4
]}

Xu, Dan ^{[4
]}

Yang, Ke ^{[5
]}

Fei, Jian ^{[4
]}

Zhou, Tong ^{[1
]}

机构：

[1] Shanghai Jiao Tong Univ, Ruijin Hosp, Dept Pediat, Sch Med, Shanghai 200025, Peoples R China

[2] Nanjing Med Univ, Dept Clin Lab, Affiliated Changzhou 2 Peoples Hosp, Changzhou 213000, Jiangsu, Peoples R China

[3] Shanghai Jiao Tong Univ, Xinhua Hosp, Dept Pediat, Sch Med, Shanghai 200092, Peoples R China

[4] Shanghai Jiao Tong Univ, Ruijin Hosp, Dept Gen Surg, Sch Med, Shanghai 200025, Peoples R China

[5] Shanghai Jiao Tong Univ, Ruijin Hosp, Inst Cardiovasc Dis, Sch Med, Shanghai 200025, Peoples R China

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2019年 / 519卷 / 03期

基金：

中国国家自然科学基金;

关键词：

DC-SIGN; mTOR; RUNX1; Renal tubular epithelial cells; TNF-ALPHA; INFLAMMATION; INNATE; RUNX1;

D O I：

10.1016/j.bbrc.2019.09.042

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Renal tubular epithelial cells (RTECs) play pivotal roles in the innate immune response in kidneys. Dendritic cell specific intracellular adhesion molecule-3 grabbing nonintegrin (DC-SIGN) functions as both the innate immune recognition receptor and the adhesion molecule. In our previous study, we found that DC-SIGN expression was induced in RTECs during renal inflammation. However, the underlying mechanism remains unclear. Here, we used the human renal proximal tubular epithelial cell lines (HK-2) to investigate the mechanism of TNF-alpha-induced expression of DC-SIGN. Our results showed that TNF-alpha up-regulated the expressions of DC-SIGN and Runt-related transcription factor 1 (RUNX1) in a time-dependent manner and that it up-regulated DC-SIGN promoter-driven luciferase activity in a dose-dependent manner. The mTOR inhibitor rapamycin and mTOR siRNA blocked the TNF-alpha-induced upregulation of DC-SIGN expression. Meanwhile, DC-SIGN expression was also inhibited by RUNX1 siRNA and its inhibitor Ro5-3335. In addition, both mTOR and RUNX1 inhibitors attenuated TNF-alpha-induced the increase in DC-SIGN promoter-driven luciferase activity. Finally, we found that HK-2 cells exposed to rapamycin or mTOR siRNA reduced the TNF-alpha-induced up-regulation of RUNX1. In conclusion, these results indicated that the mTOR-RUNX1 pathway participates in the regulation of TNF-alpha-induced DC-SIGN expression in RTECs. (C) 2019 Elsevier Inc. All rights reserved.

引用

页码：620 / 625

页数：6

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