A necroptotic-independent function of MLKL in regulating endothelial cell adhesion molecule expression

被引：36

作者：

Dai, Jialin ^{[1
,2
]}

Zhang, Chonghe ^{[1
,2
]}

Guo, Lin ^{[1
,2
]}

He, Hao ^{[1
,2
]}

Jiang, Kai ^{[1
]}

Huang, Yingying ^{[2
,3
]}

Zhang, Xixi ^{[2
,4
]}

Zhang, Haibing ^{[2
,4
]}

Wei, Wu ^{[2
,3
]}

Zhang, Yaoyang ^{[1
,2
]}

Lu, Lihua ^{[5
]}

Hu, Junhao ^{[1
,2
]}

机构：

[1] Chinese Acad Sci, Shanghai Inst Organ Chem, Interdisciplinary Res Ctr Biol & Chem, Shanghai, Peoples R China

[2] Univ Chinese Acad Sci, Beijing, Peoples R China

[3] Chinese Acad Sci, Univ Chinese Acad Sci, Shanghai Inst Biol Sci,CAS Key Lab Computat Biol, Shanghai Inst Nutr & Hlth,CAS MPG Partner Inst Co, Shanghai, Peoples R China

[4] Chinese Acad Sci, Shanghai Inst Nutr & Hlth, CAS Key Lab Nutr Metab & Food Safety, Shanghai, Peoples R China

[5] Tongji Univ, Sch Med, Shanghai First Matern & Infant Hosp, Dept Neonatol, Shanghai, Peoples R China

来源：

CELL DEATH & DISEASE | 2020年 / 11卷 / 04期

基金：

美国国家科学基金会;

关键词：

MIXED LINEAGE KINASE; DOMAIN-LIKE PROTEIN; RIP1; KINASE; NECROSIS; BINDING; ACTIVATION; TRANSLOCATION; DOWNSTREAM; DEATH; GENE;

D O I：

10.1038/s41419-020-2483-3

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Mixed-lineage kinase domain-like protein (MLKL) is known as the terminal executor of necroptosis. However, its function outside of necroptosis is still not clear. Herein, we demonstrate that MLKL promotes vascular inflammation by regulating the expression of adhesion molecules ICAM1, VCAM1, and E-selectin in endothelial cells (EC). MLKL deficiency suppresses the expression of these adhesion molecules, thereby reducing EC-leukocyte interaction in vitro and in vivo. Mechanistically, we show that MLKL interacts with RBM6 to promote the mRNA stability of adhesion molecules. In conclusion, this study identified a novel role of MLKL in regulating endothelial adhesion molecule expression and local EC-leukocyte interaction during acute inflammation.

引用

页数：16

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