2. Academic Validation
  3. A necroptotic-independent function of MLKL in regulating endothelial cell adhesion molecule expression

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

  • Cell Death Dis. 2020 Apr 24;11(4):282. doi: 10.1038/s41419-020-2483-3.
Jialin Dai 1 2,  Chonghe Zhang 1 2,  Lin Guo 1 2,  Hao He 1 2,  Kai Jiang 1,  Yingying Huang 2 3,  Xixi Zhang 2 4,  Haibing Zhang 2 4,  Wu Wei 2 3,  Yaoyang Zhang 1 2,  Lihua Lu 5,  Junhao Hu 6 7
Affiliations

Affiliations

  • 1 Interdisciplinary Research Center on Biology and Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai, China.
  • 2 University of Chinese Academy of Sciences, Beijing, China.
  • 3 CAS Key Laboratory of Computational Biology, CAS-MPG Partner Institute for Computational Biology, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
  • 4 CAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences, Shanghai, China.
  • 5 Department of Neonatology, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, China. dr_lulihua@tongji.edu.cn.
  • 6 Interdisciplinary Research Center on Biology and Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai, China. jhhu@sioc.ac.cn.
  • 7 University of Chinese Academy of Sciences, Beijing, China. jhhu@sioc.ac.cn.
PMID: 32332696 DOI: 10.1038/s41419-020-2483-3
Abstract

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.

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