Dr.Xiaoliang Sun

Issuing time:2021-09-17 11:15

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Name:

Xiaoliang Sun

Title:

Group leader of bioinformatics and   mathematical modelling

Affiliation:

Department of Molecular Systems Biology,   University of Vienna, Austria

Email:

xiaoliang.sun@univie.ac.at

100-word biography:

Xiaoliang Sun obtained his bachelor and   master degree in biomedical engineering from Southeast University, China, in   2001 and 2006 respectively, and PhD in bioinformatics from Max Planck Institute for Molecular Plant Physiology, Germany, in 2011. Since 2016 he has   been core member of Vienna Metabolomics Center and since 2018 group leader in   bioinformatics and mathematical learning in University of Vienna, Austria. He   has developed statistics and mathematical modelling algorithms with multi-omics   data, and pioneered in the inverse engineering of genome-scale omics data   that lead to identifications of key regulatory points in the biochemical   networks.

Title:

Inverse Data-Driven Modeling and Multiomics Analysis Reveals Phgdh as a   Metabolic Checkpoint of Macrophage Polarization and Proliferation

Abstract:


Mechanistic   or mammalian target of rapamycin complex 1 (mTORC1) is an important regulator   of effector functions, proliferation, and cellular metabolism in macrophages.   The biochemical processes that are controlled by mTORC1 are still being   defined. Here, we demonstrate that integrative multi-omics in conjunction   with a data-driven inverse modelling approach, identifies a biochemical node   that influences overall metabolic profiles and reactions of mTORC1-dependent   macrophage metabolism. Using a combined approach of metabolomics, proteomics,   mRNA expression analysis, and enzymatic activity measurements, we demonstrate   that Tsc2, a negative regulator of mTORC1 signaling, critically influences   the cellular activity of macrophages by regulating the enzyme   phosphoglycerate dehydrogenase (Phgdh) in an mTORC1-dependent manner. More   generally, while lipopolysaccharide
   (LPS)-stimulated macrophages repress Phgdh activity, IL-4-stimulated   macrophages increase the activity of the enzyme required for the expression   of key anti-inflammatory molecules and macrophage proliferation. Thus, we   identify Phgdh as a metabolic checkpoint of M2 macrophages.

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