Dataset Information

Proteome and phosphoproteome analysis of CMV-infected macrophages

ABSTRACT: Macrophages, which populate barrier tissues already in the embryo, are primary targets for CMV. Here we show that upon infection macrophages undergo a morphological, immunophenotypic and metabolic transformation process with features of stemness, altered migration, enhanced invasiveness and provision of the cell cycle machinery to viral proliferation

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Macrophage

SUBMITTER: Piero Giansanti

LAB HEAD: Bernhard Kuster

PROVIDER: PXD015923 | Pride | 2021-06-02

REPOSITORIES: Pride

ACCESS DATA

Publications

Cytomegalovirus subverts macrophage identity.

Baasch Sebastian S Giansanti Piero P Kolter Julia J Riedl André A Forde Aaron James AJ Runge Solveig S Zenke Simon S Elling Roland R Halenius Anne A Brabletz Simone S Hengel Hartmut H Kuster Bernhard B Brabletz Thomas T Cicin-Sain Luka L Arens Ramon R Vlachos Andreas A Rohr Jan Christopher JC Stemmler Marc Philippe MP Kopf Manfred M Ruzsics Zsolt Z Henneke Philipp P

Cell 20210610 14

Cytomegaloviruses (CMVs) have co-evolved with their mammalian hosts for millions of years, leading to remarkable host specificity and high infection prevalence. Macrophages, which already populate barrier tissues in the embryo, are the predominant immune cells at potential CMV entry sites. Here we show that, upon CMV infection, macrophages undergo a morphological, immunophenotypic, and metabolic transformation process with features of stemness, altered migration, enhanced invasiveness, and provi ...[more]

PMID: 34115982

Similar Datasets

Project description:Acute Myeloid Leukemia (AML) is characterized by the clonal expansion of immature myeloblasts originating from leukemic stem cells (LSCs) niched within the bone marrow. Bone marrow stromal cells (BMSC) and tumor-stroma interactions play a prominent role in the evolution of this disease. BMSC-mediated protection of leukemic cells involves several mechanisms, including interactions between adhesion molecules, the secretion of cytokines/chemokines and the release of extracellular vesicles produced by the surrounding non-haemopoietic BM cells. Recent studies even suggest that autophagy in the tumor stroma is associated with leukemia progression, survival and resistance. Thus, it seems widely evident that the microenvironment profile affects the prognosis and influences the efficacy of anti-cancer therapies. Yet, although widely explored, the crosstalk between leukemic and stromal cells remains poorly understood. Syntenin (directing endocytosed SDC and receptor cargo back to cell surfaces and/or to endosomal intraluminal vesicles and exosomes) is known to coordinate inter-cellular communications. Using syntenin-knockout mice, we aimed to clarify the role of environmental-syntenin in the progression of AML, a disease in which the role of (tumor/host) syntenin was not yet investigated. To address the role of host-syntenin in AML, I extensively used the mouse FLB1 AML-like model (generous gift of O. Herault, Tours). Strikingly, FLB1 cells show a marked gain in aggressiveness when serially transplanted a syntenin-KO host. This aggressive behavior is cell-autonomous, as not reversed by back transplantation into WT hosts. Moreover, ‘aggressive’ FLB1 blasts, raised by education in a syntenin-negative in vivo background, are able to survive and grow in vitro in the absence of stroma, suggesting the cell-autonomous activation of survival pathways. Surprisingly, this gain of aggressiveness is not accompanied by a noticeable morphotypic or transcriptomic signature. However using quantitative proteomics we highlighted altered mRNA translational control. Aggressive FLB1 show a significant up-regulation of several factors, but most marked for EEF1A2, previously shown to have pro-oncogenic activities in various cancers..Globally, these findings are also consistent with the emerging notion that altered mRNA translational control is a critical factor in cancer development and progression.

Dataset Information

Proteome and phosphoproteome analysis of CMV-infected macrophages

Publications

Cytomegalovirus subverts macrophage identity.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure