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Transcriptomics reveals pathways involved in myeloid-derived suppressor cell (MDSC) supernatant attenuation of TGF-β1-induced myofibroblastic differentiation of mesenchymal stem cells (MSCs)

ABSTRACT: Transcriptomic analyses were conducted to discover potential mechanisms of TGF-β1-induced changes in MSCs and the effect of MDSC supernatant treatment.

ORGANISM(S): Mus musculus

PROVIDER: GSE193592 | GEO | 2022/02/25

REPOSITORIES: GEO

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Transcriptomics reveals pathways involved in myeloid-derived suppressor cell (MDSC) supernatant attenuation of TGF-β1-induced myofibroblastic differentiation of mesenchymal stem cells (MSCs)

Project description:Transcriptomics reveals pathways involved in myeloid-derived suppressor cell (MDSC) supernatant attenuation of TGF-β1-induced myofibroblastic differentiation of mesenchymal stem cells (MSCs)

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MDSC exacerbate acute hepatitis, mature and loose suppressor function CD40 dependent

Project description:Myeloid-derived suppressor cells (MDSC) represent a heterogeneous population of immature myeloid cells that accumulate in blood, liver, spleen and tumors upon chronic inflammation and tumor development in patients and mice. Acute hepatitis is characterized by a fast infiltration of inflammatory cells in the liver and increased enzymatic activity at this organ that could lead into liver fibrosis and cirrhosis. We have studied the biology of hepatic MDSC in acute hepatitis. Unexpectedly, hepatic MDSC, which accumulate in the liver of mice bearing subcutaneous tumors, failed to suppress inflammatory responses upon Con A injection, but instead were responsible for exacerbating acute liver damage. Phenotypic, genetic and functional studies demonstrated rapid changes of hepatic MDSC from a suppressor phenotype into a pro-inflammatory subset as early as 3 hours after Con A injection. An increase in the expression of pro-inflammatory cytokines, costimulatory molecules such as CD80, CD86 and CD40 along with a loss of suppressor function was noticed in mice upon Con A treatment. These changes were CD40-dependent and not found in CD40-/- MDSC. Interestingly, CD40 ligation of human MDSC in vitro resulted in down-regulation of arginase I expression and suppressor function. Finally, blockade of ROS production in hepatic MDSC ameliorated hepatocyte damage suggesting that MDSC mediated toxicity was ROS dependent. We believe that these findings reflect how MDSC plasticity can be modulated to promote inflammation, opening a new path for therapies targeting innate suppressive cells in cancer patients. EL4 tumors were established in C57BL/6 mice, then mice were injected either with PBS (n=3) or 12.5mg/kg Con A (n=3). Three hours later mice were sacrificed, liver CD11b+Gr-1+ cells were sorted and samples were processed for gene expression analysis.

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Expression data from granulocytic MDSC (G-MDSC) and neutrophils

Project description:Myeloid derived suppressor cells (MDSC) playing the immune suppressive roles in tumor bearing host consists of two major subsets of granulocytic and monocytic cells. Granulocytic MDSC (G-MDSC) express CD11b+ Gr-1high Ly6G+ Ly6Clow and produce high level of reactive oxygen species (ROS). Interestingly, neutrophils are well known ROS producing cells during immune defensive process and share same surface markers with G-MDSC. These similar features always brought the fundamental questions what’s the difference between G-MDSC and neutrophils but it’s not yet proven clearly. In this study, we examined the gene expression of G-MDSC and neutrophils using Affymetrix microarray G-MDSC (CD11b+Ly6G+Ly6Clow) were purifed from splenocytes in EL4 lymphoma tumor bearing mice by positive selection of Ly6G using microbeads isolation. Neutrophils were purified from ascitic fluids induced after injection of milk protein, casein by negative selection of F4/80 and positive selection of Ly6G using microbeads isolation. Their RNA was extracted and gene expression was analyzed using Affymetrix microarray.

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Expression data from granulocytic MDSC (G-MDSC) and neutrophils

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Exosome from A498 cellular supernatant

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