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Proteomic analysis of human microglia cells (HMC3) stimulated with anti-inflammatory cytokines using serum-deprived culture conditions

ABSTRACT: The immune functions of microglia in the brain are compromised in the presence of tumors that have the ability to “hijack” their pro-inflammatory nature by sending out signals that promote cancer progression. To analyze the tumor-supportive microglia phenotype, human microglia cells (HMC3) were treated with anti-inflammatory cytokines in serum-deprived cell culture media, and analyzed by LC-MS/MS using an Orbitrap QE instrument.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Brain, Cell Culture, Macrophage

DISEASE(S): Brain Cancer

SUBMITTER: Iulia M. Lazar

LAB HEAD: Iulia Lazar

PROVIDER: PXD023163 | Pride | 2021-10-07

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	HMC3_G1C1_1.msf	Msf
	HMC3_G1C1_1.raw	Raw
	HMC3_G1C1_2.msf	Msf
	HMC3_G1C1_2.raw	Raw
	HMC3_G1C1_3.msf	Msf

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Publications

Systems-Level Proteomics Evaluation of Microglia Response to Tumor-Supportive Anti-Inflammatory Cytokines.

Ahuja Shreya S Lazar Iulia M IM

Frontiers in immunology 20210909

<h4>Background</h4>Microglia safeguard the CNS against injuries and pathogens, and in the presence of certain harmful stimuli are capable of inducing a disease-dependent inflammatory response. When exposed to anti-inflammatory cytokines, however, these cells possess the ability to switch from an inflammatory to an immunosuppressive phenotype. Cancer cells exploit this property to evade the immune system, and elicit an anti-inflammatory microenvironment that facilitates tumor attachment and growt ...[more]

PMID: 34566949

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Proteomic analysis of human microglia cells (HMC3) stimulated with anti-inflammatory cytokines using serum-enriched culture conditions

Project description:The immune functions of microglia in the brain are compromised in the presence of tumors that have the ability to “hijack” their pro-inflammatory nature by sending out signals that promote cancer progression. To analyze the tumor-supportive microglia phenotype, human microglia cells (HMC3) were treated with anti-inflammatory cytokines in serum-enriched cell culture media, and analyzed by LC-MS/MS using an Orbitrap QE instrument.

2021-10-06 | PXD023166 | Pride

DNA microarray analysis of the anti-inflammatory effects of PDTC on IL-6 signaling in HepG2 cells

Project description:Interleukin-6 (IL-6) is a proinflammatory cytokine that exerts a wide range of cellular, physiological and pathophysiological responses. Pyrrolidine dithiocarbamate (PDTC) antagonizes the cellular responsiveness to IL-6 through impairment in STAT3 activation and downstream signaling. Here, a transcriptional profiling was conducted as a basis for understanding the biological properties of PDTC in human HepG2 hepatocarcinoma cells. A global comparison of mRNA identified a highly significant difference of dysregulated gene expression transduced by PDTC versus IL-6 in HepG2 cells. Through an unbiased pathway analysis method, we have uncovered the mammalian target of rapamycin (mTOR) pathway together with rapid and dynamic alterations in REDD1 (regulated in development and DNA damage response 1) expression as one of the underlying molecular mechanisms responsible for IL-6 resistance to PDTC. Quantitative PCR and Western blot analyses validated the microarray data by showing the reciprocal pattern of REDD1 expression and subsequent mTOR inhibition after stimulation with PDTC relative to IL-6. The HepG2 human hepatocarcinoma cell line (American Type Culture Collection) was routinely grown and maintained in Minimum Eagle's medium (MEM)/F12 (1:1) supplemented with 10% heat-inactivated fetal bovine serum, 50 units/ml penicillin and 50 ug/ml streptomycin under standard cell culture conditions at 37Â°C and 5% CO2 in a humid environment. Cells were seeded in 35- or 60-mm dishes and grown to ~90% confluence after which they were serum starved for 4 h followed by the addition of either vehicle, PDTC (50 ÂµM) or human recombinant IL-6 (20 ng/ml) for 2 replicates, labeled a and b, of the 5 time points: 0hr, 1hr, 2hr, 4hr and 8hr.

2012-01-05 | E-GEOD-14632 | biostudies-arrayexpress

SKBR3/HER2+ Breast Cancer Cellular Response to Brain Cell-Secreted Factors

Project description:To address the challenges associated with the investigation of brain-metastasized cancers and provide insights into the drivers of cancer cell behavior at the brain metastatic site, this study was aimed at exploring the response of SKBR3/HER2+ cells to neural factors secreted by brain cells that come first in contact with the metastasized cancer cells, i.e., human endothelial cells (HBEC5i), astrocytes (NHA), and microglia (HMC3). To this end, serum-starved breast cancer cells were exposed to the combined secretome of brain cells, allowed to grow for 24h, and analyzed by LC-MS/MS using an Orbitrap QE instrument to generate and compare the whole cell proteome profiles of treated vs non-treated cells.

2024-08-27 | PXD046330 | Pride

Proteomic breast cancer data set for exploring somatic mutations

Project description:MCF7, SKBR3 (breast cancer) and MCF10 (non-tumorigenic) cell extracts were explored by LC-MS/MS for the identification of protein-level mutations.

2019-07-25 | PXD014458 | Pride

Network analysis identifies proinflammatory plasma cell polarization for secretion of ISG15 in human autoimmunity

Project description:Plasma cells (PCs) as effectors of humoral immunity produce immunoglobulins to match pathogenic insult. However, emerging data suggests more diverse roles for PCs as regulators of immune and inflammatory responses via secretion of factors other than immunoglobulins. The extent to which such responses are pre-programmed in B-lineage cells or can be induced in PCs by the microenvironment is unknown. Here we dissect the impact of IFNs on the regulatory networks of human plasma cells. We show that core PC programs are unaffected, while PCs respond to IFNs with distinctive transcriptional responses. The ISG15-system emerges as a major transcriptional output induced in a sustained fashion by IFN-Î± in PCs and linked both to intracellular conjugation and ISG15 secretion. This leads to the identification of ISG15-secreting plasmablasts/PCs in patients with active SLE. Thus ISG15-secreting PCs represent a distinct pro-inflammatory PC subset providing an immunoglobulin-independent mechanism of PC action in human autoimmunity B-cells were isolated from the peripheral blood of three adult donors and differentiated in vitro (see individual samples for culture conditions)

2016-07-22 | E-GEOD-75007 | biostudies-arrayexpress

m6A modification profile in primary microglia with/without Igf2bp1 knockdown

Project description:Our study demonstrated that the expression of Igf2bp1 in activated microglia was significantly up-regulated, implying a role of Igf2bp1 in LPS-induced m6A modifications in microglia. To understand the roles of Igf2bp1 on LPS-induced m6A modification in microglia, we performed Igf2bp1 loss-of-function (LOF) approach. Microglia stimulated by LPS were transfected with either scrambled siRNA control or Igf2bp1 siRNA for 48 hours. To m6A modification profiles in control and Igf2bp1 LOF microglia were determined by MeRIP-seq analysis.

2022-12-31 | E-MTAB-11411 | biostudies-arrayexpress

Nucleosome Repositioning: Nicotine- and Cocaine-induced Changes

Project description:SH-SY5Y, neuroblastoma cells, were exposed to nicotine for 10, 60, and 90 minutes or cocaine for 5, 20, 40, and 60 minutes. Drugs of abuse modify behavior by altering gene expression in the brain. Gene expression can be regulated by changes in DNA methylation as well as by histone modifications, which alter chromatin structure, DNA compaction and DNA accessibility. In order to better understand the molecular mechanisms directing drug-induced changes in chromatin structure, we examined DNA-nucleosome interactions within promoter regions of 858 genes in human neuroblastoma cells (SH-SY5Y) exposed to nicotine or cocaine. Widespread, drug- and time-resolved repositioning of nucleosomes was identified at the transcription start site and promoter region of multiple genes. Nicotine and cocaine produced unique and shared changes in terms of the numbers and types of genes affected, as well as repositioning of nucleosomes at sites which could increase or decrease the probability of gene expression based on DNA accessibility. Half of the drug-induced nucleosome positions approximated a theoretical model of nucleosome occupancy based on physical and chemical characteristics of the DNA sequence, whereas the basal or drug-naive positions were generally DNA sequence independent. Thus we suggest that nucleosome repositioning represents an initial dynamic genome-wide alteration of the transcriptional landscape preceding more selective downstream transcriptional reprogramming, which ultimately characterizes the cell- and tissue-specific responses to drugs of abuse. SH-SY5Y, neuroblastoma cells, were exposed to nicotine for 10, 60, and 90 minutes or cocaine for 5, 20, 40, and 60 minutes. Two independently grown biological replicates for each time point and condition, and two controls were processed.

2015-08-07 | E-GEOD-71795 | biostudies-arrayexpress

Transcription profiling time series of hematopoietic progenitor cells treated with TNFalpha as they differentiate to dendritic cells

Project description:Dendritic Cell differentiation - Transcription Regulator cluster follow-up: The data files associated to this experiment show gene expression levels for a subset of 481 transcripts (out of 12626 genes represented on Affymetrix Genechip HG_U95Av2) corresponding to Transcription Regulators whose expression is changed during the differentiation process of Dendritic Cells as assessed in the 9 conditions tested. Another subset of genes, corresponding to a cluster of CD molecules is available from E-MEXP-1 experiment.

2011-08-15 | E-MEXP-2 | biostudies-arrayexpress

Transcription profiling of dendritic cells under 9 conditions

Project description:Dendritic Cell differentiation - CD molecule cluster follow up: The data files associated to this experiment show the gene expression levels for a subset of 152 transcripts (out of 12626 genes represented on Affymetrix Genechip HG_U95Av2) representing CD molecules specifically expressed in Dendritic Cells (DC) as assessed by the 9 conditions tested. Another subset of genes, corresponding to a cluster of Transcription regulators is available from E-MEXP-2 experiment.

2014-06-23 | E-MEXP-1 | biostudies-arrayexpress

ERG activity is regulated by endothelial FAK coupling with TRIM25/USP9x in vascular patterning

Project description:Precise vascular patterning is critical for normal growth and development. The ERG transcription factor drives Delta like ligand 4 (DLL4)/Notch signalling and is thought to act as pivotal regulators of endothelial cell (EC) dynamics and developmental angiogenesis. However, molecular regulation of ERG activity remains obscure. Using a series of EC specific Focal Adhesion Kinase (FAK)-knockout (KO) and point-mutant FAK-knockin mice, we show that loss of ECFAK, its kinase activity or phosphorylation at FAK-Y397, but not FAK-Y861, reduces ERG and DLL4 expression levels together with concomitant aberrations in vascular patterning. Rapid Immunoprecipitation Mass Spectrometry of Endogenous Proteins identified that endothelial nuclear-FAK interacts with the de-ubiquitinase USP9x and the ubiquitin ligase TRIM25 enzymes. Further in silico analysis corroborates that ERG interacts with USP9x and TRIM25. Moreover, ERG levels are reduced in FAKKO ECs via a ubiquitin-mediated post-translational modification programme involving USP9x and TRIM25. Re-expression of ERG in vivo and in vitro rescues the aberrant vessel sprouting defects observed in the absence of ECFAK. Our findings identify ECFAK as a regulator of retinal vascular patterning by controlling ERG protein degradation via TRIM25/USP9x.

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