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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Genome-wide analysis of M1 and M2 polarized macrophages with CNI-1493 treatment

ABSTRACT: Analysis of the effects of CNI-1493 treatment on M1 and M2 polarized macrophages. The purpose of this microarray is to identify genes that may be differentially expressed in M1 or M2 macrophages after treatment with CNI-1493. CNI-1493 is a known inhibitor of M1 macrophages but details of its molecular mechanism are unknown. The effect of CNI-1493 on M2 macrophages has yet to be explored, but we hypothesize that CNI-1493 treatment will attenuate pro-tumor properties of M2 macrophages. We demonstrate with this array that known macrophage markers are unchanged after treatment with CNI-1493, indicating that CNI-1493 does not change the macrophage phenotype on a transcriptional level. Additionally, no candidate genes to suggest how CNI-1493 may attenuate the pro-tumor effects of M2 macrophages are readily identifiable. Total RNA extracted from M1 or M2 macrophages after polarization with GM-CSF (25ng/ml) or M-CSF (25ng/ml) for 7 days, followed by addition of IFN-γ (20ng/ml) and LPS (100ng/ml) or IL-4 (40ng/ml) for 18 hours, respectively, from CD14+ human PBMCs, and treated with CNI-1493 (200nM)

ORGANISM(S): Homo sapiens

SUBMITTER: Anthony Hesketh

PROVIDER: E-GEOD-66805 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide analysis of M1 and M2 polarized macrophages with CNI-1493 treatment

Project description:Analysis of the effects of CNI-1493 treatment on M1 and M2 polarized macrophages. The purpose of this microarray is to identify genes that may be differentially expressed in M1 or M2 macrophages after treatment with CNI-1493. CNI-1493 is a known inhibitor of M1 macrophages but details of its molecular mechanism are unknown. The effect of CNI-1493 on M2 macrophages has yet to be explored, but we hypothesize that CNI-1493 treatment will attenuate pro-tumor properties of M2 macrophages. We demonstrate with this array that known macrophage markers are unchanged after treatment with CNI-1493, indicating that CNI-1493 does not change the macrophage phenotype on a transcriptional level. Additionally, no candidate genes to suggest how CNI-1493 may attenuate the pro-tumor effects of M2 macrophages are readily identifiable.

2015-03-12 | GSE66805 | GEO

Homo sapiens

Project description:Genome-wide analysis of M1 and M2 polarized macrophages with CNI-1493 treatment

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Expression data from M(LPS+IFNγ) and M(IL4)

Project description:Human monocyte THP-1 cells obtained from ATCC were cultured in RPMI 1640 (Invitrogen, Carlsbad, CA) containing 10% FBS and supplemented with 10 mM Hepes (Gibco BRL). THP-1 was differentiated into macrophages by 24-h incubation with 160 nM phorbol 12-myristate 13-acetate (PMA; Sigma, St. Louis, MO) followed by 24-h incubation in RPMI medium. Macrophages were further polarized to M1 macrophages by incubation with 10 pg/ml of lipopolysaccharide (LPS; Sigma) and 20 ng/ml of interferon (IFN)-γ (R&D Systems, MN) and are referred to as M(LPS+IFN-γ) cells. M2 macrophages were obtained by incubation with 20 ng/ml of interleukin (IL)-4 (R&D Systems) and are referred to as M(IL4) cells. To test the represented polarization marker of PMA differentiated-THP-1 macrophages stimulated with 20 ng ml(-1) IFNγ + 10 pg ml(-1) LPS and 20 ng ml(-1) IL-4, which are known to influence macrophage polarization in vetro into the M1 and M2 state, respectively. We used microarrays to detail the gene expression pools to identify distinct M1 and M2 state during this process.

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