Pathophysiological role of MIG-6 and ERBB2 in progesterone resistance and endometriosis-related infertility.
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ABSTRACT:
PROVIDER: PRJNA575007 | ENA |
REPOSITORIES: ENA
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Project description:In the present study, we have documented a previously unrecognized membrane vesicles called “migrasomes” (M-mig) that originate from the filament-like nanotubes of macrophage.To characterize the signatures of macrophage migrasomes (M-mig) gene expression that might underlie M-mig-associated biological function. M0-mig, M1-mig, M2-mig and HG-mig genome-wide expression profiling was carried out by using SurePrint G3 Mouse GE V2.0 8X60K Microarrays (Design ID:074809, Agilent Technologies, USA). Total RNA was quantified by the NanoDrop ND-2000 (Thermo Scientific) and the RNA integrity was assessed using Agilent Bioanalyzer 2100 (Agilent Technologies). The sample labeling, microarray hybridization and washing were performed based on the manufacturer’s standard protocols. Briefly, total RNA was transcribed to double strand cDNA, then synthesized into cRNA and labeled with Cyanine-3-CTP. The labeled cRNAs were hybridized onto the microarray. After washing, the arrays were scanned by the Agilent Scanner G2505C (Agilent Technologies). For data analysis, Feature Extraction software (version10.7.1.1, Agilent Technologies) was used to analyze array images to get raw data. Genespring (version14.9, Agilent Technologies) were employed to finish the basic analysis with the raw data. To begin with, the raw data was normalized with the quantile algorithm. Differentially expressed genes were then identified through fold change. The threshold set for up- and down-regulated genes was a fold change>=2.0. Afterwards, GO analysis and KEGG analysis were applied to determine the roles of these differentially expressed mRNAs.
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Project description:The disruption of cholesterol homeostasis leads to an increase in cholesterol levels which results in the development of cardiovascular disease. Mitogen Inducible Gene 6 (Mig-6) is an immediate early response gene that can be induced by various mitogens, stresses, and hormones. To identify the metabolic role of Mig-6 in the liver, we conditionally ablated Mig-6 in the liver using the Albumin-Cre mouse model (Albcre/+Mig-6f/f; Mig-6d/d). Mig-6d/d mice exhibit hepatomegaly and fatty liver. Serum levels of total, LDL, and HDL cholesterol and hepatic lipid were significantly increased in the Mig-6d/d mice. The daily excretion of fecal bile acids was significantly decreased in the Mig-6d/d mice. DNA microarray analysis of mRNA isolated from the livers of these mice showed alterations in genes that regulate lipid metabolism, bile acid, and cholesterol synthesis, while the expression of genes that regulate biliary excretion of bile acid and triglyceride synthesis showed no difference in the Mig-6d/d mice compared to Mig-6f/f controls. These results indicate that Mig-6 plays an important role in cholesterol homeostasis and bile acid synthesis. Mice with liver specific conditional ablation of Mig-6 develop hepatomegaly and increased intrahepatic lipid and provide a novel model system to investigate the genetic and molecular events involved in the regulation of cholesterol homeostasis and bile acid synthesis. Defining the molecular mechanisms by which Mig-6 regulates cholesterol homeostasis will provide new insights into the development of more effective ways for the treatment and prevention of cardiovascular disease.
2011-08-31 | GSE31752 | GEO
Project description:The disruption of cholesterol homeostasis leads to an increase in cholesterol levels which results in the development of cardiovascular disease. Mitogen Inducible Gene 6 (Mig-6) is an immediate early response gene that can be induced by various mitogens, stresses, and hormones. To identify the metabolic role of Mig-6 in the liver, we conditionally ablated Mig-6 in the liver using the Albumin-Cre mouse model (Albcre/+Mig-6f/f; Mig-6d/d). Mig-6d/d mice exhibit hepatomegaly and fatty liver. Serum levels of total, LDL, and HDL cholesterol and hepatic lipid were significantly increased in the Mig-6d/d mice. The daily excretion of fecal bile acids was significantly decreased in the Mig-6d/d mice. DNA microarray analysis of mRNA isolated from the livers of these mice showed alterations in genes that regulate lipid metabolism, bile acid, and cholesterol synthesis, while the expression of genes that regulate biliary excretion of bile acid and triglyceride synthesis showed no difference in the Mig-6d/d mice compared to Mig-6f/f controls. These results indicate that Mig-6 plays an important role in cholesterol homeostasis and bile acid synthesis. Mice with liver specific conditional ablation of Mig-6 develop hepatomegaly and increased intrahepatic lipid and provide a novel model system to investigate the genetic and molecular events involved in the regulation of cholesterol homeostasis and bile acid synthesis. Defining the molecular mechanisms by which Mig-6 regulates cholesterol homeostasis will provide new insights into the development of more effective ways for the treatment and prevention of cardiovascular disease. Eight week old Mig-6f/f vs Mig-6d/d male mice after undergoing a 24 hour fast
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Project description:The objective of the study was to discover new functions of chemokine CXCL9/MIG, a cationic chemokine that has antimicrobial properties. Human monocytic cell line, THP-1 cells were stimulated 4 hours with chemokine MIG or CCL2/MCP-1 (a chemokine that is not positively charged and has no antimicrobial activity). By using a 21,000 oligo-based DNA human microarray we analyzed gene expression profiles induced by MIG and by MCP-1. The gene expression profile induced by MIG was >85% different from that induced by MCP-1. MIG increased transcription of genes encoding various chemokines (including CCL3/MIP-1alpha, CCL4/MIP-1beta, CCL2/MCP-1 and CXCL8/IL-8), cytokines (TNF-alpha), indicating that MIG has an immunomodulatory effect on THP-1 cells. Additionally, MIG strongly up-regulated a set of genes identified as having tumor suppressor functions, including BTG2, BTG1, P21, IGFBP3, DSCR1 and genes encoding markers for mature leukocyte differentiation (PLAU, LPL, PLAUR etc). In parallel, MIG down-regulated the expression of oncogenes (MYC), and genes related to cell proliferation and cell cycle progression. This gene profile strongly suggested that the chemokine MIG had anti-proliferative activity and might induce THP-1 cells to undergo terminal differentiation.
2010-07-01 | E-FPMI-5 | biostudies-arrayexpress