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Inflammatory markers in ABCG1-/- lungs

ABSTRACT: Transcriptional profiling of cytokines and its receptors in lungs from 8 month old chow-fed wild-type and ABCG1-/- mice Keywords: genotype comparison; inflammatory mediators

ORGANISM(S): Mus musculus

PROVIDER: GSE8976 | GEO | 2008/07/30

SECONDARY ACCESSION(S): PRJNA102433

REPOSITORIES: GEO

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Inflammatory markers in ABCG1-/- lungs

Project description:Transcriptional profiling of cytokines and its receptors in lungs from 8 month old chow-fed wild-type and ABCG1-/- mice Keywords: genotype comparison; inflammatory mediators 4 individual mice per group; RNA from inferior left lobe; WT vs. ABCG1-/-

2010-05-25 | E-GEOD-8976 | biostudies-arrayexpress

Adrenal Abcg1 controls cholesterol flux and steroidogenesis

Project description:Cholesterol is the precursor of all steroids, but how cholesterol flux is controlled in steroidogenic tissues is poorly understood. The cholesterol exporter ABCG1 is an essential component of the reverse cholesterol pathway and its systemic inactivation results in neutral lipid redistribution to macrophages. However, the function of ABCG1 in steroidogenic organs is not explored. To model this question, we inactivated the ortholog Abcg1 gene in the mouse adrenal cortex. Abcg1 disruption led to an adrenal-specific increase in transcripts involved in cholesterol uptake and de novo synthesis, and to an 80% increase in corticosterone production. Importantly, this phenotype was not recapitulated by inactivation of the cholesterol exporter Abca1. The absence of any change in lipid profile suggested that adrenal Abcg1 is not involved in cholesterol export to a clinically relevant extent.

2023-09-05 | GSE242081 | GEO

Effects of deletioin of cholesterol efflux genes Abca1 and Abcg1 on other gene expressions in macrophages

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Mus musculus

Project description:Inflammatory markers in ABCG1-/- lungs

| PRJNA102433 | ENA

Adrenal Abcg1 controls cholesterol flux and steroidogenesis

Project description:Adrenal Abcg1 controls cholesterol flux and steroidogenesis

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Single cell RNA sequencing of myeloid cells from lungs of young and aged mice

Project description:Single cell RNA sequencing from lungs of young (2-3 month old) and aged (20-22 month old) mice.

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Oxaliplatin resistance is enhanced by saracatinib via upregulation of ABCG1 and Wnt/β-catenin signaling in hepatocellular carcinoma

Project description:Background:Oxaliplatin-resistant hepatocellular carcinoma (HCC) is associated with increased insulin-like growth factor 1 (IGF1) paracrine signaling, and the IGF1 receptor can be downregulated by inhibition of Src kinases. Therefore, we sought to determine whether Src inhibition and oxaliplatin treatment exerted synergistic effects on HCC cell lines. Methods: The antitumor effects of combined treatment with saracatinib and oxaliplatin on proliferation were evaluated in HCC cells as well as in saracatinib- and oxaliplatin-resistant HCC cell lines using cell viability assays, plate colony formation assays, and cell cycle distribution detection. RNA sequencing was used to explore the resistance mechanism, and the effects on ABCG1 and Wnt signaling in oxaliplatin resistance were confirmed. Results: Chemotherapy with oxaliplatin and saracatinib individually induced strong anti-HCC effects, while combined or sequential treatment of HCC cells with these two drugs exhibited reduced efficacy compared to treatment with the single drugs. Furthermore, treatment with saracatinib caused oxaliplatin resistance. RNA sequencing revealed 458 genes that were altered by treatment with saracatinib and oxaliplatin. Of these, the gene encoding the ATP-binding cassette transporter G1 ABCG1 and Wnt-associated genes were significantly upregulated. Upregulation of ABCG1 and oxaliplatin resistance were associated with activation of Wnt signaling. Interference with ABCG1 expression or inhibition of Wnt signaling resulted in reversal of the saracatinib-induced oxaliplatin resistance in the HCC cell lines. Conclusions: These studies demonstrated that combined or sequential chemotherapy with oxaliplatin and saracatinib reduced antitumor efficacy, and this antagonism was attributed to the upregulation of ABCG1 and activation of Wnt signaling pathway by saracatinib.

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Project description:HIV Tg rats exhibit pulmonary hypertension and pulmonary artery remodeling. In an effort to begin to understand cell signaling pathways which are altered in lungs from HIV transgenic rats, we used microarray analysis. n=3 samples of lung tissue from 3 month old male HIV transgenic rat and n=3 samples of lung tissue from 3 month oldmale F344 (control) rat

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PCR array of inflammatory cytokines and receptors in mouse lungs with NF-kappaB RelA mutant in alveolar epithelial cells during LPS stimulation

Project description:A murine model of RelA mutated throughout the alveolar epithelium was generated. Mice were anesthetized and intratracheally instilled with 50M-NM-<g LPS into the left lung lobe. Mice were euthanized after 6 hours after instillation, and left lung lobes were collected to isolate RNA. We used SABioscience Mouse Inflammatory Cytokines and Receptors PCR Array to evaluate whether the expressions of lung cytokines and receptors during LPS stimulation are dependent on alveolar epithelial NF-M-NM-:B RelA or not. qPCR gene expression profiling. RNA were collected from six different mouse lungs in each genotype (wild-type and alveolar epithelial RelA mutant). Equal amount of RNA (200ng) was pooled from six different mouse lungs, and 1M-NM-<g of total RNA (1.2M-NM-<g) was used to the PCR array.

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