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Expression data from bone marrow cultures treated with adiponectin - evidence for lipopolysaccharide contamination

ABSTRACT: The adipocyte-derived hormone adiponectin potently inhibits osteoclast formation in vitro. Gene expression profiling of murine bone marrow cells treated with adiponectin was used to identify candidate genes that mediate the effect of adiponectin to inhibit osteoclastogenesis in these cultures. However, we found that contamination by lipopolysaccharide confounds the study of adiponectin activity. Bone marrow cells were cultured for up to five days and RNA was extratced from cells treated with adiponectin and from untreated controls at different time points.

ORGANISM(S): Mus musculus

SUBMITTER: Dorit Naot

PROVIDER: E-GEOD-35466 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from bone marrow cultures treated with adiponectin - evidence for lipopolysaccharide contamination

Project description:The adipocyte-derived hormone adiponectin potently inhibits osteoclast formation in vitro. Gene expression profiling of murine bone marrow cells treated with adiponectin was used to identify candidate genes that mediate the effect of adiponectin to inhibit osteoclastogenesis in these cultures. However, we found that contamination by lipopolysaccharide confounds the study of adiponectin activity.

2012-02-02 | GSE35466 | GEO

Gene expression analysis in macrophages stimulated 18 h with Adiponectin

Project description:Bone marrow derived macrophages (BMDM) generated from c57bl/6j mice bone marrow cells were stimulated for 18 h with 12 microgram/ml adiponectin, RNA from non-stimulated or 18 h adiponectin-stimulated BMDM subjected to a agilent microarray analysis Three different non-stimulated and 3 different 18 h adiponectin (12 microgram/ml) RNA samples were subjected to a micrrorray analysis

2014-07-03 | E-GEOD-49332 | biostudies-arrayexpress

Gene regulation by full length human adiponectin

Project description:Transcriptionnal profiling of 4 human cell lines treated during 3 hours with human adiponectin Keywords: transcriptionnal analysis Four human cell lines (Hela, HepG2, Panc-1, Hek293) were grown until confluence. These cell lines were serum depleted during 2 hours and then treated with human adiponectin (2,5 µg/ml) during 3 hours. Each adiponectin stimulated cell line was compared to depleted cell line. Depleted cell line was considered as control.

2010-12-09 | E-GEOD-14070 | biostudies-arrayexpress

Uncoupling effects of ERalfa on LKB1/AMPK interaction upon adiponectin exposure in breast cancer

Project description:Adipose tissue is a metabolic and endocrine organ that secretes numerous bioactive molecules called adipocytokines. Among these, adiponectin has been argued to have a crucial role in obesity-associated breast cancer. The key molecule of adiponectin signaling is AMP-activated protein kinase (AMPK), mainly activated by Liver Kinase B1 (LKB1). Here, we demonstrated how the ERalfa/LKB1 interaction may negatively interfere with the capability of LKB1 to phosphorylate AMPK and then inhibit its downstream signaling TSC2/mTOR/p70S6k. In MCF-7 cells upon adiponectin AMPK signaling was not working, keeping its downstream protein Acetyl-CoA Carboxylase (ACC) still active. In contrast, in MDA-MB-231 cells the phosphorylation of AMPK and ACC was enhanced with consequent inhibition of both lipogenesis and cell growth. Thus, upon adiponectin, ERalfa signaling switched the energy balance of breast cancer cells towards a lipogenic phenotype. In other words, adiponectin in all the concentrations tested played an inhibitory role on ERalpha-negative breast cancer cell growth and progression either in vitro or in vivo. In contrast, low adiponectin levels, similar to those circulating in obese patients, worked on ERalfa-positive cells as a growth factor, stimulating their growth and progression. The latter effect seems to be blunted in vivo only in the presence of high adiponectin concentration. Based on the present results, it can be concluded that if we prospectively address adiponectin as a pharmacological tool, a separate therapeutic treatment should be carefully assessed in ERalfa-positive and negative breast-cancer patients.

2020-02-27 | E-MTAB-6120 | biostudies-arrayexpress

Adiponectin regulates expression of hepatic genes critical for glucose and lipid metabolism.

Project description:The effects of adiponectin on hepatic glucose and lipid metabolism at transcriptional level are largely unknown. We profiled hepatic gene expression in adiponectin knockout (KO) and wild-type (WT) mice by RNA-Seq. Comparing to WT mice, adiponectin KO mice exhibited decreased mRNA expression of rate-limiting enzymes in several important glucose and lipid metabolic pathways including glycolysis, TCA cycle, fatty-acid activation and synthesis, triglyceride synthesis and cholesterol synthesis. In addition, binding of the transcription factor Hnf4a to DNAs encoding several key metabolic enzymes was reduced in KO mice, suggesting that adiponectin might regulate hepatic gene expression via Hnf4a. Phenotypically, adiponectin KO mice possessed smaller epididymal fat pads and showed reduced body weights comparing to WT mice. When fed a high fat diet, adiponectin KO mice showed significantly reduced lipid accumulation in the livers. These lipogenic defects are consistent with the downregulation of lipogenic genes in the KO mice. Mice were fasted overnight before euthanization. Liver tissues from WT or adiponectin KO male mice (n = 9-10) at 12 weeks of age were harvested and subjected to total RNA extraction using an RNeasy Plus Mini Kit (Qiagen, Valencia, CA). Total RNA from nine to ten mice of the same strain was pooled together as one biological sample. The mRNA sequencing samples were prepared using the Illumina sample preparation protocol (RS-930-1001, Illumina, Inc. San Diego, CA). The cDNA fragments of 200–250 bp were purified on an agarose gel and then enriched by PCR with Phusion polymerase. The cDNA libraries were sequenced by an Illumina Genome analyzer II at the Whitehead Genome Technology Core.

2012-09-04 | E-GEOD-38144 | biostudies-arrayexpress

Effect of adiponectin deficiency on pulmonary responses to subacute ozone exposure in mice

Project description:Adiponectin is an adipose-derived hormone with anti-inflammatory activity. Following subacute ozone exposure (0.3 ppm for 24-72 h), pulmonary neutrophilic inflammation is augmented in adiponectin deficient mice. The purpose of this study was to use microarrays to examine the impact of adiponectin deficiency on changes in pulmonary gene expression induced by ozone, a common air pollutant. Lungs were harvested from wildtype and mice that were genetically deficient in adiponectin. Mice were exposed either to room air or to ozone (0.3 ppm) for 72 h. RNA was extracted and microarray analysis of gene expression performed. Both male and female mice were used.

2013-08-27 | E-GEOD-50183 | biostudies-arrayexpress

Gene expression analysis in macrophages stimulated 18 h with Adiponectin

2014-07-03 | GSE49332 | GEO

Adipocyte XBP1s regulates systemic insulin sensitivity by modulating adiponectin multimerization

Project description:The physiological role of the spliced form of X-box-binding protein 1 (XBP1s), a key transcription factor of the endoplasmic reticulum (ER) stress response, in adipose tissue remains largely unknown. Here we show that overexpression of XBP1s promotes adiponectin multimerization in adipocytes, thereby regulating systemic glucose homeostasis. Ectopic expression of XBP1s in adipocytes improves glucose tolerance and insulin sensitivity in both lean and obese (ob/ob) mice. The beneficial effect of adipocyte XBP1s on glucose homeostasis is associated with elevated serum levels of HMW adiponectin and indeed, is adiponectin dependent. Mechanistically, XBP1s promotes adiponectin multimerization rather than activating its transcription likely through a direct regulation of the expression of several ER-chaperones involved in adiponectin maturation, including Grp78, Pdia6, ERp44 and DsbA-L. Thus, we conclude that XBP1s is an important regulator of adiponectin multimerization, which may lead to a new therapeutic approach for the treatment of type 2 diabetes and hypoadiponectinemia. Epididymal adipose tissue from wild type and XBP1-overexpressing mice was subjected to gene expression profiling.

2013-11-21 | E-GEOD-36031 | biostudies-arrayexpress

Signaling between mammalian adiponectin and a mosquito adiponectin receptor reduces Plasmodium transmission

Project description:Signaling between mammalian adiponectin and a mosquito adiponectin receptor reduces Plasmodium transmission

| PRJNA817525 | ENA

Endogenous renal adiponectin drives gluconeogenesis through enhancing pyruvate and fatty acid utilization

Project description:Adiponectin is an important secretory protein, primarily produced in adipose tissue. However, low but detectable expression of adiponectin can be observed in cell types beyond adipocytes, particularly in kidney tubular cells, but its local renal role is unknown. We assessed the role of renal adiponectin by utilizing male doxycycline inducible kidney tubular cell-specific adiponectin overexpression or knockout mice. Kidney-specific adiponectin overexpression induces a doubling of phosphoenolpyruvate carboxylase expression and enhanced pyruvate-mediated glucose production, tricarboxylic acid cycle intermediates and an upregulation of fatty acid oxidation (FAO). The inhibition of FAO reduces the adiponectin-induced enhancement of glucose production, highlighting the role of FAO in the induction of renal gluconeogenesis. In contrast, kidney-specific adiponectin deleted mice exhibit enhanced glucose tolerance as well as a lower utilization and greater accumulation of lipid species. In summary, renal adiponectin is a potent inducer of gluconeogenesis by driving enhanced FAO in the kidney and underline the important systemic role of renal gluconeogenesis.

2023-09-20 | GSE242095 | GEO

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