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Microarray analysis of genes regulated by SHP in wild-type and ob/ob mice.

ABSTRACT: Liver gene expression was compared in wild type, SHP knockout, ob/ob, and ob/ob SHP double mutant mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE40775 | GEO | 2012/09/12

SECONDARY ACCESSION(S): PRJNA174860

REPOSITORIES: GEO

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Microarray analysis of genes regulated by SHP in wild-type and ob/ob mice.

Project description:Liver gene expression was compared in wild type, SHP knockout, ob/ob, and ob/ob SHP double mutant mice. A total of eight samples were analyzed using Affymetrix arrays. Each of the four genotypes studied were assayed in duplicate.

2012-09-12 | E-GEOD-40775 | biostudies-arrayexpress

MicroRNA profiling of mouse wild type and SHP knock-out liver

Project description:The microRNA expression profiles between wild type 2-month old mouse liver and small heterodimer partner (SHP) knockout mouse liver was compared using microRNA array.

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Gene expression analysis of FXR null, SHP null, and double FXR/SHP null mice

Project description:Bile acid (BA) homeostasis is maintained through a feedback loop operated by the nuclear hormone receptors FXR and SHP. Here we show that contrary to the current models placing FXR upstream of SHP in a linear regulatory pathway, the phenotypic consequence of the combined loss of both receptors is much more severe than the relatively modest impact of the loss of either Fxr or Shp alone. This is highlighted by the dramatic elevation of hepatic and serum BA levels in the double knockout (DKO) mice as early as three weeks of age coupled with a commensurate increase in Cyp7A1 expression and alterations in BA homeostatic genes. In addition, we find several genes necessary for C21 steroid biosynthetic pathway as novel targets for FXR and SHP. The elevated BAs result in severe hepato-pathology but the DKO mice surprisingly do not develop complete liver failure and live for over a year. Their survival is accompanied by an adaptive proliferation of the resident liver progenitor cell population, known as oval cells. Overall, these data demonstrate that FXR and SHP function coordinately to maintain BA homeostasis, and identify DKO mice as a novel genetic model for juvenile cholestatic disorders and for oval cell activation. Liver samples collected from FXR-/-, SHP-/-, and FXR-/-/SHP-/- animals at 3 or 5 weeks were hybridized to Illumina mouse REF-8 v1.1 arrays in duplicate.

2010-12-10 | E-GEOD-20599 | biostudies-arrayexpress

Gene expression analysis of FXR null, SHP null, and double FXR/SHP null mice

2010-12-10 | GSE20599 | GEO

Genome wide transcriptomics analyses of livers reveal induction of N-glycosylation upon loss of nuclear receptors FXR and SHP

Project description:We performed high-throughput RNA-sequencing on livers from hepatocyte specific Fxr-/- Shp-/- double knockout mice, and identified upregulation of N-glycan protein modification machinery. This correlated positively with Golgi structural defects and alterations in the hepatic secretome. This study identifies a new role for hepatic FXR-SHP axis in Golgi dynamics and N-glycosylation, apart from its traditional function in nutrient metabolism.

2021-03-09 | GSE164447 | GEO

Gene expression in livers of Lepob/ob (ob/ob) mice v.s. wild type C57BL/6J mice

Project description:To identify novel transcriptional factors involved in dysfunctional hepatic lipids homeostasis in obesity, mRNA microarray analysis were performed to of livers of ob/ob mice, a widely used obese model, and C57BL/6J control mice. Chow-fed ob/ob and C57BL/6J mice were housed in a 12 h of light and 12 h of dark cycle and fed ad libitum a regular chow diet. Mice were sacrificed at 16:00 (Zeitgeber Time 8 during light phase). Total RNA was prepared from each liver using TRIzol (Invitrogen). Equal aliquots of total RNA from each of four mouse livers in each group were pooled and used for biotin labeling as described in the Affymetrix technical bulletin. Then the transcriptional profiles of samples were probed using the Gene-Chip Mouse Genome 430 2.0 arrays.

2014-06-29 | E-MTAB-2678 | biostudies-arrayexpress

Mus musculus strain:C57BL/6 wild-type and ob/ob mice

Project description:The identification of glucose-responsive genes in the liver of WT and ob/ob mice.

| PRJDB8330 | ENA

Mus musculus strain:C57BL/6J wild-type and ob/ob mice

Project description:The identification of differentially expressed genes in skeletal muscle of wild-type and ob/ob mice

| PRJDB10695 | ENA

Mus musculus strain:C57BL/6J wild-type and ob/ob mice

Project description:The identification of glucose-responsive genes in the skeletal muscle of WT and ob/ob mice.

| PRJDB13195 | ENA

Feeding activates FGF15-SHP-TFEB-mediated lipophagy in the gut

Project description:Lysosome-mediated macroautophagy, including lipophagy, is activated under nutrient deprivation but is repressed after feeding. We show that feeding unexpectedly activates intestinal lipophagy in a manner dependent on both the orphan nuclear receptor, small heterodimer partner (SHP/NR0B2), and the late fed-state gut hormone, fibroblast growth factor-15/19 (FGF15/19). Postprandial intestinal triglycerides (TGs) and apolipoprotein-B48 (ApoB48), the TG-rich chylomicron marker, were elevated in SHP-knockout and FGF15-knockout mice. Genomic analyses in mouse intestine revealed that SHP partners with the key lysosomal activator, transcription factor-EB (TFEB), upregulating autophagy/lipolysis network genes after feeding. In HT29 intestinal cells, FGF19 treatment activated lipophagy in a manner dependent on both SHP and TFEB, reducing TG and ApoB48 levels. Mechanistically, feeding-induced FGF15/19 signaling increases nuclear localization of TFEB and SHP via PKCβ/ζ-mediated phosphorylation, leading to transcriptional induction of Ulk1 and Atgl. Collectively, these results demonstrate that after feeding, FGF15/19-activated SHP and TFEB paradoxically activate gut lipophagy, limiting postprandial TG levels. As excess lipids cause dyslipidemia and obesity, the FGF15/19-SHP-TFEB axis that reduces intestinal TGs via lipophagic activation provides promising therapeutic targets for obesity-associated metabolic disease.

2022-04-22 | GSE197549 | GEO

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