RNA-seq of livers from female mice treated for eight weeks with the glucagon analogue, NNC9204-0043, compared to female mice treated with PBS (control group)
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Illumina NovaSeq 6000
ORGANISM(S): Mus musculus
SUBMITTER: Christian Johansen
PROVIDER: E-MTAB-12040 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Chronic glucagon receptor inhibition with a glucagon receptor antibody decreases amino acid catabolism and ureagenesis, while increasing plasma triglyceride concentrations, plasma very-low density lipoprotein cholesterol concentrations, and liver triglyceride concentrations. To dissect the molecular mechanism underlying these effects, RNA sequencing of liver biopsies from female mice treated for eight weeks with the glucagon receptor antibody, REGN1193, or a control antibody, REGN1945, were performed.
2022-10-09 | E-MTAB-12048 | biostudies-arrayexpress
Project description:Chronic glucagon receptor activation induced by a long-acting glucagon analogue causes thickening of the parietal layer of Bowman’s capsule, causes mesangial area expansion, and formation of albuminuria. To dissect the molecular mechanism underlying these effects, RNA sequencing of kidney biopsies from female mice treated for eight weeks with either the long-acting glucagon analogue, NNC9204-0043, or PBS were performed
2023-12-01 | E-MTAB-12520 | biostudies-arrayexpress
Project description:Chronic glucagon receptor inhibition induced by a glucagon receptor antibody causes decrease in mesangial cell area and increases kidney weight. To dissect the molecular mechanism underlying these effects, RNA sequencing of kidney biopsies from female mice treated for eight weeks with the glucagon receptor antibody, REGN1193, or a control antibody, REGN1945, were performed.
2023-12-01 | E-MTAB-12518 | biostudies-arrayexpress
Project description:RNA-seq analysis was performed using RNA isolated from three tumor models (GL261 glioma, LLC Lewis lung carcinoma, B16F10 melanoma) implanted subcutaneousy in C57BL/6 mice, or in ICR scid mice. Mice were untreated or were treated with cyclophosphamide (CPA) given on a 6-day repeating metronomic schedule (CPA/6d), except as noted. Results from these global transcriptome analysis indicated substantial elevation of basal GL261 immune infiltration and strong activation by CPA/6d treatment of GL261 immune stimulatory pathways and their upstream regulators, but without preferential depletion of negative immune regulators compared to LLC and B16F10 tumors. In LLC tumors, where CPA/6d treatment was found to be anti-angiogenic, CPA/6d suppressed VEGFA target genes and down regulated cell adhesion and leukocyte transendothelial migration genes. In GL261 tumors implanted in adaptive immune-deficient scid mice, where CPA/6d-induced GL261 regression is incomplete and late tumor growth rebound can occur, T cell receptor signaling and certain cytokine-cytokine receptor responses seen in B6 mice were deficient. Extending the CPA treatment interval from 6 to 9 days (CPA/9d) â which results in a strong but transient natural killer cell response followed by early tumor growth rebound â induced fewer cytokines and increased expression of drug metabolism genes. Taken together, these findings elucidate molecular response pathways activated by intermittent metronomic CPA treatment and identify deficiencies that characterize immune-unresponsive tumor models and drug schedules. RNA isolated from various tumor cell lines implanted s.c in C57BL/6 mice or scid mice, untreated or treated with cyclophosphamide (CPA) given on a metronomic schedule, were prepared and used for stranded or unstranded RNA-seq.
2016-08-01 | E-GEOD-71491 | biostudies-arrayexpress
Project description:Autophagy is an evolutionally conserved catabolic process that recycles nutrients upon starvation and maintains cellular energy homeostasis1-3. Its acute regulation by nutrient sensing signaling pathways is well described, but its longer-term transcriptional regulation is not. The nuclear receptors PPARα and FXR are activated in the fasted or fed liver, respectively4,5. Here we show that both regulate hepatic autophagy. Pharmacologic activation of PPARα reverses the normal suppression of autophagy in the fed state, inducing autophagic lipid degradation, or lipophagy. This response is lost in PPARα knockout (PPARα-/-) mice, which are partially defective in the induction of autophagy by fasting. Pharmacologic activation of the bile acid receptor FXR strongly suppresses the induction of autophagy in the fasting state, and this response is absent in FXR knockout (FXR-/-) mice, which show a partial defect in suppression of hepatic autophagy in the fed state. PPARα and FXR compete for binding to shared sites in autophagic gene promoters, with opposite transcriptional outputs. These results reveal complementary, interlocking mechanisms for regulation of autophagy by nutrient status. Mouse liver PPARα cistromes in fed 8-week-old male WT or PPARα KO mice treated with or without its synthetic agonist ligand GW7647twice a day were generated by deep sequencing in quadruplicate using illumina
2014-09-27 | E-GEOD-61817 | biostudies-arrayexpress
Project description:Farnesoid X receptor (FXR) is a ligand activated nuclear receptor belonging to the nuclear receptor superfamily. Bile acids (BAs) are the endogenous ligand for FXR. FXR is a master regulator of BA homestasis, including BA synthesis, metabolism, transport, and enterohepatic circulation of BAs. Besides, FXR is involved in regulating diverse physioligical function in both humans and mice. GW4064 is a synthetic FXR agonist which selectively activates FXR and induce the transcription of FXR target genes. In this study, we treated wild type C57BL/6J mice with GW4064 at 100mg per kg body weight or vehicle control. Mice were treated three times, first dose at 8 am, second dose at 6 pm, third dose at 8 am the second day. Mice were sacrificed 2 hours after the last dose, and liver tissues were harvested for analysis. Animal protocols and procedures were approved by the Institutional Animal Care and Use Committee (IACUC) at the University of Kansas Medical Center. Total RNA from livers was prepared with TRIzol Reagent (Invitrogen, CA), and the whole transcription expression levels were determined using Mouse Gene 1.0 ST Array system manufactured by Affymetrix, Inc..
2014-07-24 | E-GEOD-57305 | biostudies-arrayexpress
Project description:Androgens are required for prostate development, growth and physiology, by activating the androgen receptor (AR) upon activation by testosterone and dihydrotestosterone (DHT), the AR undergoes conformational changes, dimerizes and translocates to the cell nucleus regulation important genes releted to cell survival. Understanding the mechanisms of androgen regulation in the prostate gland is important, because the prostate is affected by several different diseases, in particular prostate cancer (PCa). Several ways exist to treat prostate cancer and promote epithelial cell death. Treatments involving androgen manipulation include surgical castration (bilateral orchiectomy), antiandrogens (usually AR antagonists), or substances that inhibit androgen synthesis (5 alpha-reductase inhibitors, gonadotrophin-releasing hormone blockers). 17 beta-estradiol exerts anti-androgen effects by blocking the hypothalamic production of gonadotropin-releasing hormone and thereby inhibiting the production of testosterone by the testes , but also acts locally via interactions with either of the estrogen receptors found in the gland. It is known that the kinetics of apoptosis are different in the rat ventral prostate (VP) of castrated rats (Cas group) and in rats subjected to 17 beta-estradiol high dose (group E2) or their combination (group Cas+E2), with an evident additive effect in the latter situation (Garcia-Florez et al, 2005). The microarray approach was done to figure out what genes are expressed and how the cells of ventral prostate gland responses when the androgen is not available comparing three diferent androgen deprivation methods (sirurgical castration, high dose of 17-beta estradiol and both treatment combined). Forty-eight 21-day-old male Wistar rats were obtained from the Multidisciplinary Center for Biological Research (CEMIB), University of Campinas. The animals were kept under normal light conditions (12-h light:dark cycle) and received filtered tap water and Purina rodent chow ad libitum. On the 90th day after birth, the rats were divided in four groups (n=3) and assigned to different treatment groups. To cause androgen deprivation, we utilized three different procedures with different effects on epithelial cell apoptosis. Animals in the first group were castrated (Cas) by orchiectomy via scrotal incision under ketamine (150 mg/Kg body weight) and xylazin (10 mg/kg body weight) anesthesia. Animals in the second group received a 25 mg/Kg body weight dose of 17β-estradiol diluted in corn oil (E2 group). The third group received a combination of both treatments (Cas+E2 group) (combined orchiectomy and 17β-estradiol). In the control group (Ct; normal androgen and estrogen), the animals received only the vehicle. Three days after the treatments, the rats were killed by anesthetic overdose, and the ventral prostate was dissected out for the microarray and immunohistochemistry analyses.
2015-03-28 | E-GEOD-56289 | biostudies-arrayexpress
Project description:We report that the phytoestrogen genistein acts as a tissue-specific androgen receptor modulator in mouse using a novel androgen reporter mouse line and gene expression profiling. Genistein is a partial androgen agonist/antagonist in prostate, brain, and testis but not in skeletal muscle or lung. Gene expression profiling has been done from prostates of intact and castrated male mice treated with genistein or vehicle. Gene expression profiling was also done from prostates of estradiol-treated intact male mice. Gene expression profiling from prostates of castrated and intact male mice after 5-day genistein- or vehicle-treatment or after 4-day estradiol- or vehicle-treatment.
2011-08-18 | E-GEOD-31341 | biostudies-arrayexpress
Project description:We have demonstrated that water-soluble zinc ionophores can be administered to mice at relatively high doses and inhibit the growth of A549 lung cancer cells grown in xenograft models. Gene expression profiles of tumor specimens harvested from mice four hours after treatment confirmed that the activation of stress responsive genes occurs in vivo. These findings lead us to propose that the pharmacologic delivery of zinc to tumors using water solubilized ionophores is a potential approach to cancer therapy. Experiment Overall Design: 1.25 million A549 cells were injected subcutaneously/intramuscularly into the right hind flank of 6 week old CD-1 nude mice that had been irradiated with 4 Gy of total body irradiation from a 137Cs radiation source one day prior to tumor implantation. When the average size of tumors reached approximately 100 mm3, mice were randomized by tumor size to treatment groups, typically containing 6-8 mice per group. Tumor and body weight measurements were performed three times per week. Tumor volume was calculated using the equation V (mm3) = a x b2/2, where a is the largest diameter and b is the smallest diameter. No significant body weight loss was observed. To perform gene expression profiling, mice were treated intravenously with one dose (100 μmol/kg) PCI-5002, PCI-5003, or control vehicle (4 mice per group) when the average A549 tumor size reached 500 mm3. After four hours, tumors were harvested and snap frozen immediately on dry ice. Tumor tissue was homogenized, and total RNA was isolated and subjected to analysis using Human Genome U133 Plus 2.0 Arrays as described above.
2008-06-15 | E-GEOD-6962 | biostudies-arrayexpress
Project description:We investigated whether transcription-coupled repair deficient mice (Cockayne syndrome B knockout mice (Csb-/-)), known to be sensitive to oxidative stressors, have a different response to ozone than its repair-proficient control, Csb heterozygote (Csb+/-) mice.
2006-11-13 | E-TABM-137 | biostudies-arrayexpress