Total RNA-seq analysis of mouse liver following LNA treatment in vivo to identify mRNA targets of mmu-miR-802-5p and mmu-miR-1948-5p. Overall design: Male and female 9-wk ICR mice were injected with LNAs complementary to mmu-miR-1948-5p and mmu-miR-802-5p, respectively. Liver RNA was analyzed by RNA-seq 3 days or 6 days after LNA treatment.
Functional Roles of Sex-Biased, Growth Hormone-Regulated MicroRNAs miR-1948 and miR-802 in Young Adult Mouse Liver.
Sex, Age, Specimen part, Cell line, Treatment, Subject
View SamplesRNA-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) - which results in a strong but transient natural killer cell response followed by early tumor growth rebound - 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. Overall design: 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.
Metronomic cyclophosphamide activation of anti-tumor immunity: tumor model, mouse host, and drug schedule dependence of gene responses and their upstream regulators.
No sample metadata fields
View SamplesGene expression in livers of adult male mice subjected to continuous GH infusion using Alzet osmotic minipumps for 1, 4 or 7 days was assayed by RNA-seq, as part of a study of growth hormone regulation of hepatic lincRNAs (PMID:26459762) and protein-coding genes (PMID:28694329). Overall design: RNA isolated from livers obtained from untreated male mice, or from male mice subjected to continuous GH tratment for 1, 4 or 7 days were prepared and used for unstranded RNA-seq.
Feminization of Male Mouse Liver by Persistent Growth Hormone Stimulation: Activation of Sex-Biased Transcriptional Networks and Dynamic Changes in Chromatin States.
No sample metadata fields
View SamplesrRNA-depleted RNA isolated from livers of intact male and female mice and from male mice treated with a continuous infusion of growth hormone for either 10 hr or 1 days was analyzed by RNA-seq Overall design: Liver RNA was isolated from 8 week old male mice treated with a continuous GH infusion (cGH) for either 10 hours or 1 day. Sham pump males served as a control. RNA-seq data are compared to untreated adult females to identify genes that show sex differences in liver expression and also respond to cGH. RNA samples were pooled to make 3 biological replicates per condition comprised of 2-4 individuals each.
Feminization of Male Mouse Liver by Persistent Growth Hormone Stimulation: Activation of Sex-Biased Transcriptional Networks and Dynamic Changes in Chromatin States.
Sex, Age, Cell line, Treatment, Subject
View SamplesGene expression in intact and hypophysectomized adult mouse liver was assayed by RNA-seq analysis of total liver RNA, as part of a study of growth hormone regulation of hepatic lincRNAs. Overall design: Eight independent pools: two intact males, two intact females, two hypophysectomized males and two hypophysectomized females, comprised of total RNA isolated from 3-5 individual livers / pool, were prepared and used for unstranded RNA-seq.
Hepatic Long Intergenic Noncoding RNAs: High Promoter Conservation and Dynamic, Sex-Dependent Transcriptional Regulation by Growth Hormone.
No sample metadata fields
View SamplesWe investigated the effects of a single pulse of growth hormone on the transcriptional activation of STAT5 target genes in hypophysectomized male mouse liver. This GEO series is part of a larger study, where we investigated the impact of a single pulse of GH given to hypophysectomized mice on local liver chromatin accessibility [DNase hypersensitive site analysis], transcription rates [hnRNA analysis], and gene expression [quantitative PCR and RNA-Seq] determined 30, 90 or 240 min later. The STAT5-dependent but sex-independent early GH response genes Igf1 and Cish showed rapid, GH pulse-induced increases in chromatin accessibility and gene transcription, reversing the effects of hypophysectomy. Rapid increases in liver chromatin accessibility and transcriptional activity were also induced in hypophysectomized male mice for some (Ces2b, Ugt2b38) but not for other liver STAT5-dependent male-biased genes (Cyp7b1). Moreover, in pituitary-intact male mice, Igf1, Cish, Ces2b and Ugt2b38 all showed remarkable cycles of chromatin opening and closing, and associated cycles of induced gene transcription, which closely followed each endogenous pulse of liver STAT5 activity. Thus, the endogenous rhythms of male plasma GH pulsation dynamically open and then close liver chromatin at discrete, localized regulatory sites in temporal association with transcriptional activation of Igf1, Cish and a subset of STAT5-dependent male-biased genes. Overall design: Liver RNA was isolated from hypophysectomized male mice that were untreated, or were treated with a single pulse of GH and euthanized 30, 90 or 240 minutes later. 8 Individual RNA samples were pooled to make 2 biological replicates per condition for RNA-seq analysis.
Activation of Male Liver Chromatin Accessibility and STAT5-Dependent Gene Transcription by Plasma Growth Hormone Pulses.
Sex, Age, Specimen part, Cell line, Treatment, Subject
View SamplesWe investigated the effects of a single pulse of growth hormone on the transcriptional activation of STAT5 target genes in hypophysectomized male mouse liver. This GEO series is part of a larger study, where we investigated the impact of a single pulse of GH given to hypophysectomized mice on local liver chromatin accessibility [DNase hypersensitive site analysis], transcription rates [hnRNA analysis], and gene expression [quantitative PCR and RNA-Seq] determined 30, 90 or 240 min later. The STAT5-dependent but sex-independent early GH response genes Igf1 and Cish showed rapid, GH pulse-induced increases in chromatin accessibility and gene transcription, reversing the effects of hypophysectomy. Rapid increases in liver chromatin accessibility and transcriptional activity were also induced in hypophysectomized male mice for some (Ces2b, Ugt2b38) but not for other liver STAT5-dependent male-biased genes (Cyp7b1). Moreover, in pituitary-intact male mice, Igf1, Cish, Ces2b and Ugt2b38 all showed remarkable cycles of chromatin opening and closing, and associated cycles of induced gene transcription, which closely followed each endogenous pulse of liver STAT5 activity. Thus, the endogenous rhythms of male plasma GH pulsation dynamically open and then close liver chromatin at discrete, localized regulatory sites in temporal association with transcriptional activation of Igf1, Cish and a subset of STAT5-dependent male-biased genes. Overall design: Liver RNA was isolated from untreated hypophysectomized male mice and from hypophysectomized male mice treated with a single pulse of GH and euthanized 30, 90 or 240 minutes later. 8 Individual RNA samples were pooled to make 2 biological replicates per condition for RNA-seq analysis.
Activation of Male Liver Chromatin Accessibility and STAT5-Dependent Gene Transcription by Plasma Growth Hormone Pulses.
Sex, Age, Specimen part, Cell line, Treatment, Subject
View SamplesGene expression in adult male mouse liver was assayed by nuclear RNA-seq, as part of a study of hepatic lincRNAs. Overall design: Three independent pools, comprised of nuclear RNA isolated from 4 individual male livers per pool, were prepared and used for RNA-seq.
Hepatic Long Intergenic Noncoding RNAs: High Promoter Conservation and Dynamic, Sex-Dependent Transcriptional Regulation by Growth Hormone.
No sample metadata fields
View SamplesGene expression in adult female mouse liver was assayed by nuclear RNA-seq, as part of a study of hepatic lincRNAs. Overall design: Three independent pools, comprised of nuclear RNA isolated from 4 individual livers per pool, were prepared and used for unstranded RNA-seq.
Hepatic Long Intergenic Noncoding RNAs: High Promoter Conservation and Dynamic, Sex-Dependent Transcriptional Regulation by Growth Hormone.
No sample metadata fields
View SamplesGene expression in adult male and female mouse liver was assayed by RNA-seq, as part of a study on hepatic lincRNAs. Overall design: Total liver RNA was prepared from 12 individual male and 12 individual female mice. Four independent pools, comprised of RNA isolated from 6 individual male or female livers (2 pooled biological replicates for each sex) were then prepared and used for RNA-seq.
Hepatic Long Intergenic Noncoding RNAs: High Promoter Conservation and Dynamic, Sex-Dependent Transcriptional Regulation by Growth Hormone.
No sample metadata fields
View Samples