The effect of Rapamycin on the transcriptome of old mouse liver
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PROVIDER: PRJNA209711 | ENA |
REPOSITORIES: ENA
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Project description:Analysis of the effect of gene expression in the livers of old mice (25 months of age) fed rapamycin short term (6 months) Rapamycin from 19 months of age.
2014-02-07 | GSE48331 | GEO
Project description:Analysis of the effect of gene expression in the livers of old mice (25 months of age) fed rapamycin chronically (21 months) from 4 months of age.
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Project description:Analysis of the effect of gene expression in the livers of old mice (25 months of age) fed rapamycin short term (6 months) Rapamycin from 19 months of age. Total RNA extracted from livers of 25 month old C57BL6/N male and female mice started on control or 14 ppm rapamycin (Rapa) from 19 months of age on 6 months of treatment. Number of samples total: 42, with 10 samples in Control males, 12 samples in Rapa males, 9 samples in Control Females, and 11 samples in Rapa Females
2014-02-07 | E-GEOD-48331 | biostudies-arrayexpress
Project description:Analysis of the effect of gene expression in the livers of old mice (25 months of age) fed rapamycin chronically (21 months) from 4 months of age. Total RNA extracted from livers of 25 month old C57BL6/J male and female mice started on control or 14 ppm rapamycin (Rapa) from 4 months of age on 21 months of treatment. Number of samples total: 69, with 19 samples in Control males, 13 samples in Rapa males, 16 samples in Control Females, and 21 samples in Rapa Females
2014-02-07 | E-GEOD-48333 | biostudies-arrayexpress
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Project description:Liver from RICTOR knockout mice show normal levels of mTORC1 signaling in response to refeeding. With this experiment we sought to compare the effects of Rictor depletion to the effects of mTORC1 inhibition by rapamycin in liver from mice that were fasted and refed.
2013-09-23 | GSE46582 | GEO
Project description:Liver from RICTOR knockout mice show normal levels of mTORC1 signaling in response to refeeding. With this experiment we sought to compare the effects of Rictor depletion to the effects of mTORC1 inhibition by rapamycin in liver from mice that were fasted and refed. Mice were either fasted for 24hr (n=5), or fasted for 22hr then treated with either 10mg/kg rapamycin suspended in 0.9% NaCl and 2% ethanol at a concentration of 1mg/ml (547mM), or vehicle only. After an additional 2 hr, one group of mice (0 hr time, n=3) was sacrificed, the liver immediately removed, and flash frozen in liquid nitrogen. The remaining mice were given ad libitum access to food and sacrificed after 3hr (n=3), 6hr (n=3), or 12 hr (n=3). Two other nonfasted groups of mice (n=2) were injected with either vehicle or rapamycin and sacrificed after 24hr. Submitter cannot locate the CEL files.
2013-09-23 | E-GEOD-46582 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below.
2014-02-07 | GSE48334 | GEO
Project description:Effect of continuous GH treatment on old rat liver. Male rats, 2-year-old, were treated with vehicle or human GH (0.34 microgram/gram body weight) for 3 weeks. Keywords: response of old rat liver to growth hormone
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Project description:Glycogen storage disease type III (GSDIII) is a rare metabolic disorder due to glycogen debranching enzyme (GDE) deficiency. Reduced GDE activity leads to pathological glycogen accumulation in liver, and in cardiac and skeletal muscles, responsible for impaired hepatic metabolism, heart function impairment, and muscle weakness. To date, there is no curative treatment for GSDIII. The large 4.6 kb coding sequence of GDE represents a major limitation toward the development of clinically relevant AAV gene transfer strategy for GSDIII. We previously reported that liver and heart/muscle correction of the GSDIII phenotype can be achieved in a mouse model of GSDIII by using two distinct overlapping AAV vectors encoding GDE. Here, results of a long-term stability of an approach based on a dual AAV vector encoding for GDE under the control of a recently developed tandem liver-muscle promoter suggests that stable but partial correction of the muscle phenotype can be achieved at very long-term (12 months). In liver, the dual AAV had an only transient efficacy supporting the need for an optimization of the approach. We then assessed the efficacy of rapamycin, an autophagy inducer used in the clinic as an immunosuppressive drug that has shown efficacy in GSDIII. Combination of rapamycin with the dual vector expressing GDE resulted in better correction of glycogen accumulation and muscle strength impairment than AAV vector alone thus supporting a synergic effect of the two treatments. The combined treatment synergic effect was also demonstrated at the molecular level by transcriptomic analysis that indicated a better rescue of the lysosomal pathway in muscle, possibly due to the induction of autophagy by rapamycin and the clearance of glycogen achieved with the combination therapy. In GSDIII mice liver, rapamycin was also able to counteract an unexpected immune reaction to the AAV vector that seems specific of this model. In conclusion, these results indicate that correction of both liver and muscle can be achieved in symptomatic GSDIII mice by an overlapping vector expressing GDE with a tandem promoter when combined with rapamycin treatment. These data also indicate that the effect of rapamycin on AAV gene transfer although disease- and tissue-specific has a net positive impact on dual AAV gene therapy for GSDIII thus opening the way to the clinical translation of this combination approach.
2024-05-17 | GSE232166 | GEO