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MRNA Expression Data from Murine Hearts of Transgenic Clock delta 19/delta 19 mice (Clock mice) and Wild type (WT) mice Fed a High-Fat (HFD) or Standard Chow (SC) Diet for 24 weeks

ABSTRACT: mRNA Expression Data from Murine Hearts of Transgenic Clock delta 19/delta 19 mice (Clock mice) and Wild type (WT) mice Fed a High-Fat (HFD) or Standard Chow (SC) Diet for 24 weeks

PROVIDER: PRJNA433250 | ENA |

REPOSITORIES: ENA

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mRNA Expression Data from Murine Hearts of Clock delta 19/delta 19 Mice over 24 hours in normal light-dark environment (12:12)

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mRNA Expression Data from Murine Hearts of Transgenic Clock delta 19/delta 19 mice (Clock mice) and Wild type (WT) mice Fed a High-Fat (HFD) or Standard Chow (SC) Diet for 24 weeks

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mRNA Expression Data from Murine Hearts of Clock delta 19/delta 19 Mice over 24 hours in normal light-dark environment (12:12)

Project description:mRNA Expression Data from Murine Hearts of Clock delta 19/delta 19 Mice over 24 hours in normal light-dark environment (12:12)

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miRNA Expression data from murine hearts of transgenic Clock delta 19/delta 19 mice (Clock mice) and wild type (WT) mice at 4 and 21 months of age

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The miRNAs expression in liver of Clock∆19 mutant mouse

Project description:Circadian clock controls the physiological functions of a lot of tissues including liver by an autoregulatory transcription-translational feedback loop, of which CLOCK is a core positive component. And, many studies have indicated that microRNAs (miRNAs) regulate liver function. However, little is known about the molecular interpretation of how CLOCK-regulated miRNAs are link to liver function. To better understand this, we performed the expression profiles of miRNAs in the liver of Clock△19 mutant mice to obtain the putative CLOCK-regulated miRNAs. A total of 61 miRNAs were differentially expressed (FCA≥2) in the liver of Clock mutant mice at zeitgeber time 2 (ZT2) and 57 miRNAs at zeitgeber time 14 (ZT14) as compared with control mice. Then, we analyzed the pathways of differentially expressed miRNAs to evaluate the roles of these miRNAs. According to the pathway analysis, the circadian rhythms and circadian entrainment pathway were found, and the target genes of differentially expressed miRNAs were mainly involved in pathways in cancer, PI3K-Akt signaling pathway and MAPK signaling pathway. The protein-protein interaction (PPI) analysis indicated that the hub genes were mostly associated with the pathway in cancer and circadian rhythms. Moreover, we verified the expression level of five miRNAs across the circadian cycle. Although the expression levels of miR-195 and miR-340 were up-regulated, the rhythms of these two miRNAs were always remained. The results identify a number of miRNAs that may be regulated by CLOCK, and these miRNAs play a role in the various physiological processes of the liver, which will provide a reference to better understanding the potential regulatory mechanisms in the liver.

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Hepatic transcriptome by Next Generation Sequencing of WT and clock mutant mice fed a HFD ad libitum or time-restricted feeding.

Project description:Increased susceptibility of circadian clock mutant mice to metabolic diseases has led to the understanding that a molecular circadian clock is necessary for metabolic homeostasis. Circadian clock produces a daily rhythm in activity-rest and an associated rhythm in feeding-fasting. Feeding-fasting driven programs and cell autonomous circadian oscillator act synergistically in the liver to orchestrate daily rhythm in metabolism. However, an imposed feeding-fasting rhythm, as in time-restricted feeding, can drive some rhythm in liver gene expression in clock mutant mice. We tested if TRF alone, in the absence of a circadian clock in the liver or in the whole animal can prevent obesity and metabolic syndrome. Mice lacking the clock component Bmal1 in the liver, Rev-erb alpha/beta in the liver or cry1-/-;cry2-/- (CDKO) mice rapidly gain weight and show genotype specific increased susceptibility to dyslipidemia, hypercholesterolemia and glucose intolerance under ad lib fed condition. However, when the mice were fed the same diet under time-restricted feeding regimen that imposed 10 h feeding during the night, they were protected from weight gain and other metabolic diseases. Transcriptome and metabolome analyses of the liver from there mutant mice showed TRF reduces de novo lipogenesis, increased beta-oxidation independent of a circadian clock. TRF also enhanced cellular defense to metabolic stress. These results suggest a major function of the circadian clock in metabolic homeostasis is to sustain a daily rhythm in feeding and fasting. The feeding-fasting cycle orchestrates a balance between nutrient stress and cellular response to maintain homeostasis.

2018-08-30 | GSE102072 | GEO

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