The miRNAs expression in liver of Clock∆19 mutant mouse
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ABSTRACT:
PROVIDER: PRJNA588779 | ENA |
REPOSITORIES: ENA
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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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Project description:Circadian clocks drive 24-h rhythms of physiology and behavior. The circadian clock of hepatocytes has been shown to regulate glucose metabolism, and we were interested if rescuing liver clock function can reverse metabolic impairments in hyperphagic/obese Clock-D19 mutant mice. We compared transcripomte regulation in livers (at Zeitgeber time ZT10) of wild-type (C57BL/6J) and Clock-D19 mice and Clock-D19 mice with genetic rescue of liver clock function using hydrodynamic tail vein injection of a WT-CLOCK expression plasmid
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Project description:The oscillation status of the circadian clock during late gestation is not clear. To gain a better understanding on the oscillation state of the clock and possible influences by maternal cues, we performed transcriptome analyses on the fetal liver tissue during late gestation. Fetal liver transcriptome data were analyzed and compared to adult mouse data in the public database: GSE11923 and GSE13093 (only samples GSM327130 to GSM327141). Re-analyzed (gc-RMA) data from GSE11923 and GSE13093 linked below as supplementary files. Fetal mouse liver tissues were collected at four hours intervals across embryonic day 18 and day 19. Groups 1 and 2.
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Project description:Molecular analysis of circadian rhythm in mice. Liver tissue of wildtype, Clock mutant and Cry deficient C57BL/6 8- to 10-week-old male mice examined. Keywords = circadian rhythm Keywords: other
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Project description:The mammalian circadian clock system is made up of individual cell and tissue clocks that function as a coherent network, however it remains unclear which rhythmic functions of the liver clock are autonomous or rely on clocks in other tissues. Here, using mice which only have a functioning liver clock, we investigate the autonomous vs non-autonomous reatures of the liver clock and diurnal rhythmicity in the liver
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Project description:Molecular analysis of circadian rhythm in mice. Liver tissue of wildtype, Clock mutant and Cry deficient C57BL/6 8- to 10-week-old male mice examined.
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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.
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Project description:A functional interaction between peroxisome proliferator-activated receptor alpha (PPARalpha) and components of the circadian clock has been suggested; however, it remains to be clarified whether those transcriptional factors interact with each other to regulate the expression of their target genes. In this study, we used a ligand of PPARalpha, bezafibrate, to search the PPARalpha-regulated genes that express in a CLOCK-dependent circadian manner. Microarrays analyses using hepatic RNA isolated from bezafibrate treated-wild type, Clock mutant (Clk/Clk), and PPARalpha-null mice revealed that 136 genes are transcriptionally regulated by PPARalpha in a CLOCK-dependent manner.
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