Expression data from skeletal muscle biopsies of healthy adults
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Brian Lam
PROVIDER: E-GEOD-49297 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Cholesterol has attracted significant attention as a possible lifespan regulator. It has been reported that serum cholesterol levels have an impact on mortality due to age-related disorders such as cardiovascular disease. Diet is also known to be an important lifespan regulator. Dietary restriction retards the onset of age-related diseases and extends lifespan in various organisms. Although cholesterol and dietary restriction are known to be lifespan regulators, it remains to be established whether cholesterol is involved in dietary restriction-induced longevity. Here, we show that cholesterol deprivation suppresses longevity induced by intermittent fasting, which is one of the dietary restriction regimens that effectively extend lifespan. We also found that cholesterol is required for the fasting-induced upregulation of transcriptional target genes such as the insulin/IGF-1 pathway effector DAF-16 and that cholesterol deprivation suppresses the long lifespan of the insulin/IGF-1 receptor daf-2 mutant. Remarkably, we found that cholesterol plays an important role in the fasting-induced nuclear accumulation of DAF-16. Moreover, knockdown of the cholesterol-binding protein NSBP-1, which has been shown to bind to DAF-16 in a cholesterol-dependent manner and to regulate DAF-16 activity, suppresses both fasting-induced longevity and DAF-16 nuclear accumulation. Furthermore, this suppression was not additive to the cholesterol deprivation-induced suppression, which suggests that NSBP-1 mediates, at least in part, the action of cholesterol to promote fasting-induced longevity and DAF-16 nuclear accumulation. These findings identify a novel role for cholesterol in the regulation of lifespan. Two independent replicates were performed. Total RNA was extracted with TRIzol (Invitrogen). The extracted RNA was purified with PureLink RNA Micro Kit (Invitrogen) and analyzed with Agilent 2100 Bioanalyzer to assess the RNA integrity. The microarray procedures were performed according to Affymetrix protocols. Hybridized arrays were scanned using an Affymetrix GeneChip Scanner.
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Project description:Treatment with insulin-like growth factor-I (IGF-I) during feed deprivation attenuates the weight loss response in both mammals and fish, therefore the reduction in plasma IGF-I concentrations during fasting likely serves as a signal that contributes to the catabolic response. To better understand the physiological mechanisms responsible for this effect rainbow trout were administered IGF-I during a 2 wk period of feed deprivation and changes in gene expression in white muscle were determined using microarray analysis. Weight loss was reduced by 15% (P<0.05) in IGF-I treated fish. A total of 440 transcripts were identified as differentially regulated (P<0.05) between saline and IGF-I treated fish. Genes related to protein degradation were down-regulated and included protease and peptidase genes and genes involved in ubiquitin-proteasome and cathepsin-mediated proteolytic pathways. IGF-I increased expression of myosin binding protein H and coronin-1C, while decreasing expression of other myofibrillar and cytoskeleton-associated genes like troponin-C and parvalbumin-2. Polyadenylate-binding protein 2, a transcription factor that positively regulates myoD and myogenin expression, was upregulated with IGF-I treatment. Additional genes that were differentially regulated are associated with lipid and carbohydrate metabolism, mitochondrial biogenesis and electron transport, gene transcription, signal transduction and regulation of apoptosis. In summary, these data suggest that IGF-I plays a central role in regulating protein degradation, especially via the ubiquitin-proteasomal pathway, and that reductions in protein degradation and the subsequent effects on other physiological systems are largely responsible for the IGF-I-induced reduction in weight loss. Eight approximately 1-year old full-sibling rainbow trout families were housed in individual tanks, according to family, at the National Center for Cool and Cold Water. Each fish was pit-tagged at 7-months of age. At the beginning of the study, fish were anesthetized with tricaine methanesulfonate (MS-222), weighed, and an osmotic pump was surgically inserted into the peritoneal cavity of each fish (n=4 fish/family/treatment, N=16 fish). The osmotic pump contained either recombinant human IGF-I, which released hormone at 25 ug/kg/day, or saline, which was the vehicle used to resuspend IGF-I. Feed was withheld 2-days prior to surgery and for the experimental 2 week period. Fish were harvested using as overdose of MS-222, weighed, and white muscle samples were removed, frozen in liquid N, and stored at -80 C until analysis. Muscle RNA was isolated from muscle of the two families that exhibited the greatest difference in weight loss between IGF-I and saline treatments; families 64 and 107. Hybridizations were performed using a dye-swap design with an IGF-I and saline treated fish within the same family, therefore a total of 16 slides were hybridized using Alexa 647 and Alexa 555 dyes.
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