Effects of ursolic acid and tomatidine on skeletal muscle mRNA expression in aged mice.
ABSTRACT: For additional details see Ebert et al, Identification and Small Molecule Inhibition of an ATF4-dependent Pathway to Age-related Skeletal Muscle Weakness and Atrophy. Weight-matched cohorts of 22-month-old male C57BL/6 mice were provided ad libitum access to standard chow (control) or standard chow supplemented with 0.27% ursolic acid (UA) or 0.05% tomatidine (TM) for 2 months. After the 2 month treatment period, quadriceps femoris muscles were harvested. mRNA levels in muscles harvested from ursolic acid or tomatidine fed mice were normalized to levels in muscles fed control diet.
Project description:For additional details see Ebert et al, Identification and Small Molecule Inhibition of an ATF4-dependent Pathway to Age-related Skeletal Muscle Weakness and Atrophy. Quadriceps femoris muscles were harvested from 22-month-old muscle-specfic ATF4 knockout (ATF4 mKO) mice and littermate controls. mRNA levels in ATF4 mKO muscles were normalized to levels in littermate control muscles.
Project description:PGC1b transgenic mice were generated to selectively over-express PGC1b in skeletal muscles using human skeletal alpha-actin gene promoter. The gene expression profiles were collected from Tibialis anterior (TA) muscles of wild type (WT) and PGC1b transgenic (TG) mice. Tibialis anterior muscles from three month old WT and PGC1b transgenic male mice.
Project description:Neurofibromatosis type 1 (NF1) is a multi-system disease caused by mutations in the NF1 gene encoding a Ras-GAP protein, neurofibromin, which negatively regulates Ras signalling. Besides neuroectodermal malformations and tumours, the skeletal system is often affected (e.g. scoliosis and long bone dysplasia), demonstrating the importance of neurofibromin for development and maintenance of the musculoskeletal system. Here we focus on the role of neurofibromin in skeletal muscle development. Nf1 gene inactivation in the early limb bud mesenchyme using Prx1-cre (Nf1Prx1) resulted in muscle dystrophy characterised by fibrosis, reduced number of muscle fibres, and reduced muscle force. To gain insight into the molecular changes of the observed muscle dystrophy and fibrosis and to compare these with other known muscle dystrophies, we performed transcriptional profiling of the entire triceps muscles of threemonth-old wild type (wt) and mutant animals using Affymetrix high-density microrrays. We analyzed triceps muscles from 4 three-month-old wt controls and 4 three-month-old Nf1Prx1 mice using the Affymetrix Mouse Gene 1.0 ST platform. Array data was processed by the Affymetrix Exon Array Computational Tool. RNA isolated from each animal was hybridized to a separate microarray.
Project description:Bile acids are not only physiological detergents facilitating nutrient absorption, but also signaling molecules regulating metabolic homeostasis. We reported recently that transgenic expression of CYP7A1 in mice stimulated bile acid synthesis and prevented Western diet-induced obesity, insulin resistance and hepatic steatosis. The aim of this experiment is to determine the impact of induction of hepatic bile acid synthesis on liver metabolism by determining hepatic gene expression profile in CYP7A1 transgenic mice. CYP7A1 transgenic mice and wild type control mice were fed either standard chow diet or high fat high cholesterol Western diet for 4 month. Hepatic gene expressions were measured by microarray analysis. Our results indicate that hepatic bile acid synthesis is closely linked to cholesterogenesis and lipogenesis, and maintaining bile acid homeostasis is improtant in hepatic metabolic homeostasis. Male aged matched (~ 12-14 weeks) CYP7A1 transgenic mice and their wild type control littermates were fed a standard chow diet or a high fat (42%) high cholesterol (0.2%) diet (Harlan Teklad #88137) for 4 month Four groups (4 mice/group) are included in the experiments: Group 1: WT _ Chow Group 2: CYP7A1-tg + chow Group 3: WT + Western diet Group 4: CYP7A1-tg _ Western diet Total liver mRNA was isolated with a RNeasy kit (Qiagen) and used for microarray analysis.
Project description:Transcriptional profiling of cytokines and its receptors in lungs from 8 month old chow-fed wild-type and ABCG1-/- mice Keywords: genotype comparison; inflammatory mediators 4 individual mice per group; RNA from inferior left lobe; WT vs. ABCG1-/-
Project description:Muscle denervation causes skeletal muscle atrophy. The goal of these studies was to determine the effects of denervation on skeletal muscle mRNA levels in C57BL/6 mice. For additional details see Ebert et al, Stress-Induced Skeletal Muscle Gadd45a Expression Reprograms Myonuclei and Causes Muscle Atrophy. JBC epub. June 12, 2012. Left sciatic nerves of C57BL/6 mice were transected. Seven days later bilateral tibialis anterior muscles were harvested. mRNA levels in denervated muscles were normalized to levels in contralateral innervated muscles.
Project description:ATF4 is a fasting-induced trascription factor that promotes skeletal muscle atrophy. The goal of these studies was to determine how of loss of ATF4 affects skeletal muscle mRNA expression. For additional details see Ebert et al, Stress-Induced Skeletal Muscle Gadd45a Expression Reprograms Myonuclei and Causes Muscle Atrophy. JBC epub. June 12, 2012. Muscle-specfic ATF4 knockout (ATF4 mKO) mice and littermate controls were fasted for 24 hours and then tibialis anterior muscles were harvested. mRNA levels in ATF4 mKO muscles were normalized to levels in littermate control muscles.
Project description:Mice were fed for 6 months with a normal chow (NC) or a high fat diet (HFD). After 6 months of diet, high fat fed mice with Low, Medium and High body weight, but with similar glucose intolerance, were selected. These selected mice as well as NC mice were then treated with Rimonabant or Vehicle for 1 month. After treatment, mice were sacrificed and visceral and subcutaneous adipose tissues were collected and immediately frozen in liquid nitrogen. Total RNA from each sample was further extracted, purified, quality-controled before and after amplification, Cy5-labeled and co-hybridized with a Cy3-labeled mouse Universal Reference total RNA on the mouse 17K microarray. Keywords: diet response, pharmacological response Each individual RNA sample was hybridized with a mouse Universal Reference Total RNA
Project description:Gadd45a is a stress-induced protein that causes skeletal muscle atrophy. The goal of these studies was to determine the effects of Gadd45a overexpression on mRNA levels in mouse skeletal muscle. For additional details see Ebert et al, Stress-Induced Skeletal Muscle Gadd45a Expression Reprograms Myonuclei and Causes Muscle Atrophy. JBC epub. June 12, 2012. Tibialis anterior (TA) muscles from muscle-specfic ATF4 knockout mice (ATF4 mKO) were transfected with either 20 mg empty plasmid (pcDNA3) (left TA) or 20 mg pCMV-FLAG-Gadd45a (right TA) and harvested 7 days later. mRNA levels in Gadd45a-transfected muscles were normalized to levels in control transfected muscles.
Project description:We identified that the adiponectin gene expression in rainbow trout muscle decreased by restrected feeding. In order to identify the genes differently expressed by the same treatment, micrarray analysis was conducted Fish were fed ad libitum once a week (RF, restricted feed group) or fed ad libitum twice per day (control). After 1 month, the muscle was desected from 4 individuals from each group.