Project description:The role of murine peroxisome proliferator-activated receptor-delta (PPARd) in mammary tumorigenesis was assessed. Microarrays were used to analyse global gene expression to determine changes in MMTV-PPARd transgenic mice versus wild-type mice and the effect of GW501516.
Project description:The role of murine peroxisome proliferator-activated receptor-delta (PPARd) in mammary tumorigenesis was assessed. Microarrays were used to analyse global gene expression to determine changes in MMTV-PPARd transgenic mice versus wild-type mice and the effect of GW501516. RNA was isolated (RNeasy Mini Kit, Qiagen) from mammary gland tissue of transgenic and wild-type mice maintained on normal rodent chow or 0.005% GW501516
Project description:The PPAR (Peroxisome proliferator-activated receptor) family of nuclear receptors has three members: PPARg, PPARa and PPARd. Although they share similar structures, their biological functions are distinct. PPARg controls lipid storage and adipogenesis, while PPARd is associated with fat burning. The highly specific synthetic ligand for PPARd, GW501516, is a promising drug candidate for obesity and diabetes. Here we use Affymetrix microarray to analyze gene expression profile in mouse embryo fibroblasts treated with 100 nM GW501516 for 0, 2, 8 and 24 hours. These data may provide new clues into the molecular mechanism by which GW501516 ameliorates obesity and diabetes.
Project description:The role of PDK1 on mammary tumorigenesis and its interaction with PPARdelta, was assessed. Transgenic mice were generated in which PDK1 was expressed in the mammary epithelium. We used microarrays to analyse global gene expression changes in MMTV-PDK1 transgenic mice versus wild-type mice and determine any differential responses to GW501516 treatment. RNA was isolated (RNeasy Mini Kit, Qiagen) from mammary gland tissue from nulliparious transgenic and wild-type mice maintained on normal rodent chow or a diet supplemented with GW501516 for 1 week.
Project description:The PPAR (Peroxisome proliferator-activated receptor) family of nuclear receptors has three members: PPARg, PPARa and PPARd. Although they share similar structures, their biological functions are distinct. PPARg controls lipid storage and adipogenesis, while PPARd is associated with fat burning. The highly specific synthetic ligand for PPARd, GW501516, is a promising drug candidate for obesity and diabetes. Here we use Affymetrix microarray to analyze gene expression profile in mouse embryo fibroblasts treated with 100 nM GW501516 for 0, 2, 8 and 24 hours. These data may provide new clues into the molecular mechanism by which GW501516 ameliorates obesity and diabetes. Wild type mouse embryonic fibroblasts (MEFs) stably infected with retroviruses MSCVpuro expressing PPARd were plated at 0.5 million per 10 cm dish. After overnight incubation, cells were treated with 100nM GW501516 for 0h, 2h, 8h and 48h. Cells were collected at subconfluent condition. Total RNAs were sequentially purified with Trizol (Invitrogen) and RNeasy kit (Qiagen) and analyzed in triplicate on Mouse Genome 430 2.0 Array (Affymetrix) at NIDDK Microarray Core Facility following standard protocols.
Project description:The role of PDK1 on mammary tumorigenesis and its interaction with PPARdelta, was assessed. Transgenic mice were generated in which PDK1 was expressed in the mammary epithelium. We used microarrays to analyse global gene expression changes in MMTV-PDK1 transgenic mice versus wild-type mice and determine any differential responses to GW501516 treatment.
Project description:We collected whole genome testis expression data from hybrid zone mice. We integrated GWAS mapping of testis expression traits and low testis weight to gain insight into the genetic basis of hybrid male sterility.
Project description:Investigation of whole genome gene expression level changes in GW501516 (a Ppard ligand) or Il-4 treated Ppard-overexpressing RAW 264.7 macrophages as compared to vehicle. Alternative activation of adipose tissue resident macrophages inhibits obesity-induced metabolic inflammation. In the current study we profile genes regulated by two M2 inducers, Il-4 or Ppard agonists and find that alternative activation promotes the cell survival program, while inhibiting that of inflammation-related cell death.