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Expression data from normal rat and steroid induced necrosis of femoral head rat

ABSTRACT: The steriod-induced necrosis of femoral head(SINFH) is a serious clinical problem and the underlying mechanism of this disease remains unknown. As its etiology and pathogenesis are not clear, there hasn’t been an effective treatment yet. In-depth studies on its pathogenesis will provide important information for the prevention and treatment of this devastated disease. Animal model researches are helpful to a better understanding of its etiology and pathogenesis, to early diagnosis and treatments and provide the basis for clinical treatment It has been proved that the occurrence of SINFH is related to gene itself and its polymorphism. These studies, in which only one or a few genes were investigated, could not provide a comprehensive understanding to the pathogenesis of SINFH. We used microarrays to compare the gene expression profile of SINFH rats with that of normal rats and identified gene expression changes between SINFH rats and normal rats.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE26316 | GEO | 2010/12/28

SECONDARY ACCESSION(S): PRJNA136763

REPOSITORIES: GEO

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Project description:The steriod-induced necrosis of femoral head(SINFH) is a serious clinical problem and the underlying mechanism of this disease remains unknown. As its etiology and pathogenesis are not clear, there hasn’t been an effective treatment yet. In-depth studies on its pathogenesis will provide important information for the prevention and treatment of this devastated disease. Animal model researches are helpful to a better understanding of its etiology and pathogenesis, to early diagnosis and treatments and provide the basis for clinical treatment It has been proved that the occurrence of SINFH is related to gene itself and its polymorphism. These studies, in which only one or a few genes were investigated, could not provide a comprehensive understanding to the pathogenesis of SINFH. We used microarrays to compare the gene expression profile of SINFH rats with that of normal rats and identified gene expression changes between SINFH rats and normal rats. Adult healthy male Wistar rats(body weight 200±10g) were randomly divided into control and experimental groups. All the rats were given injection of E. coli endotoxin at a dose of 20μg/kg body weight into abdominal cavity for two times with a 24 hour interval. 24 hours after the second administration of E. coli endotoxin, methylprednisolone 40mg/kg was administered into the left gluteus muscle of experimental group rats for three times with a 24 hour interval. Rats were then killed 6 weeks after steroid administration. In experiment, immediately after death the left femoral heads were isolated. Femoral heads were used for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain the gene expression profile of SINFH rats and that of normal rats in order to identified gene expression changes between SINFH rats and normal rats by comparing the gene expression profile of SINFH rats with that of normal rats. To that end, we have established the gene expression profiles of normal and SINFH disease of rat femoral head and found out differentially expressed genes.

Project description:Uterine leiomyomata, or fibroids, are benign tumors of the uterine myometrium that significantly affect up to 30% of reproductive-age women. Despite being the primary cause of hysterectomy in the United States, accounting for up to 200,000 procedures annually, the etiology of leiomyoma remains largely unknown. Due to the lack of an effective medicinal therapy for these tumors, this disease continues to have a tremendous negative impact on women’s health. As a basis for understanding leiomyoma pathogenesis and identifying targets for pharmacotherapy, we conducted transcriptional profiling of leiomyoma and unaffected myometrium from humans and Eker rats, the best characterized preclinical model of leiomyoma. A global comparison of mRNA from leiomyoma versus myometrium in human and rat identified a highly significant overlap of dysregulated gene expression in leiomyoma. An unbiased pathway analysis using a method of gene set enrichment based on the Sigpathway algorithm detected the mammalian target of rapamycin (mTOR) pathway as one of the most highly upregulated pathways in both human and rat tumors. Activation of this pathway was confirmed in both human and rat leiomyomata at the protein level via Western. Inhibition of mTOR in female Eker rats with the rapamycin analog WAY-129327 for 2 weeks decreased mTOR signaling and cell proliferation in tumors, and treatment for 4 months significantly decreased tumor incidence, multiplicity and size. These results identify dysregulated mTOR signaling as a component of leiomyoma etiology across species and directly demonstrate the dependence of these tumors on mTOR signaling for growth in the Eker rat. Modulation of this pathway warrants additional investigation as a potential therapy for uterine leiomyoma. Experiment Overall Design: We analyzed 1-3 leiomyoma or normal myometrium biopsies from each 23 woman undergoing hysterectomy for the treatment of uterine fibroids. tment and compared it leiomyoma and normal myometrium from the Eker rat model of uterine fibroids (N=14-15)

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Expression data from normal rat and steroid induced necrosis of femoral head rat

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