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PROVIDER: PRJDB20139 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The transitional Gene Expression Profiling of Ovarian Follicle Treated with Indomethacin and RU486 in Rats
2015-07-31 | E-GEOD-54584 | ExpressionAtlas
Project description:It is well-known that indomethacin (the cyclooxygenase 1 & 2 inhibitor) and RU486 (or mifepristone, the progesterone receptor antagonist) block follicular rupture in rats. To characterize genetic alterations in unruptured follicles, gene expression profiles in ovarian follicle were analyzed in indomethacin- and RU486-treated female Sprague-Dawley rats. Ovaries are collected at 22:00 on the proestrus day and 10:00 on the following estrus day after a single dose of indomethacin and RU486. Histopathologically, changes depicting responses to LH surge were observed in ovaries, uteri and vagina. Total RNA was extracted from pre-ovulatory follicles or unruptured follicles collected by laser microdissection and analyzed by GeneChip. Among genes showing statistically significant changes compared to control groups, following changes were considered relevant to induction of unruptured follicles. In indomethacin-treated rats, Wnt4 was down-regulated, suggesting effect on tissue integrity and steroid genesis. In RU486-treated rats, Adamts1, Adamts9, Edn2, Ednra, Lyve1, Plat, and Pparg were down-regulated. These changes suggest effects on proteolysis for extracellular matrix or surrounding tissue (Adamts1 & 9, and Plat), constriction of smooth muscle surrounding follicles (Edn2, Ednra, and Pparg), follicular fluid (Lyve1), and angiogenesis (Pparg). Down-regulation of angiogenesis related genes (Angpt2, Hmox1, and Vegfa) was observed in both treatment groups. Here, we clarify genetic alterations induced by the inhibition of cyclooxygenase or progesterone receptor.
2014-02-01 | GSE54584 | GEO
Project description:Altered Gene Expression Profile in Ovarian Follicle in Rats Treated with Indomethacin and RU486
| PRJNA237063 | ENA
Project description:Indomethacin (an inhibitor of prostaglandin synthesis) and RU486 (mifepristone, progesterone receptor antagonist) are well known compounds which impair follicle rupture in rats, nevertheless the histopahotlogical figures of these follicle were different in detail due to the difference of the pathway which each compound inhibits. To characterize these unruptured follicles further and to investigate the genes which were altered in each rat treated with indomethacin or mifepristone, gene expression profile in ovarian follicle were analyzed in female sprague-Dawley rats. Peri- or post ovulatory follicles were collected by laser microdissection and extracted RNA was analyzed by genechip after single dosage of mifepristone or indomethacin. Animals were singly administered orally Indomethacin (IM) at 4mg/kg at 16:00 or RU486 (RU) at 100 mg/kg at 10:00 on the proestrus day, and sacrificed by exsanguination under anesthesia at 22:00 on the proestrus day (PeF: peri-ovulatory follicle), and 10:00 on the estrus day (PoF: post-ovulatory follicle). Ovaries were also collected from untreated rats at 22:00 on the proestrus day, and 10:00 on the estrus day as control groups. Three animals were contained per each treatment group at each timing. The ovaries were removed and embedded in OCT (Tissue-Tek, Sakura Finetek, Torrance, CA), frozen in dry-ice-cold isopentan, and stored at -70 C until used. Frozen sections (8 micro meter thick) were mounted on the membrane slides (MMI, Glatteburg, Zurich, Switzerland), and stained with HistogeneTM LCM frozen section staining kit (Arcturus Engineering, Mountain View, CA). Then, 15 follicles in each phase were retrieved by Laser Micro Dissection system (LMD, CellCut Plus, MMI). The collected follicle sections were lysed by the buffer RLT in the collection tube supplied in RNeasy Micro Kit (Qiagen, Hilden, Germany), and total RNA was extracted according to manufacturer's instructions.
2014-02-01 | E-GEOD-54584 | biostudies-arrayexpress
Project description:The Transitional Gene Expression Profiling in Ovarian Follicle during the Process of Ovulation in Normal cycling Rats (CBX137)
| PRJDB20104 | ENA
Project description:Transcription profiling by array of methamphetamine (METH)-treated rats with high or low behavioural responses against saline-treated controls
2015-11-02 | E-MEXP-948 | ExpressionAtlas
Project description:Epidemiological studies have shown that the regular use of non-steroidal anti-inflammatory (NSAIDs) drugs is associated with a reduced risk of various cancers. In addition, in vitro and experiments in mouse models have demonstrated that NSAIDs decrease tumor initiation and/or progression of several cancers. However, there are limited preclinical studies investigating the effects of NSAIDs in ovarian cancer. Here, we have studied the effects of two NSAIDs, diclofenac and indomethacin, in ovarian cancer cell lines and in a xenograft mouse model. Diclofenac and indomethacin treatment decreased cell growth by inducing cell cycle arrest and apoptosis. In addition, diclofenac and indomethacin reduced tumor volume in a xenograft model of ovarian cancer. To identify possible molecular pathways mediating the effects of NSAID treatment in ovarian cancer, we performed microarray analysis of ovarian cancer cells treated with indomethacin or diclofenac. Interestingly, several of the genes found downregulated following diclofenac or indomethacin treatment are transcriptional target genes of E2F1. E2F1 was downregulated at the mRNA and protein level upon treatment with diclofenac and indomethacin, and overexpression of E2F1 rescued cells from the growth inhibitory effects of diclofenac and indomethacin. In conclusion, NSAIDs diclofenac and indomethacin exert an anti-proliferative effect in ovarian cancer in vitro and in vivo and the effects of NSAIDs may be mediated, in part, by downregulation of E2F1.
2014-06-20 | GSE45052 | GEO
Project description:Epidemiological studies have shown that the regular use of non-steroidal anti-inflammatory (NSAIDs) drugs is associated with a reduced risk of various cancers. In addition, in vitro and experiments in mouse models have demonstrated that NSAIDs decrease tumor initiation and/or progression of several cancers. However, there are limited preclinical studies investigating the effects of NSAIDs in ovarian cancer. Here, we have studied the effects of two NSAIDs, diclofenac and indomethacin, in ovarian cancer cell lines and in a xenograft mouse model. Diclofenac and indomethacin treatment decreased cell growth by inducing cell cycle arrest and apoptosis. In addition, diclofenac and indomethacin reduced tumor volume in a xenograft model of ovarian cancer. To identify possible molecular pathways mediating the effects of NSAID treatment in ovarian cancer, we performed microarray analysis of ovarian cancer cells treated with indomethacin or diclofenac. Interestingly, several of the genes found downregulated following diclofenac or indomethacin treatment are transcriptional target genes of E2F1. E2F1 was downregulated at the mRNA and protein level upon treatment with diclofenac and indomethacin, and overexpression of E2F1 rescued cells from the growth inhibitory effects of diclofenac and indomethacin. In conclusion, NSAIDs diclofenac and indomethacin exert an anti-proliferative effect in ovarian cancer in vitro and in vivo and the effects of NSAIDs may be mediated, in part, by downregulation of E2F1. The serous ovarian adenocarcinoma cell lines HEY, OVCAR5 and UCI-101 were grown in culture then seeded in 60 mm dishes and treated for 24 hours with 300 mM diclofenac, indomethacin or no treatment (Control). RNA was isolated and one sample from each group was labeled and hybridized to Illumina Sentrix bead arrays.
2014-06-20 | E-GEOD-45052 | biostudies-arrayexpress
Project description:Gene expression in hepatocytes and bile ducts from ANIT-treated rats
2015-09-15 | E-GEOD-20498 | ExpressionAtlas
Project description:Transcription profiling by array of skin wound samples from rats treated with the 5alpha-reductase inhibitor MK-434
2015-10-22 | E-MEXP-1232 | ExpressionAtlas