Gene Profiling Male Fetal Rat Gubernaculum After Insulin-like 3 (Insl3) Exposure
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE19658 | GEO | 2010/07/02
SECONDARY ACCESSION(S): PRJNA122561
REPOSITORIES: GEO
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Project description:Insl3 is a testis-derived hormone that induces growth and differentiation of the fetal gubernaculum. The goal of this study was to identify genes showing altered expression in fetal gubernaculum following Insl3 exposure. The number of biological replicates processed initially were six controls, five 10 nM Insl3, and six 100 nM Insl3. Following data collection, two 10 nM Insl3 samples (biological replicates 4 and 5) were deemed to be outliers based upon Principal Component Analysis and a relatively low yield of biotin-labeled cRNA. The two outlier samples were not included in the statistical analysis.
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Project description:This study aimed to investigate the direct mechanism(s) of action ofMono-(Ethyl-Hexyl) phthalate (MEHP) on the rat fetal testis with particular emphasis to Leydig cell steroidogenesis, by means of an in vitro system based on culture for 3 days of fetal testes from 14.5 days post-coïtum old rats. We first confirmed that an exposure to MEHP led to a dose-dependent decrease of testosterone and demonstrated that dihydrotestosterone (DHT) production was also inhibited. We then demonstrated that in 10µM MEHP-exposed testis basal 17alpha-hydroxy-progesterone (17OHP) production was increased (+40%) while androstenedione levels decreased (-55%). Furthermore, the addition of the latter steroid but none of the other precursors rescued testosterone thus establishing further that MEHP specifically blocked steroidogenesis at the level of the 17,20 lyase activity of the P450c17 enzyme (CYP17), which converts 17OHP to androstenedione. Furthermore and accordingly, both levels of testicular CYP17 protein (western blot) and cyp17a1 gene (qPCR, microarrays) were found to decrease under MEHP exposure. The microarray analysis also showed that among the few other testicular genes cyp17a1 whose expression was inhibited by MEHP were the genes encoding for the Leydig cell insulin-like peptid 3 (INSL3), involved in the control of testicular descent, and for inhibin A (INHA), that regulates follicular-stimulating hormone secretion.Under in vitro conditions where MEHP is not metabolized and remains at low intratesticular concentration, our findings show in particular that this phthalate directly inhibits several important Leydig cell factors involved in testis development and function. Transcription profiling of rat fetal testes explants, vehicle or monoethylhexylphthalate (MEHP)-treated (1uM, 10uM) 3 condition experiment, 1-3 biological replicates per treatment. 2 technical replicates per sample.
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Project description:During male development, the testes move from a high intraabdominal position and descend into the scrotum. The gubernaculum, an inguinoscrotal ligament connecting the testis to the lower abdomen, is believed to play a critical role in this process. The first stage of testicular descent is controlled by INSL3, insulin like3 hormone, produced in testicular Leydig cells. Deletion of Insl3 or its receptor, Rxfp2, in mice causes cryptorchidism. We produced Cre/loxP regulated shRNA transgenic mice targeting RXFP2 expression. We have shown that the transgene was able to reduce Rxfp2 gene expression and thus behaved as a hypomorphic allele of Rxfp2. Variable degrees of uni-and bilateral cryptorchidism was detected in males with the activated shRNA transgene on an Rxfp2+/- background. Conditional suppression of Rxfp2 in the gubernaculum led to cryptorchidism. Gene expression analysis of a mutant cremasteric sac using Illumina microarrays indicated abnormal expression of a significant number of genes in Wnt/β-catenin and Notch pathways. We have demonstrated profound changes in the expression pattern of β-catenin, Notch1, desmin, and androgen receptor (AR) in Rxfp2-/- male embryos, indicating the role of INSL3 in proliferation, differentiation, and survival of specific cellular components of the gubernaculum. We have shown that INSL3/RXFP2 signaling is essential for myogenic differentiation and maintenance of AR-positive cells in the gubernaculum. Males with the deletion of β-catenin or Notch1 in the gubernacular ligament demonstrated abnormal development. Our data indicates that β-catenin and Notch pathways are potential targets of INSL3 signaling during gubernacular development.
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Project description:During male development, the testes move from a high intraabdominal position and descend into the scrotum. The gubernaculum, an inguinoscrotal ligament connecting the testis to the lower abdomen, is believed to play a critical role in this process. The first stage of testicular descent is controlled by INSL3, insulin like3 hormone, produced in testicular Leydig cells. Deletion of Insl3 or its receptor, Rxfp2, in mice causes cryptorchidism. We produced Cre/loxP regulated shRNA transgenic mice targeting RXFP2 expression. We have shown that the transgene was able to reduce Rxfp2 gene expression and thus behaved as a hypomorphic allele of Rxfp2. Variable degrees of uni-and bilateral cryptorchidism was detected in males with the activated shRNA transgene on an Rxfp2+/- background. Conditional suppression of Rxfp2 in the gubernaculum led to cryptorchidism. Gene expression analysis of a mutant cremasteric sac using Illumina microarrays indicated abnormal expression of a significant number of genes in Wnt/β-catenin and Notch pathways. We have demonstrated profound changes in the expression pattern of β-catenin, Notch1, desmin, and androgen receptor (AR) in Rxfp2-/- male embryos, indicating the role of INSL3 in proliferation, differentiation, and survival of specific cellular components of the gubernaculum. We have shown that INSL3/RXFP2 signaling is essential for myogenic differentiation and maintenance of AR-positive cells in the gubernaculum. Males with the deletion of β-catenin or Notch1 in the gubernacular ligament demonstrated abnormal development. Our data indicates that β-catenin and Notch pathways are potential targets of INSL3 signaling during gubernacular development. Total RNA obtained from the cremasteric sac of cryptorchid Tg(shRxfp1) males compared to the wild-type control cremasteric sac.
2010-11-10 | E-GEOD-25222 | biostudies-arrayexpress
Project description:High dose level dibutyl phthalate (DBP) exposure of fetal rat testes in vivo inhibits testosterone production (i.e. endocrine disruption). Here, fetal testis mRNA levels were profiled following exposure to a DBP dose level that did not significantly reduce testosterone levels. The goal was to identify the constellation of gene expression changes that do not correlate with endocrine disruption. Fischer 344 rats were exposed via oral gavage of the dam to vehicle (corn oil) or 50 mg/kg (body weight) DBP daily from gestational day (GD) 12 to 20. The day after mating was defined as gestational day 0. Six hours after the final exposure on GD20, fetal testes were dissected and mRNA levels quantified using Affymetrix Rat Expression 230 2.0 microarrays.
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