Project description:[Original title] In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces disruption of the prostate glands and fibrosis in rhesus monkeys. We investigated the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure on the prostate in rhesus monkey offspring. Dams received 0, 30 or 300 ng/kg TCDD subcutaneously on Day 20 of gestation, and then 5% of the initial dose was injected every 30 days until Day 90 after delivery. The offspring were maintained until reaching sexual maturity, and examined histopathologically. Dose-dependent decreases in the prostate glands and widespread fibrosis were observed in offspring. It is noteworthy that 7 years from the final lactational TCDD exposure, inflammatory cell infiltration and disruption of the prostate glands were also observed. Differential mRNA expression associated with fibrosis, inflammatory response and disruption of cell components were demonstrated by microarray analysis, and up-regulation of TGM4, TGFB1, COL1A1 and MMP2 was confirmed with Real-time PCR. In conclusion, in utero and lactational exposure to TCDD induced dose-proportional prostatic fibrosis, indicating prostatic dysfunction and inducible semen quality reduction in second-generation rhesus monkeys.
Project description:[Original title] In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces disruption of the prostate glands and fibrosis in rhesus monkeys. We investigated the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure on the prostate in rhesus monkey offspring. Dams received 0, 30 or 300 ng/kg TCDD subcutaneously on Day 20 of gestation, and then 5% of the initial dose was injected every 30 days until Day 90 after delivery. The offspring were maintained until reaching sexual maturity, and examined histopathologically. Dose-dependent decreases in the prostate glands and widespread fibrosis were observed in offspring. It is noteworthy that 7 years from the final lactational TCDD exposure, inflammatory cell infiltration and disruption of the prostate glands were also observed. Differential mRNA expression associated with fibrosis, inflammatory response and disruption of cell components were demonstrated by microarray analysis, and up-regulation of TGM4, TGFB1, COL1A1 and MMP2 was confirmed with Real-time PCR. In conclusion, in utero and lactational exposure to TCDD induced dose-proportional prostatic fibrosis, indicating prostatic dysfunction and inducible semen quality reduction in second-generation rhesus monkeys. Dam received 0, 30 or 300 ng/kg TCDD subcutaneously on Day 20 of gestation, and then 5% of the initial dose was injected every 30 days until Day 90 after delivery. The offspring were maintained until reaching sexual maturity, and the prostates from 3 offspring in each group were evalutated by histopathological examination, microarray analysis and Real-time quantitative PCR. Supplementary file: Fold_change comparison results of 'control group vs 30 ng/kg group' and 'control group vs 300 ng/kg group'.
Project description:Splenic tissue was isolated from four adult male Indian-origin Rhesus monkeys serologically positive for non-pathogenic SHIV 89.6 and from matched uninfected four adult male Indian-origin Rhesus monkeys respectively. The corresponding RNA was processed by cDNA microarray analysis. Keywords: SIV infection
Project description:Splenic tissue was isolated from four adult male Indian-origin Rhesus monkeys serologically positive for non-pathogenic SHIV 89.6 and from matched uninfected four adult male Indian-origin Rhesus monkeys respectively. The corresponding RNA was processed by cDNA microarray analysis. Sample RNA extracted from the tissue samples. Reference RNA was prepared from a pool of Rhesus monkeys' RNA. Microarray hybridization was carried out by labeling Reference RNA as Cy3 and sample RNA as Cy5. The sample was incubated at 55C for 16hr.