Lung in neonatal mice: Control vs. transplacental treated with dimethylarsinic acid (DMA)
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ABSTRACT:
PROVIDER: PRJNA591977 | ENA |
REPOSITORIES: ENA
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Project description:The gene expression profling between Control and transplacental treated with 200 ppm dimethylarsinic acid (DMA) for 10 days in lung of neonatal male mice.
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Project description:ChIP-seq profiling by Histone H3K9me3 antibody between Control and transplacental treated with 200 ppm dimethylarsinic acid (DMA) for 10 days in lung of neonatal male mice.
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Project description:Lung in neonatal mice: Control vs transplacental treated with dimethylarsinic acid (DMA)
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Project description:We revealed that an enhancement of rice growth by 2'-deoxymugineic acid (DMA) application was observed not only under high pH conditions where iron availability for plant uptake was reduced but also under normal pH conditions. This result indicates that DMA application improves not only Fe availability for plants but also plant productivity. To explain a mechanism caused by the DMA application, molecular regulation in rice treated with or without DMA was analyzed using microarray analysis and qRT-PCR. Results provide insight into advantages of DMA application in rice seedlings.
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Project description:We revealed that an enhancement of rice growth by 2'-deoxymugineic acid (DMA) application was observed not only under high pH conditions where iron availability for plant uptake was reduced but also under normal pH conditions. This result indicates that DMA application improves not only Fe availability for plants but also plant productivity. To explain a mechanism caused by the DMA application, molecular regulation in rice treated with or without DMA was analyzed using microarray analysis and qRT-PCR. Results provide insight into advantages of DMA application in rice seedlings. Gene expression patterns induced by DMA and EDTA in root and shoot were analyzed with control experiment (no chelator). One independent experiment was performed at each pH (pH 5.8 or pH 8.0).
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Project description:Transcriptional profiling of the parietal cortex was performed in postnatal day 22 rats with obstructive hydrocephalus. An intracisternal injection of kaolin was done on postnatal day one, and severe hydrocephalus developed over 3 weeks. Hydrocephalic animals were compared to age-matched saline controls. The goal was to determine the effects of kaolin-induced neonatal hydrocephalus on gene expression.
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Project description:Intrahepatic cholestasis of pregnancy (ICP) is estimated to impact between 0.4% and 5% of pregnancies worldwide. This disease is associated with elevated maternal bile acids and frequently untoward neonatal outcomes such as respiratory distress and asphyxia. Multiple candidate genes have been implicated, but none have provided insight into the mechanisms of neonatal respiratory distress and death. Herein our studies demonstrate that maternal cholestasis (due to Abcb11 deficiency) produces 100% neonatal death within 24h due to atelectasis producing pulmonary hypoxia, which recapitulates the respiratory distress and asphyxia of human ICP. We show that these neonates have elevated pulmonary bile acids that are associated with disrupted structure of pulmonary surfactant. Maternal absence of Nr1i2 superimposed upon Abcb11 deficiency strongly increased neonatal survival and is directly related to reduced maternal bile acid concentrations. The mechanism accounting for reduced serum bile acids in the mothers deficient in both Nr1i2 and Abcb11 appears related to disrupted reabsorption of intestinal bile acids due to changes in transporter expression. These findings provide novel insights into pulmonary failure by revealing bile acids capability to disrupt the structure of surfactant producing collapsed alveoli, pulmonary failure and ultimately death. These findings have important implications for neonatal health especially when maternal bile acids are elevated during pregnancy and highlight a potential pathway and targets amenable to therapeutic intervention to ameliorate this condition. We used microarrays to measure changes in gene expression profiles in lung tissues from Abcb11+/- lungs after interbreeding C57BL/6 wild-type female or C57BL/6 Abcb11-/- female mice against either C57BL/6 wild-type male mice or C57BL/6 Abcb11-/- male mice to create only heterozygote offspring. We also measured profiles in liver tissues from age-matched C57BL/6 wild-type and C57BL/6 Abcb11-/- mice. Lung tissues were collected from day E17.5, E18.5 and neonatal (N0) mice. Liver tissues were collected from 1.5-month-old C57BL/6 wildtype and Abcb11-/- mice.
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Project description:Intrahepatic cholestasis of pregnancy (ICP) is estimated to impact between 0.4% and 5% of pregnancies worldwide. This disease is associated with elevated maternal bile acids and frequently untoward neonatal outcomes such as respiratory distress and asphyxia. Multiple candidate genes have been implicated, but none have provided insight into the mechanisms of neonatal respiratory distress and death. Herein our studies demonstrate that maternal cholestasis (due to Abcb11 deficiency) produces 100% neonatal death within 24h due to atelectasis producing pulmonary hypoxia, which recapitulates the respiratory distress and asphyxia of human ICP. We show that these neonates have elevated pulmonary bile acids that are associated with disrupted structure of pulmonary surfactant. Maternal absence of Nr1i2 superimposed upon Abcb11 deficiency strongly increased neonatal survival and is directly related to reduced maternal bile acid concentrations. The mechanism accounting for reduced serum bile acids in the mothers deficient in both Nr1i2 and Abcb11 appears related to disrupted reabsorption of intestinal bile acids due to changes in transporter expression. These findings provide novel insights into pulmonary failure by revealing bile acids capability to disrupt the structure of surfactant producing collapsed alveoli, pulmonary failure and ultimately death. These findings have important implications for neonatal health especially when maternal bile acids are elevated during pregnancy and highlight a potential pathway and targets amenable to therapeutic intervention to ameliorate this condition.
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