Ontology highlight
ABSTRACT:
PROVIDER: PRJNA982530 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24909457_1.fastq.gz | Fastqsanger.gz | |||
| SRR24909457_2.fastq.gz | Fastqsanger.gz | |||
| SRR24909458_1.fastq.gz | Fastqsanger.gz | |||
| SRR24909458_2.fastq.gz | Fastqsanger.gz | |||
| SRR24909459_1.fastq.gz | Fastqsanger.gz |
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Project description:Transcriptomic analysis of lungs from newborn rats born to vitamin D adequate and vitamin D deficient mothers Vitamin D deficiency during pregnancy is common and is related to several maternal and fetal morbidities. Past studies suggest that vitamin D plays a role in normal lung development and we have shown that vitamin D regulates lung alveolar and vascular growth and preserves lung structure in experimental bronchopulmonary dysplasia (BPD) through improved pro-angiogeneic signaling. In addition, maternal vitamin D deficiency causes abnormal airway, alveolar, and vascular growth, as well as impaired lung function and airway hyper-reactivity in newborn rats. However, the mechanisms responsible for these physiologic effects are unknown. To gain insight into the role that maternal vitamin D status has on fetal lung development we used an unbiased transcriptomic approach to identify pathways altered in the lungs of offspring from vitamin D deficient dams.
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Project description:Tuberculosis is a global health threat that affects millions of people every year, and treatment-limiting toxicity remains a considerable source of treatment failure. Recent reports have characterized the nature of hPXR-mediated hepatotoxicity and systemic toxicity of antitubercular drugs. The antitubercular drug isoniazid plays a role in such pathologic states as acute intermittent porphyria, anemia, hepatotoxicity, hypercoagulable states (deep vein thrombosis, pulmonary embolism, or ischemic stroke), pellagra (vitamin B3 deficiency), peripheral neuropathy, and vitamin B6 deficiency. However, the mechanisms by which isoniazid administration leads to these states are unclear. To elucidate the mechanism of rifampicin- and isoniazid-induced liver and systemic injury, we performed tandem mass tag mass spectrometry-based proteomic screening of mPxr–/– and hPXR mice treated with combinations of rifampicin and isoniazid. Proteomic profiling analysis suggested that the hPXR liver proteome is affected by antitubercular therapy to disrupt [Fe–S] cluster assembly machinery, [2Fe–2S] cluster-containing proteins, CYP450 enzymes, heme biosynthesis, homocysteine catabolism, oxidative stress responses, vitamin B3 metabolism, and vitamin B6 metabolism. These findings provide insight into the etiology of some of these processes and potential targets for subsequent investigations.
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Project description:Rationale: Growth/differentiation factor 15 (GDF15) is a stress cytokine with numerous proposed roles including stress erythropoiesis. Higher circulating GDF15 levels are prognostic of mortality during acute respiratory distress syndrome, but the sources and downstream effects of GDF15 during pathogen-mediated injury remain unclear. Methods: We quantified GDF15 in plasma and lower respiratory tract (LRT) biospecimens from critically-ill humans with acute respiratory failure. Publicly available data from SARS-CoV-2 infection were re-analyzed. We utilized mouse models of acute lung injury mediated by P. aeruginosa exoproducts in wildtype mice and in mice genetically deficient for Gdf15 and its putative receptor, Gfral.Results: Plasma levels of GDF15 associated with worse outcomes and LRT GDF15 levels in critically-ill humans. Intra-tracheal P. aeruginosa Type 2 secretion system exoproducts (PA SN) were sufficient to induce airspace and plasma release of GDF15 in wildtype mice, which was attenuated during epithelial-specific Gdf15 deficiency. SARS-CoV-2 infection induced GDF15 expression in human lung epithelium. Mice with global Gdf15 deficiency had decreased airspace hemorrhage, an attenuated cytokine profile, and altered lung transcriptional profile during PA SN injury, which was not recapitulated in mice deficient for Gfral. Airspace GDF15 reconstitution did not significantly modulate key lung cytokine levels but did increase circulating erythrocyte counts.Conclusions: Lung epithelium releases GDF15 during pathogen injury, which associates with plasma levels in both humans and mice and can increase erythrocyte counts in mice. Potential local and other extra-pulmonary roles for GDF15 remain undefined.
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Project description:The recently described roles of vitamin C as an epigenetic regulator playsa crucial role in normal physiological development and pathological conditions.However, the epigenetic regulatory role of vitamin C in renal homeostasis andpathogenesis remains largely unknown. We aim to reveal that vitamin C deficiency promoted acute tubular necrosis,and provide a potential mechanism for epigenetic therapy in preventing the progression of chronic kidney disease.
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