Plant damage promotes the interaction of lipoxygenases (LOX) with fatty acids yielding 9-hydroperoxides, 13-hydroperoxides and complex arrays of oxylipins. The action of 13-LOX on linolenic acid enables production of 12-oxo-phytodienoic acid (12-OPDA) and its downstream products, termed jasmonates. As signals, jasmonates have related yet distinct roles in the regulation of plant resistance against insect and pathogen attack. A similar pathway involving 9-LOX activity on linolenic and linoleic acid leads to the 12-OPDA positional isomer, 10-oxo-11-phytodienoic acid (10-OPDA) and 10-oxo-11-phytoenoic acid (10-OPEA), respectively; however, physiological roles for 9-LOX cyclopentenones have remained unclear. In developing maize (Zea mays) leaves, southern leaf blight (Cochliobolus heterostrophus) infection results in dying necrotic tissue and the localized accumulation of 10-OPEA, 10-OPDA and a series of related 14- and 12-carbon metabolites, collectively termed death acids. 10-OPEA accumulation becomes wound-inducible within fungal-infected tissues and at physiologically relevant concentrations acts as a phytoalexin by suppressing the growth of fungi and herbivores including Aspergillus flavus, Fusarium verticillioides, and Helicoverpa zea. Unlike previously established maize phytoalexins, 10-OPEA and 10-OPDA display significant phytotoxicity. Both 12-OPDA and 10-OPEA promote the transcription of defense genes encoding glutathione S-transferases, cytochrome P450s, and pathogenesis-related proteins. In contrast, 10-OPEA only weakly promotes the accumulation of multiple protease inhibitor transcripts. Consistent with a role in dying tissue, 10-OPEA application promotes cysteine protease activation and cell death which is inhibited by overexpression of the cysteine protease inhibitor maize cystatin-9. Functions for 10-OPEA and associated death acids are consistent with specialized roles in local defense reactions.
Maize death acids, 9-lipoxygenase-derived cyclopente(a)nones, display activity as cytotoxic phytoalexins and transcriptional mediators.
Specimen part
View SamplesUterine leiomyosarcoma (ULMS) is a poorly understood gynecologic cancer with few effective treatments. This study explores molecular events involved in ULMS with the goal of identifying strategies.
A small-molecule inhibitor targeting the mitotic spindle checkpoint impairs the growth of uterine leiomyosarcoma.
Specimen part
View SamplesComparison of gene expression level of 3T3-L1, PMEF and ES cell derived adipocytes to eWAT samples.
Highly efficient differentiation of embryonic stem cells into adipocytes by ascorbic acid.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Protective role of IL-6 in vascular remodeling in Schistosoma pulmonary hypertension.
Sex, Specimen part, Disease, Disease stage, Treatment
View SamplesRationale: Schistosomiasis is one of the most common causes of pulmonary arterial hypertension worldwide, but the pathogenic mechanism by which the host inflammatory response contributes to vascular remodeling is unknown. We sought to identify signaling pathways that play protective or pathogenic roles in experimental Schistosoma-induced pulmonary vascular disease by whole-lung transcriptome analysis. Methods: Wildtype mice were experimentally exposed to S. mansoni ova by intraperitoneal sensitization followed by tail vein augmentation, and the phenotype assessed by right ventricular catheterization and tissue histology, RNA and protein analysis. Whole-lung transcriptome analysis by microarray and RNA sequencing was performed, the latter analyzed using 2 bioinformatic methods. Functional testing of the candidate IL-6 pathway was determined using IL6-knockout mice and the STAT3 inhibitor STI-201. Results: Wild-type mice exposed to S. mansoni had increased right ventricular systolic pressure and thickness of the pulmonary vascular media. Whole lung transcriptome analysis identified the IL6-STAT3-NFATc2 pathway as being upregulated, which was confirmed by PCR and immunostaining of lung tissue from S. mansoni-exposed mice and patients who died of the disease. Mice lacking IL6 or treated with STI-201 developed pulmonary hypertension associated with significant intima remodeling after exposure to S. mansoni. Conclusions: Whole lung transcriptome analysis identified upregulation of the IL6-STAT3-NFATc2 pathway, and IL6 signaling was found to be protective against Schistosoma-induced intimal remodeling.
Protective role of IL-6 in vascular remodeling in Schistosoma pulmonary hypertension.
Sex, Specimen part, Disease, Disease stage, Treatment
View SamplesA comparative analysis of gene expression of 3 different experiments; 1. Perinate or adult-tagged GFP+YFP+ and bulk GFP+YFP- Tregs, 2. FL or BM-derived Tregs 3. Perinate or adult thymic Tregs.
Immune tolerance. Regulatory T cells generated early in life play a distinct role in maintaining self-tolerance.
Sex, Age, Specimen part
View SamplesA comparative analysis of gene expression of perinate or adult Aire-GFP+ and GFP- MECs in WT or Aire-KO thymus
Immune tolerance. Regulatory T cells generated early in life play a distinct role in maintaining self-tolerance.
Sex, Age, Specimen part
View SamplesDiffering from other experimental models, intranasal infection with vaccine strain of Venezuelan equine encephalitis virus, VEEV, (TC83) caused high titer infection in the brain and 90100% mortality in the C3H/HeN murine model. Intranasal infection with VEEV (TC83) caused persistent viral infection in the brains of mice without functional T-cells (-TCR -/-). While wild-type C57BL/6 mice clear infectious virus in the brain by 13 dpi, -TCR -/- maintain infectious virus in the brain to 92 dpi.
Natural killer cell mediated pathogenesis determines outcome of central nervous system infection with Venezuelan equine encephalitis virus in C3H/HeN mice.
Sex, Specimen part
View SamplesFull title: Prepubertal Human Spermatogonia and Mouse Gonocytes Share Conserved Gene Expression of Germline Stem Cell Regulatory Molecules
Prepubertal human spermatogonia and mouse gonocytes share conserved gene expression of germline stem cell regulatory molecules.
Age
View SamplesThis study shows that the TLR4/MyD88 pathway in intestinal mesenchymal cells promotes intestinal carcinogenesis in the APCmin mouse model. Overall design: 3' RNA-Seq (QuantSeq) profiling of ColVIcre+ wt and MyD88 knockout primary mouse intestinal mesenchymal cells before and after treatment with LPS for 6 hours. 3 replicates per group.
Innate Sensing through Mesenchymal TLR4/MyD88 Signals Promotes Spontaneous Intestinal Tumorigenesis.
Specimen part, Cell line, Treatment, Subject
View Samples