BPH/5 mice are an inbred strain with “borderline hypertension” that spontaneously develops both maternal and fetal hallmarks of preeclampsia. RNA-Seq analysis of BPH/5 uterine implantation sites at embryonic day 7.5, the peak of decidualization, identifies differential expression of inflammatory response genes, including members of the complement family, compared to C57 controls. Overall design: RNA-Seq was performed on RNA isolated from E7.5 BPH/5 and C57 implantation sites (n=4).
Angiogenic factor imbalance precedes complement deposition in placentae of the BPH/5 model of preeclampsia.
Cell line, Subject
View SamplesWe asked whether combining Notch and VEGF blockade would enhance suppression of tumor angiogenesis and growth, using the NGP neuroblastoma model. NGP tumors were engineered to express a Notch1 decoy construct (N1D), which restricts Notch signaling, and then treated with either the anti-VEGF antibody bevacizumab or vehicle. Combining Notch and VEGF blockade led to blood vessel regression, increasing endothelial cell apoptosis and disrupting pericyte coverage of endothelial cells. Combined Notch and VEGF blockade did not affect tumor weight, but did additively reduce tumor viability. Our results indicate that Notch and VEGF pathways play distinct but complementary roles in tumor angiogenesis, and show that concurrent blockade disrupts primary tumor vasculature and viability further than inhibition of either pathway alone.
Notch and VEGF pathways play distinct but complementary roles in tumor angiogenesis.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Transcription factor <i>TFCP2L1</i> patterns cells in the mouse kidney collecting ducts.
Specimen part
View SamplesGene expression analysis of mouse kidney after conditional inactivation of transcription factor Tfcp2l1
Transcription factor <i>TFCP2L1</i> patterns cells in the mouse kidney collecting ducts.
Specimen part
View SamplesMicroarrays were used to examine gene expression changes that may be present in the fallopian tube epithelium of morphologically normal BRCA1 mutation positive and negative subjects. Fallopian tube epithelia has been implicated as an early point of origin for serous carcninoma. By examining the early events present in the microenvironment of this tissue between BRCA1 mutation carriers and non-carriers, we hoped to elucidate mechanisms that may lead to the development of epithelial ovarian cancer.
Identification of abrogated pathways in fallopian tube epithelium from BRCA1 mutation carriers.
Specimen part
View SamplesOur mouse model of BE in which overexpression of IL-1b in the squamous esophagus induces chronic inflammation leads to metaplasia and dysplasia at the squamo-columnar junction (SCJ) in the mouse gastro-esophageal junction resembles the human disease. Adult L2-IL1b mice were employed to investigate changes to the transcriptional landscape at the SCJ during disease progression from BE to EAC following pharmaceutical or genetic perturbations of interest to BE biology.
Notch Signaling Mediates Differentiation in Barrett's Esophagus and Promotes Progression to Adenocarcinoma.
No sample metadata fields
View SamplesThe purpose of this study was to identify molecular alterations potentially involved in predisposition to adnexal serous carcinoma (SerCa) in the non-malignant fallopian tube epithelium (FTE) of BRCA1/2-mutation carriers, given recent evidence implicating the distal FTE as a common source for SerCa.
Gene expression profiles of luteal phase fallopian tube epithelium from BRCA mutation carriers resemble high-grade serous carcinoma.
Age
View SamplesThis SuperSeries is composed of the SubSeries listed below.
PrtT-regulated proteins secreted by Aspergillus fumigatus activate MAPK signaling in exposed A549 lung cells leading to necrotic cell death.
Specimen part, Cell line, Treatment
View SamplesResponse of A549 cells treated with Aspergillus fumigatus wild type germinating conidia (WT_GC) or PrtT protease deficient mutant conidia (PrtT-GC) or inert acrylic 2-4 micron beads (Beads) for 8h
PrtT-regulated proteins secreted by Aspergillus fumigatus activate MAPK signaling in exposed A549 lung cells leading to necrotic cell death.
Specimen part, Cell line, Treatment
View SamplesResponse of A549 cells treated with Aspergillus fumigatus wild type culture filtrate (WT-CF) or PrtT protease deficient mutant culture filtrate (PrtT-CF) for 8h
PrtT-regulated proteins secreted by Aspergillus fumigatus activate MAPK signaling in exposed A549 lung cells leading to necrotic cell death.
Specimen part, Cell line, Treatment
View Samples