AEC II cell differentiation in miR142 overexpressing mice
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ABSTRACT:
PROVIDER: PRJNA416787 | ENA |
REPOSITORIES: ENA
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Project description:We observed that loss of miR142 leads to the increased expression of surfactant protein C and decreased Podoplanin. This indicates increased differentiation of alveolar progenitors towards AEC II lineage. In order to understand what are the genes that are being regulated during AEC II cell differentiation in miR142 overexpressing mice we are performing this experiment.
2019-11-01 | GSE106410 | GEO
Project description:We observed that loss of miR142 leads to the increased expression of surfactant protein C and decreased Podoplanin.This indicates increased differentiation of alveolar progenitors towards AEC II lineage. In order to understand 1)what are the genes that are being regulated during AEC II cell differentiation in miR142KO mice we are performing this experiment.
2019-11-01 | GSE106244 | GEO
Project description:AEC II cell differentiation in miR142 KO mice
| PRJNA415986 | ENA
Project description:Our previous data obtained by using immunohistochemistry showed, that Fgf10+/- (50% Fgf10 expression compared to WT) in hyperoxic condition at postnatal day 3 (P3) compared to WT has less vessel count in the lung and less muscularization of small capillaries in the lung. Furthermore, Fgf10+/- showed a drastic increase in mortality upon hyperoxic lung injury. Main question to be answer by this experiment is as followed: Does AEC II from Fgf10+/- mice in normoxia show different expression profiles at P3 compared to AEC II from WT? To adress this question we harvest lungs at P3 from WT and Fgf10+/- . For this the mice were sacrificed by Ketamin/ Dormitor ip, lungs were perfused transcardiac with PBS and directly frozen in liquid nitrogen.
2016-12-31 | GSE76300 | GEO
Project description:A GFP-expressing recombinant A/Puerto Rico/8/1934 influenza virus was used to infect C57BL/6 wild type mice and on day 3 post infection, lung alveolar epithelial cells (AEC) were isolated and sorted based on GFP expression. GFP+ AEC represent the infected AEC and GFP- AEC represent the bystander AEC. AEC were also sorted from uninfected mice to serve as controls.
2018-08-29 | GSE119123 | GEO
Project description:In this study, type II alveolar epithelial cells (AEC II) were isolated from normal, hyperoxia exposed (day 0) and recovery (day 1,3,5 and 7) rats with high purity (~95%). Total RNA from isolated cells were used for dual color DNA microarray hybridization with 3DNA 50 kit version 2. Keywords: time-course
2010-06-11 | E-GEOD-2707 | biostudies-arrayexpress
Project description:In this study, type II alveolar epithelial cells (AEC II) were isolated from normal, hyperoxia exposed (day 0) and recovery (day 1,3,5 and 7) rats with high purity (~95%). Total RNA from isolated cells were used for dual color DNA microarray hybridization with 3DNA 50 kit version 2. Keywords: time-course
2006-06-06 | GSE2707 | GEO
Project description:The transcriptional basis for disrupted epidermal differentiation arising from TP63 AEC mutations remains to be elucidated. Here we present an organotypic model of AEC dysfunction that phenocopies differentiation defects observed in AEC patient skin. Transcriptional analysis of model AEC tissue revealed impaired induction of differentiation regulators, including OVOL1, GRHL3, KLF4, PRDM1 and ZNF750. Genome wide binding analyses of TP63 during epidermal differentiation showed direct binding of OVOL1, GRHL3, and ZNF750 promoters suggesting AEC mutants prevent normal activation of these targets by direct transcriptional interference. Remarkably, exogenous ZNF750 restores impaired epidermal differentiation caused by AEC mutation. Thus, repression of ZNF750 is central to disrupted epidermal differentiation in model AEC tissue. Gene expression analysis: To establish a differentiation signature for primary human keratinocytes, with p63i-depleted, and ΔNp63α AEC mutants overexpressed, total RNA was isolated in biologic duplicate from cells in different conditions and hybridized to Affymetrix HG-U133 2.0 Plus arrays.
2012-06-17 | E-GEOD-33495 | biostudies-arrayexpress
Project description:The transcriptional basis for disrupted epidermal differentiation arising from TP63 AEC mutations remains to be elucidated. Here we present an organotypic model of AEC dysfunction that phenocopies differentiation defects observed in AEC patient skin. Transcriptional analysis of model AEC tissue revealed impaired induction of differentiation regulators, including OVOL1, GRHL3, KLF4, PRDM1 and ZNF750. Genome wide binding analyses of TP63 during epidermal differentiation showed direct binding of OVOL1, GRHL3, and ZNF750 promoters suggesting AEC mutants prevent normal activation of these targets by direct transcriptional interference. Remarkably, exogenous ZNF750 restores impaired epidermal differentiation caused by AEC mutation. Thus, repression of ZNF750 is central to disrupted epidermal differentiation in model AEC tissue. ChIP-Seq analysis: Examination of p63 binding in proliferating and differentiating human keratinocytes
2012-06-18 | E-GEOD-33571 | biostudies-arrayexpress
Project description:The transcriptional basis for disrupted epidermal differentiation arising from TP63 AEC mutations remains to be elucidated. Here we present an organotypic model of AEC dysfunction that phenocopies differentiation defects observed in AEC patient skin. Transcriptional analysis of model AEC tissue revealed impaired induction of differentiation regulators, including OVOL1, GRHL3, KLF4, PRDM1 and ZNF750. Genome wide binding analyses of TP63 during epidermal differentiation showed direct binding of OVOL1, GRHL3, and ZNF750 promoters suggesting AEC mutants prevent normal activation of these targets by direct transcriptional interference. Remarkably, exogenous ZNF750 restores impaired epidermal differentiation caused by AEC mutation. Thus, repression of ZNF750 is central to disrupted epidermal differentiation in model AEC tissue.
2012-06-18 | GSE33495 | GEO