Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA350326 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Primary murine lung fibroblasts were transfected with either control (scrambled) or sequence-specific siRNA against Lysyl oxidase (Lox), Lysyl oxidase-like (Loxl1) or Lysyl oxidase-like 2 (Loxl2) genes. Cells were harvested 48 hours after the transfection. Multiple changes in gene expression were found in the corrected p values in this microarray study.
2016-10-25 | GSE89121 | GEO
Project description:Human placental development is characterized by invasion of extravillous cytotrophoblasts (EVCTs) into the uterine wall during the first trimester of pregnancy. Peroxisome proliferator-activated receptor gamma (PPARG) plays a major role in placental development, and activation of PPARG by its agonists results in inhibition of EVCT invasion in vitro. To identify PPARG target genes, microarray analysis was performed using GeneChip technology on EVCT primary cultures obtained from first-trimester human placentas. Gene expression was compared in EVCTs treated with the PPARG agonist rosiglitazone versus control. A total of 139 differentially regulated genes were identified, and changes in the expression of the following 8 genes were confirmed by reverse transcription-quantitative polymerase chain reaction: a disintegrin and metalloproteinase domain12 (ADAM12), connexin 43 (CX43), deleted in liver cancer 1 (DLC1), dipeptidyl peptidase 4 (DPP4), heme oxygenase 1 (HMOX-1), lysyl oxidase (LOX), plasminogen activator inhibitor 1 (PAI-1) and PPARG. Among the upregulated genes, lysyl oxidase (LOX) was further analyzed. In the LOX family, only LOX, LOXL1 and LOXL2 mRNA expression was significantly upregulated in rosiglitazone-treated EVCTs. RNA and protein expression of the subfamily members LOX, LOXL1 and LOXL2 were analyzed by absolute RT-qPCR and western blotting, and localized by immunohistochemistry and immunofluorescence-confocal microscopy. LOX protein was immunodetected in the EVCT cytoplasm, while LOXL1 was found in the nucleus and nucleolus. No signal was detected for LOXL2 protein. Specific inhibition of LOX activity by beta-aminopropionitrile in cell invasion assays led to an increase in EVCT invasiveness. These results suggest that LOX, LOXL1 and LOXL2 are downstream PPARG targets and that LOX activity is a negative regulator of trophoblastic cell invasion. Microarray analysis was performed using GeneChip technology in EVCTs isolated from first trimester human placentae. Gene expression in rosiglitazone-treated primary EVCT cultures was compared with matched untreated controls. A total of 175 probe sets identified differentially regulated genes. One of these genes, lysyl oxidase (LOX) which was up-regulated, was further analyzed. Expression of the LOX family was determined by real time Q-PCR, Western blotting, immunohistochemistry and immunofluorescence. LOX, LOXL and LOXL2 mRNA expression was significantly upregulated in PPARg-activated EVCTs. LOX and LOXL2 protein were present throughout the trophoblast cytoplasm, while LOXL was localized to the nucleus and nucleolus. Cell invasion assays on Matrigel Transwells showed that specific inhibition of LOX activity by M-CM-^_-aminopropionitrile led to an increase in EVCT invasiveness, showing the basal inhibitory effect of LOX and LOX-like in the trophoblastic cells invasion process. Together these results show that LOX family as PPARg-target genes participate to the regulation of trophoblast invasion. Total RNA from EVCT were labelled according to the standard Affymetrix protocol. Five independent targets per treatment vs control were generated and hybridized on a GeneChip.
2013-12-04 | E-GEOD-28426 | biostudies-arrayexpress
Project description:Human placental development is characterized by invasion of extravillous cytotrophoblasts (EVCTs) into the uterine wall during the first trimester of pregnancy. Peroxisome proliferator-activated receptor gamma (PPARG) plays a major role in placental development, and activation of PPARG by its agonists results in inhibition of EVCT invasion in vitro. To identify PPARG target genes, microarray analysis was performed using GeneChip technology on EVCT primary cultures obtained from first-trimester human placentas. Gene expression was compared in EVCTs treated with the PPARG agonist rosiglitazone versus control. A total of 139 differentially regulated genes were identified, and changes in the expression of the following 8 genes were confirmed by reverse transcription-quantitative polymerase chain reaction: a disintegrin and metalloproteinase domain12 (ADAM12), connexin 43 (CX43), deleted in liver cancer 1 (DLC1), dipeptidyl peptidase 4 (DPP4), heme oxygenase 1 (HMOX-1), lysyl oxidase (LOX), plasminogen activator inhibitor 1 (PAI-1) and PPARG. Among the upregulated genes, lysyl oxidase (LOX) was further analyzed. In the LOX family, only LOX, LOXL1 and LOXL2 mRNA expression was significantly upregulated in rosiglitazone-treated EVCTs. RNA and protein expression of the subfamily members LOX, LOXL1 and LOXL2 were analyzed by absolute RT-qPCR and western blotting, and localized by immunohistochemistry and immunofluorescence-confocal microscopy. LOX protein was immunodetected in the EVCT cytoplasm, while LOXL1 was found in the nucleus and nucleolus. No signal was detected for LOXL2 protein. Specific inhibition of LOX activity by beta-aminopropionitrile in cell invasion assays led to an increase in EVCT invasiveness. These results suggest that LOX, LOXL1 and LOXL2 are downstream PPARG targets and that LOX activity is a negative regulator of trophoblastic cell invasion. Microarray analysis was performed using GeneChip technology in EVCTs isolated from first trimester human placentae. Gene expression in rosiglitazone-treated primary EVCT cultures was compared with matched untreated controls. A total of 175 probe sets identified differentially regulated genes. One of these genes, lysyl oxidase (LOX) which was up-regulated, was further analyzed. Expression of the LOX family was determined by real time Q-PCR, Western blotting, immunohistochemistry and immunofluorescence. LOX, LOXL and LOXL2 mRNA expression was significantly upregulated in PPARg-activated EVCTs. LOX and LOXL2 protein were present throughout the trophoblast cytoplasm, while LOXL was localized to the nucleus and nucleolus. Cell invasion assays on Matrigel Transwells showed that specific inhibition of LOX activity by ß-aminopropionitrile led to an increase in EVCT invasiveness, showing the basal inhibitory effect of LOX and LOX-like in the trophoblastic cells invasion process. Together these results show that LOX family as PPARg-target genes participate to the regulation of trophoblast invasion.
2013-12-04 | GSE28426 | GEO
Project description:Our previous studies have found that LOX and LOXL1 were highly upregulated in advanced liver fibrosis; herein, we aimed to investigate the roles of LOX and LOXL1 in hepatic stellate cells.
2021-12-01 | GSE155651 | GEO
Project description:Exogenous BAPN administration does not regulate gene expression in primary murine lung fibroblasts and alveolar epithelial type II (ATII) cells.
| PRJNA350327 | ENA
Project description:Expression data of stimulated murine primary lung fibroblasts
| PRJNA657428 | ENA
Project description:Lin28A and its paralog Lin28B are RNA binding proteins that regulate gene expression by inhibition of the maturation of the Per/Pri Let-7 miRNAs family and also via Let-7 independent mechanism. To study the effect of Lin28A ectopic-expression on mouse embryonic development we used a transgenic mice strain that combine a Cre-Lox system and a Tet-On system (herein Lox-stop-Lox-TetOn-Lin28A mice) and enable spatial and temporal control of transgenic Lin28A over-expression. Here we show that global Lin28A over-expression (by crossing Lox-stop-Lox-TetOn-Lin28A males with VasaCre females) in the mouse embryo prevents embryonic lung development. To study the precise developmental stage affected by Lin28A expression we preformed RNA sequencing analysis for transgenic and control lungs from E12.5, E14.5, E16.5 and E18.5 embryos. This analysis revealed that the development of the lung was delayed but not completely abrogated by Lin28A expression. We further showed that the effect of Lin28A expression in the mesenchymal cells (by crossing Lox-stop-Lox-TetOn-Lin28A males with Wt1Cre females) of the lung leads to the same phenotype as global Lin28A expression while expression in the lung epithelial cells (by crossing the Lox-stop-Lox-TetOn-Lin28A males with Nkx2.1Cre females) result in a milder developmental phenotype.
2019-09-22 | GSE122919 | GEO
Project description:Exogenous H2S administration does not regulate gene expression in primary murine alveolar type II cells
| PRJNA230698 | ENA
Project description:We derived a transcriptional signature of oncogenic KRAS by using the KF508 murine pancreatic ductal cell line with an inducible Lox-Stop-Lox (LSL) cassette in front of the KRASG12D oncogene to regulate transcription. This dataset allowed us to study the differential expression profile after oncogenic KRAS induction in mouse.
2016-11-16 | GSE89846 | GEO
Project description:Primary murine lung fibroblasts or ATII cells were either treated with vehicle or 1mM BAPN for 24 h. Overall, only one change in gene expression was found in the corrected p values in fibroblasts group in this microarray study.
2016-10-25 | GSE89119 | GEO