Caveolin-1 induced gene expression change in retinae
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE95657 | GEO | 2018/03/01
REPOSITORIES: GEO
Similar Datasets
Project description:By contrast with mammals, adult zebrafish have a high capacity to regenerate damaged or lost myocardium through proliferation of spared cardiomyocytes. The epicardial sheet covering the heart is activated by injury and aids muscle regeneration through paracrine effects and as a multipotent cell source, and has received recent attention as a target in cardiac repair strategies. While it is recognized that epicardium is required for muscle regeneration and itself has high regenerative potential, the extent of cellular heterogeneity within epicardial tissue is largely unexplored. In this study, we performed transcriptome analysis on dozens of epicardial lineage cells purified from zebrafish harboring a transgenic reporter for the pan-epicardial gene tcf21. Hierarchical clustering analysis suggested the presence of at least three epicardial cell subsets defined by expression signatures. We validated many new pan-epicardial and epicardial markers by alternative expression assays. Additionally, we explored the function of the scaffolding protein and main component of caveolae, caveolin-1 (cav1), which was present in each epicardial subset. In BAC transgenic zebrafish, cav1 regulatory sequences drove strong expression in ostensibly all epicardial cells and in coronary vascular endothelial cells. Moreover, cav1 mutant zebrafish generated by genome editing showed grossly normal heart development and adult cardiac anatomy, but displayed profound defects in injury-induced cardiomyocyte proliferation and heart regeneration. Our study defines a new platform for the discovery of epicardial lineage markers, genetic tools, and mechanisms of heart regeneration. Deep sequencing of isolated single epicardial cells
2015-12-15 | E-GEOD-75583 | biostudies-arrayexpress
Project description:By contrast with mammals, adult zebrafish have a high capacity to regenerate damaged or lost myocardium through proliferation of spared cardiomyocytes. The epicardial sheet covering the heart is activated by injury and aids muscle regeneration through paracrine effects and as a multipotent cell source, and has received recent attention as a target in cardiac repair strategies. While it is recognized that epicardium is required for muscle regeneration and itself has high regenerative potential, the extent of cellular heterogeneity within epicardial tissue is largely unexplored. In this study, we performed transcriptome analysis on dozens of epicardial lineage cells purified from zebrafish harboring a transgenic reporter for the pan-epicardial gene tcf21. Hierarchical clustering analysis suggested the presence of at least three epicardial cell subsets defined by expression signatures. We validated many new pan-epicardial and epicardial markers by alternative expression assays. Additionally, we explored the function of the scaffolding protein and main component of caveolae, caveolin-1 (cav1), which was present in each epicardial subset. In BAC transgenic zebrafish, cav1 regulatory sequences drove strong expression in ostensibly all epicardial cells and in coronary vascular endothelial cells. Moreover, cav1 mutant zebrafish generated by genome editing showed grossly normal heart development and adult cardiac anatomy, but displayed profound defects in injury-induced cardiomyocyte proliferation and heart regeneration. Our study defines a new platform for the discovery of epicardial lineage markers, genetic tools, and mechanisms of heart regeneration.
2015-12-15 | GSE75583 | GEO
Project description:Caveolae are plasma membrane invaginations found in most cells of mammals. Caveolin-1 (Cav1) encodes a major protein of the lipid rafts of these membrane structures. Cav1-null mice, though viable, show various phenotypic defects. At an early adult age, these mice show brain aging that resemble brain of one and half year old wildtype mice, and exhibit symptoms that are hallmarks of Alzheimer’s disease. It is not known if the ablation of Cav1 in these mice impacts the brain at the fetal stage that then influences brain function later in life. Single nuclei RNA sequencing was performed with fetal brain of wildtype and Cav1 knockout mice. Results showed that specific metabolism genes were differentially expressed bewteen different glial cells.
2023-09-20 | GSE214759 | GEO
Project description:Forkhead box protein 3 (FOXP3) is implicated in tumor progression and prognosis in various types of tumor cells. We have recently reported that FOXP3 inhibited proliferation of gastric cancer (GC) cells through activating the apoptotic signaling pathway. In this study, we found that over-expression of FOXP3 inhibited GC cell migration, invasion and proliferation. Then, the label-free quantitative proteomic approach was employed to further investigating the down-stream proteins regulated by FOXP3, resulting in a total of 3,978 proteins quantified, including 186 significantly changed proteins. Caveolin-1 (CAV1), as a main constituent protein of caveolae, was one of those changed proteins up-regulated in FOXP3-overexpressed GC cells, moreover, it was assigned as one of the node proteins in the protein-protein interaction network and the key protein involved in focal adhesion pathway by bioinformatics analysis. Further biological experiments confirmed that FOXP3 directly bound to the promoter regions of CAV1 to positively regulate CAV1 transcription in GC cells. In summary, our study suggested that FOXP3 can be considered as a tumor suppressor in GC via positively regulating CAV1 through transcriptional activation, and this FOXP3-CAV1 transcriptional regulation axis may play an important role in inhibiting invasion and metastasis of GC cells.
2017-11-03 | PXD007725 | Pride
Project description:Caveolae are plasma membrane invaginations found in most cells of mammals. Caveolin-1 (Cav1) encodes a major protein of the lipid rafts of these membrane structures. Cav1-null mice, though viable, show various phenotypic defects. At an early adult age, these mice show brain aging that resemble brain of one and half year old wildtype mice, and exhibit symptoms that are hallmarks of Alzheimer’s disease. It is not known if the ablation of Cav1 in these mice impacts the brain at the fetal stage that then influences brain function later in life. RNA-seq was performed to profile gene expression of fetal brain (gestation day 15) and aging brain (week 70) of Cav1 knockout mice. The data was comapred with genes expression data of fetal brain (gestation day 15) and aging brain (week 70) of wildtype mice from our earlier study.
2023-09-20 | GSE215139 | GEO
Project description:Chronic ocular inflammation is associated with many retinal degenerative diseases that result in vision loss. The immune-privileged environment and complex organization of retinal tissue allow for the retina’s essential role in visual function processes, yet confound inquiries into cell-specific inflammatory effects that lead to retinal dysfunction and degeneration. Caveolin-1 (Cav1) is an integral membrane protein expressed in many retinal cell populations and has been implicated in retinal immune regulation. However, the direction (i.e., promotion or inhibition) in which Cav1 regulates inflammatory processes in the retina (as well as in other tissues) remains unclear. Previously, we showed that global-Cav1 depletion in the retina paradoxically resulted in reduced retinal inflammatory cytokine production with concurrent elevated retinal immune cell infiltration. We hypothesized that our previous results could be explained by cell-specific Cav1 functions in the retina. Here, we utilized our Chx10 (visual system homeobox 2)-Cre knockout model to deplete Cav1 specifically in the neural retinal (NR) compartment in order to clarify the role of neural retinal-specific Cav1 (NR-Cav1) in the retinal immune response to intravitreal LPS (lipopolysaccharide) challenge. Our data support that neural retinal-derived Cav1 promotes retinal tissue inflammation as Chx10-mediated Cav1 depletion was sufficient to suppress both retinal cytokine production and immune cell infiltration following inflammatory stimulation. Additionally, we identify Traf3 (tumor necrosis factor (TNF) receptor-associated factor 3) as a highly expressed potential immune modulator in retinal tissue that is upregulated with NR-Cav1 depletion. Furthermore, this study highlights the importance for understanding the role of Cav1 (and other proteins) in cell-specific contexts.
2021-09-08 | PXD016872 | Pride
Project description:CAV1 loss-of-function mutations have been associated with the development of pulmonary arterial hypertension (PAH). CAV1 is an integral component of endothelial caveolae, specialized lipid rafts that attach to the actin cytoskeleton and modulate receptor/signal transduction coupling. CAV1 loss in pulmonary artery endothelial cells produced a proliferative, hypermigratory cellular phenotype with a disrupted cytoskeletal architecture, mirroring known features of PAH pathobiology. Gene expression on Human Pulmonary Arterial Endothelial Cells (PAECs) transfected with non-targeting siRNA control pool or siRNA (ON-TARGET plus CAV1) in the presence or absence of TNF-alpha was evaluated
2021-02-24 | GSE138991 | GEO
Project description:In conjunction with other techniques, the role of caveolin-1 in lipid metabolism was assayed by comparing the gene expression of three tissues in Cav1+/+ and Cav1-/- mice. The tissues assayed were liver, adipose tissue, and mouse embryonic fibroblasts (MEFs) primary cell line, collected 24 hours after plating. The MEFs were selected to give insights into the fundamental cellular functions of Cav1. The adipose tissue and liver were selected because they are the most important tissues or organs involved the control of the lipid metabolism in mammals. Both of them were study during fasting because lipid metabolism become essential for maintaining of mammal metabolism homeostasis and tissue/organ functions in animals.
2010-02-15 | GSE19045 | GEO
Project description:Forkhead box protein 3 (FOXP3) is associated with tumor progression and prognosis in various types of tumor cells. We have recently reported that FOXP3 inhibited proliferation of gastric cancer (GC) cells through activating the apoptotic signaling pathway. In this study, we found that over-expression of FOXP3 inhibited GC cell migration, invasion and proliferation. To further investigate the down-stream proteins regulated by FOXP3, the label-free quantitative proteomic approach was employed to analyze the gastric cells stably transfected with FOXP3-containing lentivirus or empty vector. A total of 3,978 proteins were identified and quantified, including 186 significantly changed proteins. Caveolin-1 (CAV1) was one of those changed proteins up-regulated in FOXP3-overexpressed gastric cells, moreover, it is one of the node proteins in the protein-protein interaction network and the key protein involved in focal adhesion pathway by bioinformatics analysis. As the main constituent of caveolae, caveolin-1 interacts directly with several signaling molecules and acts as a tumor suppressor in numerous carcinomas. Further biological experiments confirmed that FOXP3 directly binded to the promoter regions of CAV1 to positively regulated CAV1 transcription in GC cells. In summary, our study suggested that FOXP3 plays a tumor-suppressing role in GC via positively regulating CAV1 through transcriptional activation, and this FOXP3-CAV1 transcriptional regulation ais may play an important role in inhibiting invasion and metastasis of GC cells.
2024-08-16 | PXD054940 |
Project description:To identify genes regulated by Cav1 Affymetrix Human Genome U133 Plus 2.0 GeneChip Hep3B cells with or without knockdown of Cav1
2016-03-01 | E-GEOD-75994 | biostudies-arrayexpress