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Single-cell transcriptional response of placenta to the ablation of Caveolin-1 in mice: insights into the regulation of brain-placental axis [scRNA-Seq]

ABSTRACT: This study investigated gene expression of placental cells in a mouse model lacking Caveolin 1 (Cav1). Single-nuclei RNA-seq was performed with day-15 placenta of WT and Cav1-null mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE248126 | GEO | 2024/02/14

REPOSITORIES: GEO

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Single-cell transcriptional response of placenta to the ablation of Caveolin-1 in mice: insights into the regulation of brain-placental axis [bulk RNA-seq]

Project description:Bulk RNA-seq was performed to profile placental gene expression in mice lacking Caveolin-1.

2024-02-14 | GSE248093 | GEO

Insights into the regulation of the brain-placental axis (ChIP-seq)

Project description:Fetal sex influences the accessibility of the placental chromatin to REST. REST targeted fewer sites in the female placental compared to that of male. REST bound to 7,254 common sites in both sexes but nearly 17-fold more number of sites in the male placenta compared to the female placenta.

2023-09-01 | GSE157552 | GEO

caveolin-1 induced gene expression change in retinae

Project description:Caveolin-1 (Cav1) is the main structure protein of caveolae. Its main functional domain is the scaffolding domain that is the bind site of many interactors. A fused peptide called cavtratin is used to test Cav1 function which includes the scaffolding domain and a short internalizing peptide AP. Cav1 has been reported to be associated with glaucoma in the GWAS study. To explore its role in the retina, we explored the gene expression change after Cav1-shRNA or cavtratin was injected into the mouse eye vitreous.

2018-03-01 | GSE95657 | GEO

Effects of Caveolin 1 knockout in mice

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

Role of Caveolin 1 in metabolic programming of fetal brain

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

Cordycepin induces apoptosis by caveolin-1 mediated JNK’s regulation of Foxo3a in lung cancer A549 cells

Project description:c-Jun N-terminal kinase (JNK) plays a pivotal role in the regulation of cancer cell apoptosis. Previous studies have revealed that forkhead transcription factor (Foxo3a) is a critical effector of JNK-mediated tumor suppression. However, it is not clear whether caveolin-1 (CAV1) mediated JNK/Foxo3a pathway is involved in cancer cell apoptosis. We found that cordycepin upregulates CAV1 expression, which was accompanied by JNK phosphorylation (p-JNK), which induced Foxo3a translocation into the nucleus, resulting in the upregulation of levels of Bax protein. Furthermore, we found that CAV1 overexpression upregulated p-JNK, whereas siRNA mediated inhibition of CAV1 downregulated p-JNK, and that JNK inhibition by SP600125, a specific JNK inhibitor, significantly increased Foxo3a phosphorylation (p-Foxo3a), which attenuated Foxo3a translocation into the nucleus, indicating caveolin-1 mediated JNK’s regulation of Foxo3a. siRNA mediated inhibition of Foxo3a downregulated levels of Bax protein, attenuated A549 cell apoptosis, indicating that CAV1 mediated JNK/Foxo3a pathway induce the apoptosis of A549 lung cancer cells. Taken, together, these results indicate that cordycepin promotes CAV1 upregulation to enhance JNK/Foxo3a signaling pathway activation to induce apoptosis in lung cancer cells and support the potential of cordycepin as a therapeutic agent for lung cancer.

2016-05-24 | GSE81727 | GEO

Transcriptomic profile of human placenta derived trophoblast organoid cultures with its tissue of origin, human placental villi.

Project description:The aim of this microarray experiment was to compare the overall transcriptomic profile of human placenta derived trophoblast organoid cultures with its tissue of origin, human placental villi. As the placental villi contains both trophoblast and stromal populations, we have included placenta derived stromal cultures in this comparison.

2018-11-28 | E-MTAB-6683 | biostudies-arrayexpress

Single-cell transcriptional response of placenta to the ablation of Caveolin-1 in mice: insights into the regulation of brain-placental axis

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-02-14 | GSE248127 | GEO

Neuroretinal-derived caveolin-1 promotes endotoxin-induced inflammation in the murine retina

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

Treating the placenta with nanoparticles to prevent altered placental secretion and fetal development in response to hypoxia [Fetal Plasma]

Project description:Hypoxia-related pregnancy complications increase the risk of disease in the child in later life. No prevention is available. Previously we noted that a trophoblast barrier, an in vitro model of the placenta, reacted to oxidative stress by secreting factors that damage neighbouring cells. Application of mitochondrion-targeted antioxidant MitoQ prevented this. Here we tested the effects of MitoQ-bound nanoparticles on trophoblast barriers and in a rat model of gestational hypoxia.A single dose of MitoQ-nanoparticles, administered maternally before a hypoxic episode, reduced oxidative stress in the placental barrier without reaching the fetus and prevented changes to birthweight. MitoQ-nanoparticles further suppressed damaging signalling from the placental barriers. Altered signalling molecules in the fetal plasma and in conditioned media from rat placenta included changes to proteins with relevance to cardiovascular disease. We suggest as a future possibility, treatment of the placenta to prevent disease in the offspring in later life.

2017-08-22 | PXD004955 | Pride

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