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.
Project description: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.
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.
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.
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.
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
