Hormonal regulation of ATP binding cassette transporters

摘要: Although the knowledge of ATP-binding cassette lipid transport had grown substantially over last few years, detailed molecular mechanisms and exact functions these transporters were still awaiting clarification. In this thesis, analysis actions human steroid non-steroid hormones on cholesterol phospholipid effluxes ABC gene expression in two cell types (human monocytes derived macrophages HepG2 cells) performed. Human are source foam cells involved pathogenesis atherosclerosis, liver major site for biosynthesis catabolism by converting to bile acids. Some promoted ApoA-1 dependent others suppressed depending their influences ATP binding transporters. Beta-Estradiol enhanced phospholipids through upregulation ABCA1 ABCG1 expression. cells, beta-estradiol little or reversed effect sterol sensitive transporters, which presumbly related estrogen receptors Estrogen receptor-beta was high expressed but not cells. Upregulations genes beta-estadiol time where they started early lasted hours. Progesterone augmented expressions. Luteinizing hormone increased efflux augmentation ABCA7 mRNA. Somatostatin also enhancing Human insulin both These could be associated with an The time, concentration tissue dependent. macrophages, induction extended same occurred a more effect. maximum that upregulate 150 nM macrophages. Above concentration, declined. Posttransscription influence pronounced than its transcription. induced via MAP kinase signaling pathway. Furthermore, we speculate activation PPAR-gamma SDP1 process. Some effluxes. Hydrocortisone downregulation Triiodothyroxin decreased Glucagon declined supression ABCA1, Dexamethasone especially