title: Estrogen receptor β signaling induces autophagy and downregulates Glut9 expression.
abstract: Glut9 is highly expressed in the human kidney proximal convoluted tubular and plays a crucial role in the regulation of plasma urate levels. The gene effects were stronger among women. Our results show that 17-β-estradiol (E2) through ER (estrogen receptor) β downregulates Glut9 protein expression on human renal tubular epithelial cell line (HK2). Intriguingly, E2 does not affect the expression of Glut9 mRNA. ERβ is linked to PTEN, the PTEN gene negatively regulates the PI3K/AKT pathway, and the PI3K/AKT pathway inhibition may lead to autophagy. Further study indicates that ERβ may affect the expression of Glut9 though autophagy.
authors: a Biology Group, North Sichuan Medical College.
authors: Mei
authors: M
authors: Zeng
authors: Baofeng
authors: B
authors: Chen
authors: Yufeng
authors: Y
authors: Qing
authors: Wenguang
authors: W
authors: Xie
authors: Wantai
authors: W
authors: Dang
authors: Mingcai
authors: M
authors: Zhao
authors: Jingguo
authors: J
authors: Zhou
mesh_terms: D001343:Autophagy / Q000187:drug effects; D002460:Cell Line; D015536:Down-Regulation / Q000187:drug effects; D004958:Estradiol / Q000494:pharmacology; D047629:Estrogen Receptor beta / Q000378:metabolism*; D051246:Glucose Transport Proteins, Facilitative / Q000235:genetics* / Q000378:metabolism*; D006801:Humans; D051059:PTEN Phosphohydrolase / Q000235:genetics / Q000378:metabolism; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D059748:Proteolysis / Q000187:drug effects; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D047629:Estrogen Receptor beta; D051246:Glucose Transport Proteins, Facilitative; D012333:RNA, Messenger; C411811:SLC2A9 protein, human; D004958:Estradiol; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D051059:PTEN Phosphohydrolase
keywords: Phosphorylases; gene regulation; mechanism of action studies