Open Access17β-Estradiol and/or Estrogen Receptor β Attenuate the Autophagic and Apoptotic Effects Induced by Prolonged Hypoxia Through HIF-1α-Mediated BNIP3 and IGFBP-3 Signaling Blockage
Author(s) -
Dennis Jine-Yuan Hsieh,
Wei-Wen Kuo,
Yi-Ping Lai,
Marthandam Asokan Shibu,
Chia-Yao Shen,
PeiYing Pai,
YuLan Yeh,
Jing-Ying Lin,
Vijaya Padma Viswanadha,
ChihYang Huang
Publication year - 2015
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000374070
Subject(s) - apoptosis , estrogen receptor , hypoxia (environmental) , autophagy , endocrinology , estrogen , protein kinase b , medicine , downregulation and upregulation , tunel assay , programmed cell death , transfection , receptor , biology , chemistry , microbiology and biotechnology , cell culture , biochemistry , organic chemistry , cancer , breast cancer , oxygen , gene , genetics
The risk of heart disease is higher in males than in females. However, this advantage of females declines with increasing age, presumably a consequence of decreased estrogen secretion and malfunctioning of the estrogen receptor. We previously demonstrated that 17β-estradiol (E2) prevents cardiomyocyte hypertrophy, autophagy and apoptosis via estrogen receptor α (ERα), but the effects of ERβ on myocardial injury remained elusive. The present paper thus, investigated the cardioprotective effects of estrogen (E2) and ERβ against hypoxia-induced cell death.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom