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Oestrogen upregulates the sarcoplasmic reticulum Ca 2+ ATP ase pump in coronary arteries
Author(s) -
Hill Brent JF,
Muldrew Edwin
Publication year - 2014
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12233
Subject(s) - endoplasmic reticulum , chemistry , coronary arteries , medicine , biophysics , endocrinology , biochemistry , artery , biology
Summary The presence of circulating plasma 17 β ‐oestradiol (E2) is beneficial in women against abnormal vascular tone development, such as coronary arterial vasospasms. Several vascular diseases have demonstrated that increased expression of the sarcoplasmic reticulum Ca 2+ ‐ ATP ase pump ( SERCA 2b) serves to limit the excessive accumulation of intracellular Ca 2+ . Therefore, the hypothesis of the present study was that E2 would increase SERCA 2b expression in the coronary vasculature. Coronary arteries were dissected from hearts obtained from mature female pigs. Artery segments were cultured for 24 h in E2 (1 pmol/L or 1 nmol/L) and homogenized for western blot analysis. At 1 nmol/L, E2 induced an approximate 50% increase in immunoreactivity for SERCA 2b. In addition, E2 increased the protein expression of the known SERCA regulatory proteins, protein kinase A ( PKA ) and protein kinase G ( PKG ). The E2‐induced increase in SERCA 2b was attenuated when the culture medium was supplemented with the oestrogen receptor ( ER ) α / β antagonist ICI 182,780 and the PKG antagonist KT 5823 (10 μ mol/L, 24 h for both). The PKA antagonist ( KT 5720; 10 μ mol/L, 24 h) had no effect on SERCA 2b expression. Removal of the endothelium (using a wooden toothpick) from artery segments prior to culture decreased the E2‐mediated increase in SERCA 2b and PKG expression by 45% and 47%, respectively. Overall, the findings suggest that one of the potential cardiovascular benefits of E2 in women is upregulation of SERCA 2b, via activation of the classic ER α and ER β pathway.