title: 17Beta-oestradiol regulates the expression of Na+/K+-ATPase beta1-subunit, sarcoplasmic reticulum Ca2+-ATPase and carbonic anhydrase iv in H9C2 cells.
abstract: 1. It is necessary to improve our understanding of the effect of 17beta-oestradiol (E2) on the heart at a molecular and cellular level. In the present study, the effects of E2 on Na(+)/K(+)-ATPase, sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase (SERCA) and carbonic anhydrase IV (CAIV) in H9C2 cells were investigated. To identify the mechanism of action of E2 on these proteins, the oestrogen receptor (ER) antagonist tamoxifen was used. 2. The results indicated that 1 and 100 nmol/L E2 can enhance the activity of Na(+)/K(+)-ATPase and SERCA and upregulate the expression of the Na(+)/K(+)-ATPase beta1-subunit, SERCA2a and CAIV at both the mRNA and protein level compared with 0 and 0.01 nmol/L E2. 17beta-Oestradiol had the greatest effect at 100 nmol/L; 1 micromol/L E2 did not further protein expression compared with 100 nmol/L E2. 3. Tamoxifen (10 nmol/L) significantly decreased the activity of SERCA, as well as the expression of the Na(+)/K(+)-ATPase beta1-subunit and SERCA at the mRNA and protein level, in H9C2 cells cultured with 1 nmol/L E2. Tamoxifen alone had no significant effect on these proteins in H9C2 cells. 4. It may be hypothesized that a suitable E2 concentration has a protective effect on the heart and that the actual dose of E2 used in hormone-replacement therapy is important in menopausal women.
authors: Department of Biochemistry, Xiangya School of Medicine, Central South University, Changsha, Hunan, China.
authors: Chen-Geng
authors: CG
authors: Liu
authors: Ke-Qian
authors: KQ
authors: Xu
authors: Xia
authors: X
authors: Xu
authors: Jian-Jun
authors: JJ
authors: Huang
authors: Jing-Chuan
authors: JC
authors: Xiao
authors: Jie-Ping
authors: JP
authors: Zhang
authors: Hui-Ping
authors: HP
authors: Song
mesh_terms: D000199:Actins / Q000378:metabolism; D000818:Animals; D001639:Bicarbonates / Q000378:metabolism; D015153:Blotting, Western; D030741:Carbonic Anhydrase IV / Q000096:biosynthesis*; D002460:Cell Line; D003600:Cytosol / Q000187:drug effects / Q000201:enzymology; D004958:Estradiol / Q000494:pharmacology*; D004965:Estrogen Antagonists / Q000494:pharmacology; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000378:metabolism; D007527:Isoenzymes; D009206:Myocardium / Q000166:cytology / Q000201:enzymology / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D020133:Reverse Transcriptase Polymerase Chain Reaction; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases / Q000096:biosynthesis*; D000254:Sodium-Potassium-Exchanging ATPase / Q000096:biosynthesis*; D013629:Tamoxifen / Q000494:pharmacology
chemical_list: D000199:Actins; C503554:Atp1b1 protein, rat; D001639:Bicarbonates; D004965:Estrogen Antagonists; D007527:Isoenzymes; D012333:RNA, Messenger; D013629:Tamoxifen; D004958:Estradiol; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D030741:Carbonic Anhydrase IV; D000254:Sodium-Potassium-Exchanging ATPase