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The Coexistence of Hypertension and Ovariectomy Additively Increases Cardiac Apoptosis.

Authors: Lin, Yi-Yuan  Cheng, Yu-Jung  Hu, Jun  Chu, Li-Xi  Shyu, Woei-Cherng  Kao, Chung-Lan  Lin, Tzer-Bin  Kuo, Chia-Hua  Yang, Ai-Lun  Lee, Shin-Da 
Citation: Lin YY, etal., Int J Mol Sci. 2016 Dec 6;17(12). pii: ijms17122036. doi: 10.3390/ijms17122036.
Pubmed: (View Article at PubMed) PMID:27929425
DOI: Full-text: DOI:10.3390/ijms17122036

To investigate whether the coexistence of hypertension and ovariectomy will increase cardiac Fas receptor and mitochondrial-dependent apoptotic pathways, histopathological analysis, the TUNEL assay and Western blotting were performed on the excised hearts from three groups of female spontaneously hypertensive rats (SHR), which were divided into a sham-operated group (SHR-Sham), bilaterally ovariectomized group (SHR-OVX) and normotensive Wistar Kyoto rats (WKY). Compared with the WKY group, the SHR-Sham group exhibited decreased protein levels of ERα, ERß, p-Akt/Akt, Bcl-2, Bcl-xL and p-Bad and decreased further in the SHR-OVX group, as well as protein levels of t-Bid, Bak, Bad, Bax, cytochrome c, activated caspase-9 and activated caspase-3 (mitochondria-dependent apoptosis) increased in the SHR-Sham group and increased further in the SHR-OVX group. Compared with the WKY group, protein levels of Fas ligand, TNF-α, Fas death receptors, TNFR1, FADD and activated caspase-8 (Fas receptor-dependent apoptosis) increased in the SHR-Sham group, but did not increase in the SHR-OVX group, except Fas ligand and TNF-α. The coexistence of hypertension and ovariectomy attenuated the estrogen receptor survival pathway and appeared to additively increase the cardiac mitochondria-dependent, but not the Fas receptor-dependent apoptosis pathway, which might provide one possible mechanism for the development of cardiac abnormalities in hypertensive postmenopausal women.


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RGD Object Information
RGD ID: 13782308
Created: 2018-09-04
Species: All species
Last Modified: 2018-09-04
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.