AI Article Synopsis
- Research on human bone marrow endothelial cells (HBMEC) showed that aldosterone exposure for 8 hours led to the upregulation of 6 genes and downregulation of 4 genes related to blood clotting (hemostasis).
- The study detected the endothelial protein C receptor (EPCR) on cell membranes and found that the mineralocorticoid receptor (MCR) was present in the cell nucleus and cytoplasm.
- Aldosterone treatment increased clotting time significantly when HBMEC were exposed to activated protein C, and MCR blockers reduced coagulation time, indicating complex interactions between mineralocorticoid hormones and blood clotting mechanisms.
Article Abstract
In human bone marrow endothelial cell (HBMEC) exposed for 8 h to aldosterone, the microarray screening revealed an upregulation of the mRNAs for six genes and downregulation of mRNAs for four genes, all implicated in hemostasis. In HBMEC, immunocytochemistry revealed the presence of the membrane-bound endothelial protein C receptor (EPCR) whereas the mineralocorticoid receptor (MCR) was present as a nucleo-cytoplasmic. In HBMEC treated with aldosterone the induction of EPCR protein was evident by both FACS analysis and dot blot procedure. When aldosterone-treated HBMEC were incubated with the activated protein C (APC), the partial thromboplastin clotting time (aPTT) increased 2.5-fold over control, from 10 to 25 s. The MCR antagonists aldactone and eplerenone reduced the basal coagulation time in untreated cells to 33.5% and 42% of the control, respectively. These data add an entirely new dimension to delineating the receptor-mediated action of mineralocorticoid hormones.
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| http://dx.doi.org/10.1016/j.bbrc.2008.05.185 | DOI Listing |
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