Estrogen increases coagulation factor V mRNA levels via both estrogen receptor-alpha and -beta in murine bone marrow/bone
| Autor: | Marie K. Lindberg, Claes Ohlsson, Stanko Skrtic, Sofia Movérare, Karin Dahlman-Wright |
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| Rok vydání: | 2004 |
| Předmět: |
medicine.medical_specialty
medicine.drug_class Endocrinology Diabetes and Metabolism medicine.medical_treatment Gene Expression Mice Endocrinology Bone Marrow Internal medicine Fibrinolysis medicine Animals Estrogen Receptor beta RNA Messenger Blood Coagulation Estrogen receptor beta Oligonucleotide Array Sequence Analysis biology Estradiol Factor V Estrogen Receptor alpha General Medicine Mice Inbred C57BL medicine.anatomical_structure Coagulation Liver Receptors Estrogen Estrogen biology.protein Ovariectomized rat Female Bone marrow Estrogen receptor alpha hormones hormone substitutes and hormone antagonists |
| Zdroj: | European journal of endocrinology. 151(2) |
| ISSN: | 0804-4643 |
| Popis: | OBJECTIVES: Both oral estrogen-based hormone-replacement therapy and contraceptives increase the risk of venous thromboembolism. Several circulating factors involved in coagulation/fibrinolysis are expressed mainly in the liver whilst some are expressed in extrahepatic tissues, including bone marrow. The aim of this study was to identify estrogen-responsive target genes involved in the pathogenesis of estrogen-induced venous thromboembolism. METHODS: Ovariectomized mice were treated with 17beta-estradiol and possible effects on the expression of genes related to coagulation/fibrinolysis were investigated using DNA microarray analyses. RESULTS: None of the selected genes was regulated by 17beta-estradiol in the liver. Interestingly, 17beta-estradiol increased mRNA levels of coagulation factor V in the bone marrow/bone. Furthermore, this stimulatory effect of 17beta-estradiol on coagulation factor V expression can be mediated via both estrogen receptor-alpha and -beta. CONCLUSIONS: The expression of bone marrow-derived, but not liver-derived, coagulation factor V is increased by estrogen treatment in mice. The pathophysiological importance of this finding for estrogen-induced venous thromboembolism remains to be determined. |
| Databáze: | OpenAIRE |
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