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29. Rivaroxaban significantly inhibits the stimulatory effects of bone-modulating hormones: In vitro study of primary female osteoblasts.

Author

Somjen, Dalia, Sharfman, Zachary T., Katzburg, Sara, Sharon, Orli, Maman, Eran, Salai, Moshe, Stern, Naftali, and Dolkart, Oleg

Subjects
*RIVAROXABAN, *OSTEOBLASTS, *ORTHOPEDIC surgery, *ANTICOAGULANTS, *ENERGY metabolism, *CELL growth, *CELL lines
Abstract

Background:Anticoagulant therapy is a mainstay of treatment subsequent to major orthopedic surgeries. Evidence linking anticoagulant therapy, osteoporosis, and delayed fracture healing is not conclusive. We have previously reported that rivaroxaban significantly inhibited cell growth and energy metabolism in a human osteoblastic cell line. This study analyzed the response of primary female osteoblast cells to rivaroxaban in combination with various bone-modulating hormones.Methods:Bone samples were taken from both premenopausal (pre-Ob) and postmenopausal (post-Ob) women. Cells were isolated from each sample and cultured to sub-confluence. Each sample was then treated with Rivaroxaban (10 µg/ml) in combination with the following hormones or with the hormones alone for 24 hours: 30nM estradiol-17β (E2), 390nM estrogen receptor α (ERα) agonist PPT, 420nM estrogen receptor β (ERβ) agonist DPN, 50nM parathyroid hormone (PTH), and 1nM of vitamin D analog JKF.Results:No effects were observed after exposure to rivaroxaban alone. When pre-Ob and post-Ob cells were exposed to the bone-modulating hormones as a control experiment, DNA synthesis and creatine kinase (CK)-specific activity was significantly stimulated with a greater response in the pre-Ob cells. When the cells were exposed to rivaroxaban in combination with bone-modulating hormones, the increased DNA synthesis and CK-specific activity previously observed were completely attenuated.Conclusions: Rivaroxaban significantly inhibited the stimulatory effects of bone-modulating hormones in both pre-Ob and post-Ob primary human cell lines. This finding may have clinical relevance for patients at high risk of osteoporosis managed with rivaroxaban or other factor Xa inhibitors. [ABSTRACT FROM PUBLISHER]

Published
2017
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33. The response of cells derived from the supraspinatus tendon to estrogen and calciotropic hormone stimulations: in vitro study.

Author

Maman, Eran, Somjen, Dalia, Maman, Ettie, Katzburg, Sarah, Sharfman, Zachary T., Stern, Naftali, and Dolkart, Oleg

Subjects
*ROTATOR cuff injuries, *TENDON injuries, *ESTROGEN, *CALCIUM regulating hormones, *ESTRADIOL, *THERAPEUTICS
Abstract

Purpose: The most frequent complications after rotator cuff repair (RCR) are non-healing and re-tear. Age and gender are both proven risk factors for faulty RCR. This study analyzed the effects of female sex steroids and calciotropic hormones on tendon-derived cell characteristics. Methods: Tendon-derived cells from rat supraspinatus were treated with estradiol-17β (E2); soy isoflavones (daidzein, genistein, biochainin A); raloxifene and estrogen receptors α and β agonists and antagonists; and less-calcemic vitamin-D analog, parathyroid hormone, and vehicle control for 24 h. Cell proliferation and mRNA expression of estrogen receptor α and β, vitamin-D receptor (VDR), scleraxis, and collagen-1 were assessed. Results: E2, Biochainin A, raloxifene, and vitamin-D significantly increased tendon-derived cell proliferation. Estrogen receptor α antagonists neutralized tendon-derived cells response to estradiol 17-β; however, estrogen receptor β antagonists did not have an effect. Scleraxis expression decreased following estradiol 17-β and vitamin-D treatments. Vitamin-D significantly reduced collagen-1 expression, while estradiol 17-β had no effect. Vitamin-D and estradiol 17-β upregulated VDR expression. Conclusions: Significant tendon-derived cell proliferation can be achieved with commonly prescribed female sex and calciotropic hormones. However, collagen-1 expression remained constant or decreased following the administration of these hormones. Female sex steroids and vitamin-D promoted tendon-derived cell proliferation via estrogen receptor α and VDR, not estrogen receptor β. Amplified cell proliferation was not associated with increased scleraxis and collagen-1 expression. These results have important implications to the properties of healing tendon and possible pharmaceutical therapies for patients with torn RC. Further research is warranted to expose the underling mechanisms of these effects. [ABSTRACT FROM AUTHOR]

Published
2016
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