Reciprocal modulation by sex steroid and calciotrophic hormones of skeletal cell proliferation
Autor: | Yosef Weisman, Arie Harell, Alvin M. Kaye, N. Jaccard, Dalia Somjen |
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Rok vydání: | 1990 |
Předmět: |
Male
medicine.medical_specialty 24 25-Dihydroxyvitamin D 3 Endocrinology Diabetes and Metabolism medicine.medical_treatment Clinical Biochemistry Parathyroid hormone Biology Biochemistry Bone and Bones Endocrinology Calcitriol Internal medicine medicine Animals Testosterone Growth Plate Vitamin D Receptor Molecular Biology Creatine Kinase Cells Cultured Estradiol Cell growth Cartilage Cell Biology DNA Embryo Mammalian Rats Steroid hormone medicine.anatomical_structure Cell culture Sex steroid Parathyroid Hormone Molecular Medicine Female Cell Division Hormone |
Zdroj: | The Journal of steroid biochemistry and molecular biology. 37(4) |
ISSN: | 0960-0760 |
Popis: | We have demonstrated previously that 17β-estradiol (E 2 ) stimulates cell proliferation in skeletal tissues, as measured by increased DNA synthesis and creatine kinase (CK) specific activity, and that calciotrophic hormones modulate E 2 activity in rat osteoblastic sarcoma cells (ROS 17/2.8). Moreover, E 2 failed to stimulate DNA synthesis in vitamin D-depleted female rat bone in the absence of prior i.p. injections of 1,25(OH) 2 D 3 . We have, therefore, studied the effects of pretreatment of cells by one hormone on their response to challenge by a second hormone. We now report reciprocal interactions of sex steroids and other hormones modulating bone formation on cell proliferation parameters in primary bone and cartilage cell cultures; these interactions can selectively augment or diminish cell responsiveness to a given hormone. Pretreatment of rat epiphyseal cartilage cell cultures with 1,25(OH) 2 D 3 , 24,25(OH) 2 D 3 or parathyroid hormone (PTH) for 5 days, followed by E 2 treatment for 24 h, resulted in increased DNA synthesis compared to cultures pretreated with vehicle. Prostaglandin (PGE 2 ) pretreatment blocked further response to E 2 . In the reciprocal case, rat epiphyseal cartilage cells, pretreated with E 2 , showed an increased response to PTH, a loss of the response to PGE 2 or 24,25(OH) 2 D 3 and an inhibition of CK activity and DNA synthesis by 1,25(OH) 2 D 3 , similar to the characteristic inhibitory action of 1,25(OH) 2 D 3 in osteoblasts. By contrast, rat epiphyseal cartilage cells pretreated with testosterone showed no changes in response to PTH, 24,25(OH) 2 D 3 or PGE 2 and a decreased response to E 2 , but were stimulated by 1,25(OH) 2 D 3 . Rat embryo calvaria cell cultures behaved similarly to epiphyseal cartilage cultures except that 24,25(OH) 2 D 3 pretreatment did not increase the response to E 2 . Reciprocally, pretreatment with E 2 before exposure to calciotrophic hormones did not change the responses of rat embryo calvaria cell cultures to 1,25(OH) 2 D 3 or 24,25(OH) 2 D 3 . These findings suggest that the mutual interactions between calciotrophic hormones and E 2 , demonstrated here in vitro , could selectively affect the responses of bone and cartilage cells to E 2 by several mechanisms. These possibilities include increased E 2 receptors and E 2 -stimulated differentiation of cartilage cells to more E 2 responsive cells showing some characteristics of osteoblasts. |
Databáze: | OpenAIRE |
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