Retinole acid and glucocorticoids enhance the effect of 1,25‐dihydroxyvitamin D3 on bone γ‐carboxyglutamic acid protein synthesis by rat osteosarcoma cells

Satoru Nishimoto, Carl Salka, Marcel E. Nimni

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Abstract

Two 1,25‐dihydroxyvitamin D3‐controlled parameters in the osteoblastlike osteosarcoma cell line ROS 17/2, bone γ‐carboxyglutamic acid‐containing protein (BGP) and collagen synthesis, were measured after pretreatments with either retinoic acid (RA), or triamcinolone acetate (TRM). RA and TRM both caused double the expected increase in BGP secretion at 16 hr after treatment with 1,25‐dihydroxy vitamin D3. Triamcinolone acetate concentrations of 10−8 and 10−9 M or 10−6 M retinoic acid were effective in enhancing the 1,25‐dihydroxyvitamin D3 stimulation of BGP secretion. Treatment with RA or TRM alone did not stimulate BGP secretion. RA alone had no effect on BGP secretion, while TRM inhibited BGP secretion. Collagen synthesis is inhibited by 1,25‐dihydroxyvitamin D3. Neither retinoic acid nor triamcinolone acetate enhanced the 1,25‐dihydroxyvitamin D3‐mediated inhibition of collagen synthesis. Retinoic acid by itself inhibited collagen synthesis but did not change the 1,25 dihydroxyvitamin D3‐mediated inhibition of collagen synthesis. Triamcinolone acetate by itself or together with 1,25‐dihydroxy vitamin D3 increased collagen synthesis. We conclude that, although both triamcinolone acetate and retinoic acid increase the 1,25‐dihydroxy vitamin D3 stimulation of BGP secretion by ROS 17/2 cells, they have different effects on the regulation of collagen production. Thus, although both hormones increase the 1,25‐dihydroxy vitamin D3 receptor concentration in these cells, their actions are not mediated solely by this mechanism.

Original languageEnglish (US)
Pages (from-to)571-577
Number of pages7
JournalJournal of Bone and Mineral Research
Volume2
Issue number6
DOIs
StatePublished - Jan 1 1987
Externally publishedYes

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Triamcinolone
Osteosarcoma
Tretinoin
Glucocorticoids
Acetates
Collagen
Bone and Bones
Acids
Cholecalciferol
Proteins
Calcitriol Receptors
Hormones
Cell Line

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Orthopedics and Sports Medicine

Cite this

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title = "Retinole acid and glucocorticoids enhance the effect of 1,25‐dihydroxyvitamin D3 on bone γ‐carboxyglutamic acid protein synthesis by rat osteosarcoma cells",
abstract = "Two 1,25‐dihydroxyvitamin D3‐controlled parameters in the osteoblastlike osteosarcoma cell line ROS 17/2, bone γ‐carboxyglutamic acid‐containing protein (BGP) and collagen synthesis, were measured after pretreatments with either retinoic acid (RA), or triamcinolone acetate (TRM). RA and TRM both caused double the expected increase in BGP secretion at 16 hr after treatment with 1,25‐dihydroxy vitamin D3. Triamcinolone acetate concentrations of 10−8 and 10−9 M or 10−6 M retinoic acid were effective in enhancing the 1,25‐dihydroxyvitamin D3 stimulation of BGP secretion. Treatment with RA or TRM alone did not stimulate BGP secretion. RA alone had no effect on BGP secretion, while TRM inhibited BGP secretion. Collagen synthesis is inhibited by 1,25‐dihydroxyvitamin D3. Neither retinoic acid nor triamcinolone acetate enhanced the 1,25‐dihydroxyvitamin D3‐mediated inhibition of collagen synthesis. Retinoic acid by itself inhibited collagen synthesis but did not change the 1,25 dihydroxyvitamin D3‐mediated inhibition of collagen synthesis. Triamcinolone acetate by itself or together with 1,25‐dihydroxy vitamin D3 increased collagen synthesis. We conclude that, although both triamcinolone acetate and retinoic acid increase the 1,25‐dihydroxy vitamin D3 stimulation of BGP secretion by ROS 17/2 cells, they have different effects on the regulation of collagen production. Thus, although both hormones increase the 1,25‐dihydroxy vitamin D3 receptor concentration in these cells, their actions are not mediated solely by this mechanism.",
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AU - Nishimoto, Satoru

AU - Salka, Carl

AU - Nimni, Marcel E.

PY - 1987/1/1

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N2 - Two 1,25‐dihydroxyvitamin D3‐controlled parameters in the osteoblastlike osteosarcoma cell line ROS 17/2, bone γ‐carboxyglutamic acid‐containing protein (BGP) and collagen synthesis, were measured after pretreatments with either retinoic acid (RA), or triamcinolone acetate (TRM). RA and TRM both caused double the expected increase in BGP secretion at 16 hr after treatment with 1,25‐dihydroxy vitamin D3. Triamcinolone acetate concentrations of 10−8 and 10−9 M or 10−6 M retinoic acid were effective in enhancing the 1,25‐dihydroxyvitamin D3 stimulation of BGP secretion. Treatment with RA or TRM alone did not stimulate BGP secretion. RA alone had no effect on BGP secretion, while TRM inhibited BGP secretion. Collagen synthesis is inhibited by 1,25‐dihydroxyvitamin D3. Neither retinoic acid nor triamcinolone acetate enhanced the 1,25‐dihydroxyvitamin D3‐mediated inhibition of collagen synthesis. Retinoic acid by itself inhibited collagen synthesis but did not change the 1,25 dihydroxyvitamin D3‐mediated inhibition of collagen synthesis. Triamcinolone acetate by itself or together with 1,25‐dihydroxy vitamin D3 increased collagen synthesis. We conclude that, although both triamcinolone acetate and retinoic acid increase the 1,25‐dihydroxy vitamin D3 stimulation of BGP secretion by ROS 17/2 cells, they have different effects on the regulation of collagen production. Thus, although both hormones increase the 1,25‐dihydroxy vitamin D3 receptor concentration in these cells, their actions are not mediated solely by this mechanism.

AB - Two 1,25‐dihydroxyvitamin D3‐controlled parameters in the osteoblastlike osteosarcoma cell line ROS 17/2, bone γ‐carboxyglutamic acid‐containing protein (BGP) and collagen synthesis, were measured after pretreatments with either retinoic acid (RA), or triamcinolone acetate (TRM). RA and TRM both caused double the expected increase in BGP secretion at 16 hr after treatment with 1,25‐dihydroxy vitamin D3. Triamcinolone acetate concentrations of 10−8 and 10−9 M or 10−6 M retinoic acid were effective in enhancing the 1,25‐dihydroxyvitamin D3 stimulation of BGP secretion. Treatment with RA or TRM alone did not stimulate BGP secretion. RA alone had no effect on BGP secretion, while TRM inhibited BGP secretion. Collagen synthesis is inhibited by 1,25‐dihydroxyvitamin D3. Neither retinoic acid nor triamcinolone acetate enhanced the 1,25‐dihydroxyvitamin D3‐mediated inhibition of collagen synthesis. Retinoic acid by itself inhibited collagen synthesis but did not change the 1,25 dihydroxyvitamin D3‐mediated inhibition of collagen synthesis. Triamcinolone acetate by itself or together with 1,25‐dihydroxy vitamin D3 increased collagen synthesis. We conclude that, although both triamcinolone acetate and retinoic acid increase the 1,25‐dihydroxy vitamin D3 stimulation of BGP secretion by ROS 17/2 cells, they have different effects on the regulation of collagen production. Thus, although both hormones increase the 1,25‐dihydroxy vitamin D3 receptor concentration in these cells, their actions are not mediated solely by this mechanism.

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