A non-calcemic analog of 1α,25 dihydroxy vitamin D3 (JKF) upregulates the induction of creatine kinase B by 17β estradiol in osteoblast-like ROS 17/2.8 cells and in rat diaphysis

Sömjen, Dalia; Waisman, A.; Lee, J.-K.; Posner, Gary H.; Kaye, Alvin M.

doi:10.1016/s0960-0760(01)00065-6

Cited by 14 publications

(25 citation statements)

References 38 publications

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“…The increased responsiveness to estrogens after pretreatment with Vitamin D or Vitamin D analogs, previously demonstrated in skeletal-derived cells in vitro [7,17,18,29] and pre-pubertal female rat bone in vivo [7,16] has now been demonstrated using Vitamin D analogs in primary human bone cells. This is apparently an indirect effect of multiple Vitamin D or Vitamin D analog treatment due to an increase in estrogen receptors [14,19] (Fig.…”

Section: Discussionmentioning

confidence: 83%

“…Cells were pre-treated daily with vehicle (0.01% ethanol in medium) or Vitamin D analogs, for 3 days, starting on day 1 after seeding, at 1 nM final concentration [7]. On day 4 after seeding, 30 nM E 2 , 300 nM DHT or 3 M RAL, or RAL together with E 2 were added to the cultures for 4 h, followed by harvesting for CK assay.…”

Section: Hormonal Treatmentmentioning

confidence: 99%

“…We demonstrated that pretreatment with 1,25 upregulated responsiveness and sensitivity to 17␤-estradiol and to several selective estrogen receptor modulators (SERMS) in osteoblast-like cell lines (ROS 17/2.8 and SaoS 2) and rat bone, as measured by both the stimulation of the specific activity of CK and the increase in [ 3 H] thymidine incorporation into DNA [7,[14][15][16][17][18]. This mutual interaction between E 2 and Vitamin D was also manifested by an increase in estrogen receptors (ER) after treatment with 1,25 [17,19].…”

Section: Introductionmentioning

confidence: 99%

“…We have studied the interaction of Vitamin D analogs and estrogens in a rat model [6,7] using the increase in the specific activity of creatine kinase (CK) as a response marker. The brain type (BB) isoenzyme of creatine kinase, part of the "energy buffer" system, which regulates the cellular concentration of ATP and ADP, is the major component of the "E 2 -induced protein" of rat uterus [8] and other tissues containing estrogen (E 2 ) receptors [9].…”

Section: Introductionmentioning

confidence: 99%

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Treatment with non-hypercalcemic analogs of 1,25-dihydroxyvitamin D3 increases responsiveness to 17β-estradiol, dihydrotestosterone or raloxifene in primary human osteoblasts

Katzburg

Hendel

Waisman

et al. 2004

The Journal of Steroid Biochemistry and Molecular Biology

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Section: Discussionmentioning

confidence: 83%

Section: Hormonal Treatmentmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Treatment with non-hypercalcemic analogs of 1,25-dihydroxyvitamin D3 increases responsiveness to 17β-estradiol, dihydrotestosterone or raloxifene in primary human osteoblasts

Katzburg

Hendel

Waisman

et al. 2004

The Journal of Steroid Biochemistry and Molecular Biology

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“…Of note, JKF supplemented with CA and SB induced CD11b and CD14 to an extent similar to that seen in cells treated with 1,25D in triple combination (last columns in all panels in Fig 2). Thus, when supplemented by CA and SB, JKF may be a differentiating agent for leukemia cells approximately equipotent with 1,25D in human and murine myeloid leukemia cells, yet reportedly less calcemic [19,32].…”

Section: Carnosic Acid and Sb202190 Increase The Expression Of Celmentioning

confidence: 99%

Differentiation-inducing potency of the seco-steroid JK-1624F2-2 can be increased by combination with an antioxidant and a p38MAPK inhibitor which upregulates the JNK pathway

Zhang¹,

Posner²,

Danilenko³

et al. 2007

The Journal of Steroid Biochemistry and Molecular Biology

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Low calcemic analogs of vitamin D are candidates for differentiation therapy of human myeloid leukemias. We report here that the seco-steroid synthesized to have resistance to intracellular degradation and low calcemia-inducing activity, 1alpha-hydroxymethyl-3beta-16-ene-24,24-difluoro-25-hydroxy-vitamin D 3 (JKF), induces monocytic differentiation in four established human myeloid leukemia cell lines, HL60, U937, THP-1, NB4, and murine myeloid leukemia cells WEHI-3B D -. JKF has differentiation-inducing potency which is slightly lower than the physiologically active form of vitamin D, 1,25(OH) 2 vitamin D 3 (1,25D). However, simultaneous addition of carnosic acid (CA), an antioxidant, and SB20190 (SB), an inhibitor of p38 MAP kinase, increases the differentiation efficiency of JKF to a level similar to the level observed when 1,25D is used in such combinations. We also show for the first time that SB inhibits the phosphorylation of MAPKAPK-2, a downstream target of p38MAPK, but upregulates the phosphorylation of at least one of the isoforms of JNK (p46 JNK1) and of c-jun in all four human myeloid cell lines studied here. These studies indicate that the JNK1 pathway is positively associated with monocytic differentiation of several subtypes of myeloid leukemia cells arrested at different developmental stages. Further, since JKF is less calcemic than 1,25D, the data suggest that JKF combined with CA and SB is likely to have a therapeutic advantage over 1,25D-based experimental regimens for myeloid leukemias.

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Diabetes modulates differentially creatine kinase‐specific activity responsiveness to estradiol‐17β and to raloxifene in rat organs

Sömjen

Shen

Stern

et al. 2006

J of Cellular Biochemistry

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Diabetes mellitus increases the risk for CVD in women. While there is considerable evidence suggesting beneficial effects of estrogen on decreasing lipid peroxidation, atherosclerotic processes, and cardiovascular diseases, diabetes negates most estrogen protective effects as well as the skeletal protective effects of estrogens, which are not discernable in diabetic women. In the present study, we examined the in vivo effects of estradiol-17beta (E2), on creatine kinase (CK)-specific activity, in estrogen-responsive organs from healthy and diabetic rats. Healthy or diabetic (streptozotocin-induced) female rats were injected with either E2 (10-50 microg/rat) or raloxifene (Ral; 500-1,000 microg/rat). Twenty-four hours following the injection, animals were sacrificed; their organs removed and assayed for CK-specific activity. CK-specific activity in different organs [Left ventricle of heart (Lv), uterus (Ut), aorta (Ao), para uterine adipose tissue (Ad), epiphyseal cartilage (Ep), and diaphyseal bone (Di)] from healthy animals, was stimulated with increased doses of E2, with maximum at 20 microg/rat. Age-matched diabetic female rats exhibited a remarkable decreased response to E2 in all organs except Ut. In contrast, the response to Ral was not altered in diabetic rats. Similar results were observed in organs from ovariectomized female rats (Ovx), healthy or diabetic. These results support our previous in vitro findings, demonstrating that hyperglycemia decreases CK response to E2 but not to Ral in cultured human vascular and bone cells. In summary, diabetes mellitus decreases CK response to E2 but not that of Ral in skeletal and vascular tissues. The decreased response to E2 detected in organs derived from diabetic rats might be due to changes in nuclear and/or membrane estrogen receptors and/or other genomic and non-genomic pathways, as was shown in in vitro cellular models.

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A non-calcemic analog of 1α,25 dihydroxy vitamin D3 (JKF) upregulates the induction of creatine kinase B by 17β estradiol in osteoblast-like ROS 17/2.8 cells and in rat diaphysis

Cited by 14 publications

References 38 publications

Treatment with non-hypercalcemic analogs of 1,25-dihydroxyvitamin D3 increases responsiveness to 17β-estradiol, dihydrotestosterone or raloxifene in primary human osteoblasts

Treatment with non-hypercalcemic analogs of 1,25-dihydroxyvitamin D3 increases responsiveness to 17β-estradiol, dihydrotestosterone or raloxifene in primary human osteoblasts

Differentiation-inducing potency of the seco-steroid JK-1624F2-2 can be increased by combination with an antioxidant and a p38MAPK inhibitor which upregulates the JNK pathway

Diabetes modulates differentially creatine kinase‐specific activity responsiveness to estradiol‐17β and to raloxifene in rat organs

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