ED-71, a novel vitamin D analog, promotes bone formation and angiogenesis and inhibits bone resorption after bone marrow ablation

Okuda, Naoki; Takeda, Satoshi; Shinomiya, Kenichi; Muneta, Takeshi; Itoh, Soichiro; Noda, Masaki; Asou, Yoshinori

doi:10.1016/j.bone.2006.08.017

Cited by 28 publications

(23 citation statements)

References 36 publications

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“…We examined the changes in PTHrP expression and its putative role on the alterations of bone formation after marrow ablation (24,28). The results in these mice were further confirmed by using MC3T3-E1 osteoblastic cells incubated in high-glucose medium.…”

mentioning

confidence: 82%

Role of Parathyroid Hormone-Related Protein in the Decreased Osteoblast Function in Diabetes-Related Osteopenia

Lozano¹,

Castro²,

Dapía

et al. 2009

Endocrinology

107

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A deficit in bone formation is a major factor in diabetes-related osteopenia. We examined here whether diabetes-associated changes in osteoblast phenotype might in part result from a decrease in PTH-related protein (PTHrP). We used a bone marrow ablation model in diabetic mice by multiple streptozotocin injections. PTHrP (1-36) (100 microg/kg, every other day) or vehicle was administered to mice for 13 d starting 1 wk before marrow ablation. Diabetic mice showed bone loss in both the intact femur and the regenerating tibia on d 6 after ablation; in the latter, this was related to decreased bone-forming cells, osteoid surface, and blood vessels, and increased marrow adiposity. Moreover, a decrease in matrix mineralization occurred in ex vivo bone marrow cultures from the unablated tibia from diabetic mice. These skeletal alterations were associated with decreased gene expression (by real-time PCR) of Runx2, osterix, osteocalcin, PTHrP, the PTH type 1 receptor, vascular endothelial growth factor and its receptors, and osteoprotegerin to receptor activator of nuclear factor-kappaB ligand mRNA ratio, and increased peroxisome proliferator-activated receptor-gamma2 mRNA levels. Similar changes were induced by hyperosmotic (high glucose or mannitol) medium in osteoblastic MC3T3-E1 cells, which were mimicked by adding a neutralizing anti-PTHrP antibody or PTH type 1 receptor antagonists to these cells in normal glucose medium. PTHrP (1-36) administration reversed these changes in both intact and regenerating bones from diabetic mice in vivo, and in MC3T3-E1 cells exposed to high glucose. These findings strongly suggest that PTHrP has an important role in the altered osteoblastic function related to diabetes.

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mentioning

confidence: 82%

Role of Parathyroid Hormone-Related Protein in the Decreased Osteoblast Function in Diabetes-Related Osteopenia

Lozano¹,

Castro²,

Dapía

et al. 2009

Endocrinology

107

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“…126,127 Moreover, in vivo studies utilizing several different active vitamin D compounds have corroborated the stimulatory effect of active vitamin D on bone formation and bone accretion. 128 Especially, intriguing is the finding that paricalcitol treatment of LDL receptor knockout mice corrected low bone volume by enhancing bone mineralization and by decreasing bone resorption directly. 129 Treatment of low 25-hydroxyvitamin D levels may also be important for enhancing bone formation, since osteoblasts contain the 1a-hydroxylase enzyme, 65,68 which increases local production of 1,25-dihydroxyvitamin D. Interestingly, osteoblasts also contain megalin receptors, 68 which are known to function as 25-hydroxyvitamin D acceptor proteins that incorporate 25-hydroxyvitamin D into the cell.…”

Section: Vitamin D Receptor Activationmentioning

confidence: 98%

Adynamic bone in patients with chronic kidney disease

Andress

2008

Kidney International

112

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Adynamic bone in patients with chronic kidney disease (CKD) is a clinical concern because of its potential increased risk for fracture and cardiovascular disease (CVD). Prevalence rates for adynamic bone are reportedly increased, although the variance for its prevalence and incidence is large. Differences in its prevalence are largely attributed to classification and population differences, the latter of which constitutes divergent groups of elderly patients having diabetes and other comorbidities that are prone to low bone formation. Most patients have vitamin D deficiency and the active form, 1,25-dihydroxyvitamin D, invariably decreases to very low levels during CKD progression. Fortunately, therapy with vitamin D receptor activators (VDRAs) appears to be useful in preventing bone loss, in part, by its effect to stimulate bone formation and in decreasing CVD morbidity, and should be considered as essential therapy regardless of bone turnover status. Future studies will depend on assessing cardiovascular outcomes to determine whether the risk/reward profile for complications related to VDRA and CKD is tolerable.

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“…Eldecalcitol decreased urinary excretion of deoxypyridinoline, and also decreased bone resorption parameters (eroded surface, osteoclast surface and osteoclast number) of the bone histomorphometrical analysis [4]. Meanwhile, some studies with various rat models indicated that eldecalcitol maintained bone formation [4][5][6][7]. Serum osteocalcin as well as bone formation parameters (bone formation rate and mineral apposition rate) in the bone histomorphometry stayed within the normal range during the eldecalcitol treatment.…”

Section: Introductionmentioning

confidence: 80%

Eldecalcitol is less effective in suppressing parathyroid hormone compared to calcitriol in vivo

Harada¹,

Takeda²,

Uno³

et al. 2010

The Journal of Steroid Biochemistry and Molecular Biology

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ED-71, a novel vitamin D analog, promotes bone formation and angiogenesis and inhibits bone resorption after bone marrow ablation

Cited by 28 publications

References 36 publications

Role of Parathyroid Hormone-Related Protein in the Decreased Osteoblast Function in Diabetes-Related Osteopenia

Role of Parathyroid Hormone-Related Protein in the Decreased Osteoblast Function in Diabetes-Related Osteopenia

Adynamic bone in patients with chronic kidney disease

Eldecalcitol is less effective in suppressing parathyroid hormone compared to calcitriol in vivo

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