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M Lieberherr

Publications and source records attributed to M Lieberherr.

51 records · Page 3Linked to original sources
PubMed1987

Aluminum action on mouse bone cell metabolism and response to PTH and 1,25(OH)2D3.

Aluminum (Al) accumulation in bone is associated with low bone formation and mineralization rates; resorption may also be reduced. The mechanism of these Al-induced changes was investigated using cultured mouse osteoblast-like (OB) and osteoclast-like (OC) cells. The Al effect on bone resorption was measured by the in vitro release of 45Ca and beta-glucuronidase from mouse fetal limb-bones. Al had a biphasic effect. High concentrations (greater than 1.5 X 10(-6) M) of Al inhibited collagen and DNA synthesis, ornithine decarboxylase and alkaline phosphatase activity in OB, and depressed tartrate-resistant acid phosphatase activity in OC. Lower Al concentrations stimulated these cellular activities and 45Ca and beta-glucuronidase release from fetal bones. Al had no effect on basal cAMP levels in OB but inhibited the stimulating effect of bPTH on cAMP content. Al also altered the 1,25(OH)2D3 effects on the ornithine decarboxylase activity of OB cells. These data suggest that: (i) the low bone formation observed in vivo during Al intoxication may be due to the inhibition of collagen synthesis and to depressed cell proliferation; and (ii) Al may indirectly influence bone remodeling by interfering with the actions of bPTH and 1,25(OH)2D3 on bone cells.

Acid Phosphatase↗
PubMed1985

1,25 Dihydroxyvitamin D3 is required for growth-independent expression of alkaline phosphatase in cultured rat osteoblasts.

Osteoblastic cells were isolated from periosteum-stripped parietal bones of neonatal rat calvaria, seeded at low density (5,000 cells/35 mm of Falcon dish), and cultured for 6 days in BGJ medium supplemented with 20% of vitamin D-depleted FCS or vitamin D and calcium-depleted FCS, with daily addition of 1,25 dihydroxyvitamin D3 (10(-9) M) or 24,25-dihydroxyvitamin D3 (10(-9) M). Plating efficiency, clonal growth (number and size distribution of the colonies formed), and the alkaline phosphatase phenotype were evaluated on days 2 and 6 of culture. (1) Culture for 6 days in media not supplemented with 1,25(OH)2D3 led to a significant (P less than 0.001) loss of the alkaline phosphatase phenotype of the osteoblastic cells; the loss was greater in proliferating cells than in nonproliferating ones and occurred in both 0.12 mM or 1.1 mM ionized calcium concentrations. (2) Daily addition of 1,25(OH)2D3 (10(-9) M) but not 24,25(OH)2D3 maintained the basal percentage of Alk Pase positive cell units in non-proliferating cells and significantly reduced the loss of this phenotype in proliferating colonies. (3) This effect did not stem from an action of the hormone on cell growth. 1,25(OH)2D3 was also found to enhance the adhesiveness of the seeded osteoblasts, irrespective of the medium calcium concentration.

Alkaline Phosphatase↗
PubMed1984

Rat endometrial cells in primary culture: effects and interaction of sex hormones and vitamin D3 metabolite on alkaline phosphatase.

The present study was undertaken: 1) to investigate and compare the effects of two sex steroids, 17 beta-estradiol and progesterone, and two vitamin D3 metabolites, 24,25-dihydroxyvitamin D3 (24,25-(OH)2D3) and 1,25-dihydroxyvitamin D3 (1,25-OH)2D3) on the alkaline phosphatase activity (AP) of cultured endometrial cells of ovariectomized animals; 2) to see whether the in vitro or in vivo sex steroid pretreatment modifies the cellular AP responses to these vitamin D3 metabolites. Cells were cultured in Dulbecco's medium with 10% fetal calf serum until confluency and then for 18 h in a serum-free medium. All subsequent studies were performed in a fresh fetal calf serum-free medium. Results show that: 1) in endometrial cells from untreated ovariectomized rats, 17 beta-estradiol (10(-9) M) or progesterone (10(-9) M) induces increases in AP (40% or 30%) after 2- to 4-h incubation, respectively. A maximal increasing effect (20%) is observed with 24,25-(OH)2D3 (10(-9) M) after 4-h incubation contrasting with the total lack of action of 1,25-(OH)2D3 whatever the concentration (10(-13) to 10(-7) M) and the incubation time (1-18 h) tested. 2) After in vivo or in vitro pretreatment with each sex hormone taken separately, both 24,25-(OH)2D3 and 1,25-(OH)2D3 decrease AP whereas after pretreatment with sex steroids in association, these vitamin D3 metabolites induce an increase in AP. In conclusion, these data show that endometrial cell AP is sensitive to 24,25-(OH)2D3 and 1,25-(OH)2D3 and that the AP response of these cells is modulated by the presence of 17 beta-estradiol and/or progesterone.

Alkaline Phosphatase↗
PubMed1983

Rickets and alopecia with resistance to 1,25-dihydroxyvitamin D: two different clinical courses with two different cellular defects.

UNLABELLED: Two unrelated patients, aged 22 months and 31 months, with alopecia and rickets resistant to 1,25-dihydroxyvitamin D (1,25-(OH)2D] (vitamin D-dependency type II) presented with similar biochemical and radiologic features. They were treated with large doses of vitamin D3 derivatives [25-hydroxyvitamin D3 (25-(OH)D3), 1,25-(OH)2D3, and 1 alpha-hydroxyvitamin D3] for 28 months and 6 yr, respectively. In both patients, serum 1,25-(OH)2D levels remained high (approximately 10- to 100-fold normal) during the different therapeutic regimens. Circulating 1,25-(OH)2D and 24,25-dihydroxyvitamin D levels at various stages of the disease suggested in these children disturbances in the regulation of 25-hydroxyvitamin D (25(OH)D) 1 alpha- and 24-hydroxylase systems. In one child, all therapeutic trials were unsuccessful. Studies of her cultured skin fibroblasts showed low capacity (10% normal) for saturable (presumably receptor mediated) nuclear uptake of tritiated 1,25-(OH)2D3; the uptake process of nucleus associated 1,25-(OH)2D3 was normal in apparent affinity for 1,25-(OH)2D3 and in sedimentation velocity of nucleus-associated hormone. In the second child, correction of biochemical abnormalities, healing of rickets, and catch-up growth were obtained during similar therapeutic trials up to the age of 6 yr when a relapse occurred. This relapse has persisted for 2 yr in spite of similar or higher circulating concentrations of 25-(OH)D and 1,25-(OH)2D than those obtained previously when she was responsive to therapy. In her cultured skin fibroblasts, saturable high affinity nuclear uptake of 1,25(OH)2D was unmeasurable. IN CONCLUSION: 1) distinct patterns of clinical response can occur in patients with the syndrome of vitamin D-dependency type II, and can be associated with differing abnormalities in interaction of 1,25-(OH)2D3 with cultured skin fibroblasts; 2) aggravation of the resistance to 1,25-(OH)2D3 may occur during long term therapy in some patients.

24,25-Dihydroxyvitamin D 3↗
PubMed1981

Changes in plasma 1,25 and 24,25-dihydroxyvitamin D after renal transplantation in children.

The purpose of this investigation is to analyze changes in plasma 1,25-(OH)2D and 24,25-(OH)2D after successful renal transplantation in 20 children and young adults. Studies were performed on 8 subjects between the 1st and 10th month and on 12 others between the 20th and 30th to 36th month. Samples were assayed for plasma and urinary calcium, inorganic phosphate, creatinine, plasma bicarbonate, immunoreactive parathyroid hormone, 25-(OH)D, 24,25-(OH)2D, and 1,25-(OH)2D concentrations. Results showed the following: (1) All subjects had normal or high plasma levels of dihydroxyvitamin D metabolites. (2) In subjects with normal GFR's there was a significant inverse correlation between plasma 1,25-(OH)2D concentrations and tubular reabsorption of phosphorus. (3) These correlations were not found in subjects with subnormal creatinine clearances (50 to 100 ml/min/1.73 m2) even though plasma 1,25-(OH)2D concentrations in these subjects were similar to those with normal creatinine clearances. (4) In subjects with subnormal creatinine clearances, an increase in plasma 1,25-(OH)2D concentrations to very high levels was observed during the first months following renal transplantation.

24,25-Dihydroxyvitamin D 3↗
PubMed1979

Interaction of 24,25-dihydroxyvitamin D3 and parathyroid hormone on bone enzymes in vitro.

The in vitro effects of vitamin D3 metabolites, parathyroid extract (PTE), purified parathyroid hormone (bPTH), vitamin A, and heparin on acid and alkaline phosphatases in rat or mouse calvaria in culture were investigated. Results show that: (a) when compared to values found in half calvaria incubated for 24 h in control medium, the bone acid and alkaline phosphatase content is significantly higher in paired halves incubated with PTE (L USP/ml), bPTH (4 x 10(-8)M), heparin (5 USP/ml), vitamin A (23 USP/ml), 25-(OH)D3 (2.5 x 10(-11) to 2.5 x 10(-8)M), 24,25-(OH)2D3, and 1,25-(OH)2D3 (2.5 x 10(-12) to 2.5 x 10(-7M); (b) the presence of 24,25-(OH)2D3 at low concentrations in the incubation medium decreases significantly the PTE, bPTH, vitamin A, or heparin induced stimulation of the phosphatase activities. This interaction is also observed when measuring beta glucuronidase and glucose-6-phosphatase activities and 45Ca release from previously labeled mouse calvaria; (c) a similar activity could not be found with 1,25-(OH)2D3 suggesting that 24,25-(OH)2D3 may have a specific role in bone metabolism.

Acid Phosphatase↗
PubMed1978

The in vitro production and activity of 24, 25-dihydroxycholecalciferol in cartilage and calvarium.

Previously reported results from our laboratory have indicated that 24, 25-dihydroxycholecalciferol can be formed in vitro during incubations of cartilage tissue or cartilage cells with 25-hydroxycholecalcified. They have also demonstrated the high potency of this dihydroxymetabolite of vitamin D3 in stimulating in vitro the sulfate incorporation into proteoglycans of cartilage cells in culture and in decreasing in vitro the parathyroid hormone action on rat calvarium phosphatases activities. The present report shows that 24, 25-)OH)2 D3 can also be produced during rat calvarium incubations with 25-hydroxycholecalciferol and that therefore calvarium as well as cartilage might be both a site of formation and a site of action for 24, 25-(OH)2 D3. The review of recent experimental and clinical investigations strongly suggests that this metabolite has a physiological significance and may be specifically active on some parameters of bone mineralization. Further studies on the cartilage and calvarium abilities to convert 25-hydroxycholecalciferol into 24, 25-(OH)2 D3 shows that this transformation occurs in the mitochondrial fraction but that it does not seem modified by factors known to control the 25-hydroxycholecalciferol metabolism in the kidney. Finally the analysis of experimental and clinical results published so far does not yet bring enough information to understand the significance of this extrarenal metabolism of 25-hydroxycholecalciferol.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1977

Phosphatase content of rat calvaria after in vivo administration of vitamin D3 metabolites.

The effects of acute or chronic administration of small doses (130 pmol) of 25-hydroxycholecalciferol, 24,25-dihydroxycholecalciferol, and 1,25-dihydroxycholecalciferol on rat calvaria acid and alkaline phosphatase activities were investigated in weanling male albino Wistar rats raised on a vitamin D-deficient, low-calcium diet. The results indicate that each of these active metabolites has a different effect on calvarial phosphatase activities. 25-hydroxycholecalciferol causes a significant increase, and 24,25-dihydroxycholecalciferol a decrease in the enzymatic activity. In animals treated with 1,25-dihydroxycholecalciferol these activities are lower after one injection, but after seven daily doses they are not different from those of ethanol-injected control rats. The observed changes do not seem to be related to changes in serum calcium and/or phosphorus concentrations.

Acid Phosphatase↗
PubMedDate not supplied

[Vitamin D metabolism in rat calvarium in vitro (author's transl)].

The in vitro formation of 24, 25-(OH) 2D3 during incubation of rat calvarium with 25-(OH) D3 could be demonstrated. The in vitro synthesis of 24, 25-(OH) 2D3 has been localized in the mitochondrial fraction of the calvarium tissue. It could be detected also in calvarium cells in culture, but results indicate that the ability to synthetize 24, 25-(OH) 2D3 may be specific of some cell types only. The in vitro formation of 24, 25-(OH) 2D3 was observed with calvarium from rat neonates as well as from younger fetal rats, yet, in this latter period the in vitro formation of 24, 25-(OH) 2D3 was not found at all days of pregnancy tested in our experimental conditions (17th to 21st day).

Animals↗