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Biomedical subjects

I Binderman

Publications and source records attributed to I Binderman.

At least 55 records · Page 3Linked to original sources
PubMed1986

Stimulation of creatine kinase activity in rat organs by human growth hormone in vivo and in vitro.

Intraperitoneal injection of human GH (hGH) (4 micrograms/g BW) into 21-day-old rats causes, 24 h later, an increase in creatine kinase (CK) specific activity in kidney (1.7-fold), liver (1.6-fold), and in epiphyseal cartilage (1.8-fold). Similar stimulation was obtained when tissue explants were incubated for 24 h with hGH (1 microgram/ml); CK activity rose 1.8-fold in kidney, 1.9-fold in the liver, and 2.6-fold in epiphyseal cartilage. Highly significant stimulation of CK specific activity was obtained in these same organs in hypophysectomized rats. The increase in CK specific activity in the kidney, to some extent in the liver, but not in the epiphyseal cartilage, was also obtained on in vivo treatment with either human placental lactogen or ovine PRL. Stimulation of CK in these three organs by hGH is followed by a parallel increase in DNA synthesis. Dexamethasone, which was also found to increase CK activity in rat kidney and liver, did not affect the increase of CK by hGH in the kidney, stimulated the effect of hGH in the liver, and partially inhibited the effect of hGH in the epiphyseal cartilage. Diethylaminoethyl cellulose chromatography revealed that the basal and induced activity of CK in all cases was due to the brain type isozyme. On the basis of this evidence for a direct effect of hGH on CK brain type activity, we suggest that its stimulation is potentially a convenient and sensitive assay for biological activity of GH.

Animals↗
PubMed1986

Stimulation of creatine kinase activity by calcium-regulating hormones in explants of human amnion, decidua, and placenta.

We have used stimulation of the activity of the brain type creatine kinase (CK) isoenzyme as a response marker to examine the effects of vitamin D metabolites, PTH, and calcitonin in cultured explants of placenta, decidua, and amnion from normal human deliveries. We found a biological response to PTH in placenta and amnion and to vitamin D metabolites in all three tissues. In the amnion, CK activity increased 2.3-fold after 24 h of incubation in 2.5 nM 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3], 3.8-fold when incubated with 12.5 nM 24,25-dihydroxyvitamin D3 [24,25-(OH)2D3] and 2.7-fold when incubated with 10 U/ml bovine PTH. In the decidua, 24,25-(OH)2D3, but not 1,25-(OH)2D3 or bPTH caused a 1.7-fold increase in CK activity. In contrast, the placenta responded to 1,25-(OH)2D3 with a 1.6-fold increase in CK activity and to bPTH, with a 1.7-fold increase but did not respond to 24,25-(OH)2D3. Bovine calcitonin (100 ng/ml) had no effect on CK activity in any of the three tissues. Nearly all CK in both the unstimulated and stimulated explants was the brain type isoenzyme. CK activity increased significantly between 1 and 4 h after hormonal treatment in all experiments. The enzyme activity rose steeply with dose and reached a significant increase, and usually a plateau, at hormone concentrations considered to be physiological in vivo. [3H]Thymidine incorporation into DNA increased in parallel to stimulation of CK activity in all experiments, except that PTH did not increase DNA synthesis in the placenta. PTH did cause an increase in cAMP production in explants of amnion (1.5-fold) and placenta (2.6-fold).

Amnion↗
PubMed1985

Stimulation of skeletal-derived cell cultures by different electric field intensities is cell-specific.

Pulsed electric stimulation, coupled capacitively to different cell cultures of skeletal origin, caused immediate changes in the cellular levels of cyclic AMP and a later enhanced DNA synthesis. Changes both in cyclic AMP level and DNA synthesis were correlated with the strength of the applied electric field. Cultures of calvaria bone cells which contain mainly two cell types, parathyroid hormone responsive cells (osteoblast-like) and prostaglandin E2 responsive cells (fibroblast-like), respond to both low (13 V/cm) and to high (54 V/cm) electric field strength, with no response at intermediate (24 V/cm) field strength. Rat epiphyseal cartilage responded like bone cells both to low and high field intensities, while rat condylar cartilage responded only to the intermediate field strength. Moreover, subcultures of calvaria bone cells, which lost their osteoblastic phenotype expression during subculturing, were responsive only to low field strength. On the other hand, osteoblast-enriched cultures, derived from calvaria bone grown in low calcium, were responsive only to the high field strength. These findings suggest that the response to various electric field intensities is cell-specific and might be used as an additional parameter to characterize cell types. Our study points to the possibility that when exposing a whole organ to an electrical stimulation it is possible to affect specifically only one cell population out of the many cell types existing in the organ.

Animals↗
PubMed1985

Stimulation of creatine kinase BB activity by parathyroid hormone and by prostaglandin E2 in cultured bone cells.

Bone cells in culture responded to parathyroid hormone (PTH) and prostaglandin E2 (PGE2) by a 2-fold increase in creatine kinase (CK) activity. Combined treatment resulted in a higher response than with PTH alone. Calcitonin (CT) failed to stimulate CK activity, did not affect the response of CK to PTH, but inhibited slightly the increase in CK activity by PGE2. Bone-cell cultures grown in low [Ca2+] (0.125 mM), enriched in PTH-responsive osteoblast-like cells, responded to PTH, but not to PGE2 or CT, by increased CK activity. In both normal and low-[Ca2+] cultures, 8-bromo cyclic AMP did not affect CK activity, nor did it change the response of the cells to PTH, PGE2 or CT. The increase in CK activity was time- and dose-dependent and inhibited both by cycloheximide and by actinomycin D. The isoenzyme of CK stimulated was the CKBB form, the isoenzyme induced by other hormones. This appears to be the first report of the stimulation of CK activity by a polypeptide hormone or a prostaglandin. We suggest that stimulation of CKBB can serve as a marker for the action of a variety of hormones and growth promoters.

Animals↗
PubMed1985

Regulation of creatine kinase activity in rat osteogenic sarcoma cell clones by parathyroid hormone, prostaglandin E2, and vitamin D metabolites.

We have previously shown that both parathyroid hormone (PTH) and prostaglandin E2 (PGE2) stimulate the activity of creatine kinase BB (CKBB) in rat bone cells in culture. Therefore, morphologically distinct rat osteogenic sarcoma cells in culture were tested for stimulation of CKBB activity by hormones that regulate skeletal tissues. PTH stimulated CKBB in the osteoblast-like clone ROS 17/2; 1 alpha,25(OH)2D3 inhibited this activity while PGE2, CT and 24R,25(OH)2D3 had no significant effect. PGE2 stimulated CKBB activity in the fibroblast-like clone ROS 24/1, which was unresponsive to PTH, CT and Vitamin D metabolites. 24R,25(OH)2D3 as well as PGE2 (but not PTH, CT or 1 alpha 25(OH)2D3) stimulated CKBB in clone ROS 25/1, suggesting that this fibroblast-like clone has some chondroblast-like character. Both PTH and PGE2 stimulated the brain type isoenzyme of CK (CKBB), although the osteogenic sarcoma cell clones contain a significant proportion of the muscle type of CK (CKMM). Thus, increased CKBB activity can serve as an additional characteristic marker for the action of steroid and polypeptide hormones and for prostaglandins.

24,25-Dihydroxyvitamin D 3↗
PubMed1985

Autoradiographic localization of 24R,25-dihydroxyvitamin D3 in epiphyseal cartilage.

There is emerging evidence for specific binding sites and biologic action for 24,25(OH)2D3 in the epiphyseal cartilage. The present study was undertaken to identify the target cells of 24,25(OH)2D3 in the epiphyses of rat bone using an autoradiographic technique. Pieces of epiphyseal cartilage obtained from 4-day-old vitamin D-deficient rats were incubated for 15 or 60 min with [3H]-24,25(OH)2D3 in the presence or absence of 100-fold excess of 25(OH)D3, 1,25(OH)2D3, or 24R,25(OH)2D3. The pieces were prepared for autoradiographic study by a new modified fixation method. Cytoplasmic and nuclear concentration of radioactivity was observed in all cell layers of the epiphyseal cartilage except for the hypertrophic cartilage zone. The highest concentration of radioactivity was seen in the proliferating chondroblasts of the columnar zone. After 15 min of incubation the radioactivity was seen mainly in the cell membrane and cytoplasm, whereas at 60 min radioactivity was also prominent in the nuclei. The competition with excess of cold metabolites revealed that only 24R,25(OH)2D3 caused a significant decrease in cytoplasmic and nuclear radioactivity. These data support the biochemical studies showing that the epiphyseal cartilage is a target tissue for 24,25(OH)2D3.

24,25-Dihydroxyvitamin D 3↗
PubMed1985

Brain: body ratio and conceptional age in vascular-induced intrauterine growth retarded rabbits.

Vascular induced intrauterine growth retardation (IUGR) was achieved by total ligation of approximately 30% of the placental vessels to half the fetuses in the last third of gestation in pregnant rabbits. A correlation between brain weight, body weight and head circumference was established in fetuses and rabbit pups in the perinatal period. The brain:body ratio in restricted IUGR animals was significantly higher than their homologous normal controls. A cephalization index based on the brain:body ratio is proposed to assess adverse effects on brain maturity in the presence of IUGR induced by placental insufficiency.

Animals↗
PubMed1985

The cephalization index: a screening device for brain maturity and vulnerability in normal and intrauterine growth retarded newborns.

Predictive estimates of future neurological maldevelopment as a result of vascular induced intrauterine injury are based on the assumption that the body is more affected than the brain resulting in asymmetrical intrauterine growth retarded (IUGR) newborns. The higher the brain:body ratio, the more severe the IUGR process and the greater the risk for the brain to be affected. This prompted us to study in human newborns, a cephalization index based on the ratio of head circumference to body weight to express the degree of brain maturity and possible vulnerability in relation to gestational age. The newborn cephalization index was correlated with neurodevelopment. A trend could be delineated; in the later gestational age, the higher the cephalization index reflecting a greater degree of brain vulnerability, the more severe the clinical pathology; especially the likelihood of cerebral palsy and severe psychomotor retardation. The cephalization index may serve as an additional screening device for high risk intrauterine growth retarded newborns.

Body Weight↗
PubMed1984

Stimulation of creatine kinase BB activity by 1 alpha,25-dihydroxycholecalciferol and 24R,25-dihydroxycholecalciferol in rat tissues.

Vitamin D metabolites stimulate creatine kinase BB activity in organs of vitamin D-deficient rats. In epiphyses of long bones, creatine kinase BB activity increases 2.6-fold 24 h after injection of 24R,25-dihydroxycholecalciferol but not of 1 alpha,25-dihydroxycholecalciferol. Contrariwise, 1 alpha,25-dihydroxycholecalciferol, but not 24R,25-dihydroxycholecalciferol, increases creatine kinase BB activity in diaphyses and in kidney. Neither metabolite affects creatine kinase activity in duodenal mucosa.

24,25-Dihydroxyvitamin D 3↗
PubMed1984

Capacitative pulsed electric stimulation of bone cells. Induction of cyclic-AMP changes and DNA synthesis.

Pulsed electric stimulation, coupled capacitively to bone cells isolated from rat embryo calvaria, caused changes in the intracellular level of cyclic AMP and enhanced DNA synthesis. The capacitive method of electrical stimulation was characterized in terms of displacement currents (0.7-4.0 A) and voltages (10-54 V/cm) prevailing in the stimulation chamber. Changes, both in cyclic AMP and in incorporation of [3H]thymidine into DNA, were correlated with the strength of the applied electric field. Unlike the mechanical stimulation of bone cells, the electrical stimulus was not mediated by de novo synthesis of prostaglandins. The findings suggest that cyclic-AMP changes, induced by the capacitive electrical stimulation of bone cells, trigger DNA synthesis.

Animals↗
PubMed1984

24R,25-dihydroxyvitamin D stimulates creatine kinase BB activity in chick cartilage cells in culture.

In chick limb-bud cartilage cell cultures 24R,25-dihydroxycholecalciferol (24R,25(OH)2D3), but not 24S,25(OH)2D3, 1 alpha,25(OH)2D3 or 25(OH)D3, stimulates the activity of the brain type (BB) isozyme of creatine kinase (EC 2.7.3.2), the 'estrogen-induced protein' first identified in rat uterus. Cultures treated with bromodeoxyuridine, in which cartilage formation is inhibited, show no stimulation of creatine kinase BB by 24R,25(OH)2D3.

24,25-Dihydroxyvitamin D 3↗
PubMed1984

Biochemical pathways involved in the translation of physical stimulus into biological message.

Studies from our laboratory revealed that direct application of physical strain (PS) to cultured bone cells stimulated synthesis of prostaglandin E2 (PGE2) in a specific population of cells. We found that PGE2 induced the cellular production of cAMP in several bone cell types, whereas the induction of DNA synthesis was limited to osteoblastlike cells. Indirect evidence indicated that PS induced the osteoblastlike cells to synthesize PGE2. Other cell types, for example, chondrocytes, when activated by PS, can be induced to produce cAMP and induce DNA synthesis not mediated by PGE2. We have also found that electric stimulation of different populations of bone cells is specifically induced by a certain intensity of the electric field. It seems that electric stimulus circumvents the PGE2 effect and triggers the adenyl cyclase system in the cell directly. The electric field also induces DNA synthesis not via PGE2 production.

Adenylyl Cyclases↗
PubMed1984

Mechanical and hormonal stimulation of cell cultures derived from young rat mandible condyle.

Collagenase digestion of young rat condyles released cells which were grown in culture during two weeks. Morphologically, two populations of cells were distinguished, one of which reacted to alkaline phosphatase and resembled chondroblast or osteoblast-like cells. Parathyroid hormone stimulated a 2-fold increase in cellular cyclic AMP, whereas calcitonin had no effect. Physical forces activated cellular cyclic AMP to a 2.5-fold of control levels and increased the incorporation of radioactive thymidine into DNA by 50 per cent. In contrast to cultured bone cells, the response to physical forces was not inhibited by indomethacin in cultured condyle cells. It seems, therefore, that condyle cells are specific in their response to bone-seeking hormones and physical forces.

Animals↗
PubMed1984

The influence of bis-dequalinium acetate on bone regeneration induced by grafts of combined inorganic heterologous bone and autologous marrow.

The present study was undertaken in order to determine the influence of BDA on bone regeneration and remodeling. Pieces of Kiel bone soaked with autologous bone marrow were implanted in the axial area of rats. The implantation sites were injected with 0.3 cc of 0.005% BDA 3 to 14 days after grafting; the control group was injected with Hartmann solution. Results indicated that BDA does not interfere with the bone-remodeling process. It does, however, have an inhibitory effect on the early stage of mesenchymal cell proliferation, that is, the development of osteoblasts from bone marrow stromal cells. Extrapolation of these findings to earlier evidence regarding the mode of action of this material is currently being investigated.

Animals↗
PubMed1984

24,25-Dihydroxycholecalciferol induces the growth of chick cartilage in vitro.

Recent studies have indicated that 24R,25-dihydroxycholecalciferol [24R,25(OH)2D3] induces development of endochondral bone. It binds specifically to cytoplasmic and nuclear receptors in epiphyseal cartilage cells. In the present investigation we report the effects of 24R,25(OH)2D3 in comparison to other active vitamin-D metabolites on cell growth. This study was performed on micro-mass cell cultures which were prepared from 4.5-day-old embryonic chick skeletal mesenchyme: this culture consists of a high proportion of chondrocytes. Twelve nM 24R,25(OH)2D3 induces a 2-fold increase in [3H] thymidine incorporation into DNA after 24 h of treatment. Other metabolites, either at this or higher concentrations, had no significant effect. [3H]-leucine incorporation into protein and ornithine decarboxylase (ODC) activity were also enhanced only by 24R,25(OH)2D3 at 12 nM (2.4- and 2.0-fold, respectively). These results present supporting evidence for the specific role of 24R,25 (OH)2D3 in the growth and differentiation of developing cartilage cells.

24,25-Dihydroxyvitamin D 3↗
PubMed1983

The effects of 24R,25-dihydroxycholecalciferol and of 1 alpha,25-dihydroxycholecalciferol on ornithine decarboxylase activity and on DNA synthesis in the epiphysis and diaphysis of rat bone and in the duodenum.

The effect of cholecalciferol metabolites on ornithine decarboxylase activity and on DNA synthesis in developing long bones was investigated in vitamin D-depleted rats. In the epiphysis there was a 6.4-fold increase in ornithine decarboxylase activity 5 h after a single injection of 24R,25-dihydroxycholecalciferol but not of 24S,25-dihydroxycholecalciferol or other vitamin D metabolites. In comparison, in the diaphysis and duodenum, 1 alpha,25-dihydroxycholecalciferol, but not other vitamin D metabolites, caused a 3-3.5-fold increase in the enzyme activity. The enzyme activity in the tissues examined attained a maximal value at 5 h after the injection of the metabolites. The activity of ornithine decarboxylase in the epiphysial region increased dose-dependently as the result of a single injection of 24R,25-dihydroxycholecalciferol and attained a maximal value at a dose between 30 and 3000 ng. In addition, administration of 24R,25-dihydroxycholecalciferol, but not 24S,25-dihydroxycholecalciferol or other metabolites, caused within 24 h a 1.7-2.0-fold increase in [3H]thymidine incorporation into DNA of the epiphyses of tibial bones. In comparison, 1 alpha,25-dihydroxycholecalciferol caused a 1.5-fold increase in [3H]thymidine incorporation into DNA of the diaphyses and of the duodenum. The present data indicate that 24R,25-dihydroxycholecalciferol is involved in the regulation of epiphyseal growth, whereas 1 alpha,25,dihydroxycholecalciferol stimulates the proliferation of cells in the diaphysis of long bones and in the intestinal mucosa.

24,25-Dihydroxyvitamin D 3↗