Humoral factor in children with neonatal Bartter syndrome reduces bone calcium uptake in vitro

1998 ◽  
Vol 12 (5) ◽  
pp. 371-376 ◽  
Author(s):  
Lawrence R. Shoemaker ◽  
William Bergstrom ◽  
Kevin Ragosta ◽  
Thomas R. Welch
Keyword(s):  
Calcium Uptake ◽  
Bartter Syndrome ◽  
Humoral Factor ◽  
Bone Calcium ◽  
Neonatal Bartter Syndrome

scholarly journals HORMONE-LIKE ACTIVITY OF A THYMUS HUMORAL FACTOR ON THE INDUCTION OF IMMUNE COMPETENCE IN LYMPHOID CELLS

1974 ◽  
Vol 139 (1) ◽  
pp. 193-207 ◽  
Author(s):  
Abraham I. Kook ◽  
Nathan Trainin
Keyword(s):  
Adenyl Cyclase ◽  
Lymphoid Cells ◽  
Humoral Factor ◽  
Flufenamic Acid ◽  
Intracellular Camp ◽  
Immune Competence ◽  
Dibutyryl Camp ◽  
Spleen Cells ◽  
Antigenic Challenge

Experiments reported here were performed to understand the mechanism by which THF increases the immunocompetence of spleen cells from NTx mice. Dibutyryl cAMP or substances which increase intracellular levels of cAMP in lymphocytes such as Poly(A:U), theophylline, or PGE2 were shown to mimic the effect of THF and confer reactivity in an in vitro GvH response to spleen cells from NTx mice. Flufenamic acid, an antagonist to PGE2, was shown to inhibit the induction of competence by this substance. It was found that THF induces competence by activating membranal adenyl cyclase which leads to a rise in intracellular cAMP in thymus-derived cells only. These biochemical changes occur before antigenic stimulation and are unrelated to antigenic challenge. These findings indicate that THF exerts its effect via cAMP and are in agreement with the concepts which permit to classify THF as a thymus hormone.

In vitro study of placental trophoblast calcium uptake using JEG-3 human choriocarcinoma cells

1991 ◽  
Vol 98 (3) ◽  
pp. 333-342
Author(s):  
R.S. Tuan ◽  
C.J. Moore ◽  
J.W. Brittingham ◽  
J.J. Kirwin ◽  
R.E. Akins ◽  
...  
Keyword(s):  
Vitamin D3 ◽  
Calcium Uptake ◽  
In Vitro Model ◽  
Dependent Manner ◽  
Choriocarcinoma Cells ◽  
Vitro Model ◽  
Human Choriocarcinoma Cells ◽  
Functional Components ◽  
1,25 Dihydroxy Vitamin D3

During human fetal development, placental syncytiotrophoblasts actively transport calcium from the maternal to the fetal circulation. Two functional components, a cytosolic Ca2(+)-binding protein (CaBP) and a Ca2(+)-ATPase have been identified in the syncytiotrophoblasts of the chorionic villi. We report here the calcium uptake properties of a human choriocarcinoma cell line, JEG-3, which was used as an in vitro model cell system for the syncytiotrophoblasts. In culture, JEG-3 proliferated as large syncytial aggregates expressing typical syncytiotrophoblast markers. 45Ca uptake by JEG-3 was a substrate- and temperature-dependent, membrane-mediated active process that exhibited linear kinetics for up to 7 min. Both the CaBP and the Ca2(+)-ATPase were expressed by JEG-3, on the basis of biochemical, histochemical, immunochemical and or mRNA assays. Immunohistochemistry and in situ hybridization revealed that JEG-3 cells were heterogeneous with respect to the expression of the CaBP. The Ca2(+)-ATPase activity of JEG-3 was similar to the placental enzyme in terms of sensitivity to specific inhibitors, and was detected histochemically along the cell membrane. Fura-2 Ca2+ imaging revealed that calcium uptake by JEG-3 was not accompanied by a concomitant increase in cytosolic [Ca2+], suggesting a specific Ca2+ sequestration mechanism. The involvement of calciotropic hormonal regulation was evaluated by studying the response of JEG-3 to 1,25-dihydroxy vitamin D3. Calcium uptake was significantly stimulated in a dose-dependent manner by a 24-h treatment of the cells with 1,25-dihydroxy vitamin D3 (optimal dose approximately 0.5 nM); the CaBP level doubled whereas steady-state CaBP mRNA did not, suggesting that CaBP expression was regulated by 1,25-dihydroxy vitamin D3. These observations strongly suggest that the JEG-3 human choriocarcinoma cells should serve as a convenient in vitro model system for studying the cellular mechanism and regulation of transplacental calcium transport.

Thyroidectomy of SHR: effects on ventricular relaxation and on SR calcium uptake activity

1986 ◽  
Vol 250 (5) ◽  
pp. H861-H865 ◽  
Author(s):  
R. L. Rodgers ◽  
S. Black ◽  
S. Katz ◽  
J. H. McNeill
Keyword(s):  
Ventricular Hypertrophy ◽  
Calcium Uptake ◽  
Ex Vivo ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Mechanical Relaxation ◽  
Ventricular Relaxation ◽  
Uptake Activity ◽  
Wistar Kyoto

Ventricular hypertrophy and hypothyroidism are each characterized by impaired cardiac muscle relaxation and sarcoplasmic reticulum (SR) calcium uptake activity. A previous report also showed that hypothyroidism does not reverse ventricular hypertrophy (left-to-right ventricular weight ratios) of spontaneously hypertensive rats (SHR). We characterized the effects of thyroidectomy of 8 wk duration on relaxation of ejecting hearts and on SR calcium uptake activity from SHR and nonhypertrophic Wistar-Kyoto rat (WKY) controls. Relaxation was quantified by plotting maximum left ventricular pulse pressure (Pmax) vs. the area under the falling phase of the left ventricular pressure wave at three different pressure loads. Ventricles of euthyroid SHR were characterized by impaired relaxation and depressed SR calcium uptake activity compared with those of euthyroid WKY, confirming earlier studies. Thyroidectomy reduced ventricular relaxation and SR calcium uptake activities to about the same extent in SHR and WKY strains so that these measurements were most depressed in the SHR hypothyroid group. When all groups were considered, the extent of mechanical relaxation ex vivo and the rate of SR calcium uptake in vitro were well correlated.

scholarly journals Parathyroid hormone-related protein regulates intestinal calcium transport in sea bream (Sparus auratus)

2006 ◽  
Vol 291 (5) ◽  
pp. R1499-R1506 ◽  
Author(s):  
Juan Fuentes ◽  
Joana Figueiredo ◽  
Deborah M. Power ◽  
Adelino V. M. Canário
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Transport ◽  
Calcium Uptake ◽  
Sea Bream ◽  
Whole Body ◽  
Related Protein ◽  
Parathyroid Hormone Related Protein ◽  
Intestinal Calcium Transport ◽  
Sparus Auratus

Parathyroid hormone-related protein (PTHrP) is a factor associated with normal development and physiology of the nervous, cardiovascular, immune, reproductive, and musculoskeletal systems in higher vertebrates. It also stimulates whole body calcium uptake in sea bream ( Sparus auratus) larvae with an estimated 60% coming from intestinal uptake in seawater. The present study investigated the role of PTHrP in the intestinal calcium transport in the sea bream in vitro. Unidirectional mucosal-to-serosal and serosal-to-mucosal 45Ca fluxes were measured in vitro in duodenum, hindgut, and rectum mounted in Ussing chambers. In symmetric conditions with the same saline, bathing apical and basolateral sides of the preparation addition of piscine PTHrP 1–34 (6 nM) to the serosal surface resulted in an increase in mucosal to serosal calcium fluxes in duodenum and hindgut and a reduction in serosal to mucosal in the rectum, indicating that different mechanisms are responsive to PTHrP along the intestine. In control asymmetric conditions, with serosal normal and mucosal bathed with a saline similar in composition to the intestinal fluid, there was a net increase in calcium uptake in all regions. The addition of 6 nM PTHrP 1–34 increased net calcium uptake two- to threefold in all regions. The stimulatory effect of PTHrP on net intestinal calcium absorption is consistent with a hypercalcemic role for the hormone. The results support the view that PTHrP, alone or in conjunction with recently identified PTH-like peptides, counteracts in vivo the hypocalcemic effects of stanniocalcin.

Neonatal Bartter syndrome with unilateral multicystic dysplastic kidney disease

2003 ◽  
Vol 18 (4) ◽  
pp. 391-393
Author(s):  
Takuji Tomimatsu ◽  
Hirotsugu Fukuda ◽  
Toru Kanzaki ◽  
Shinya Hirano ◽  
Kazuko Wada ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Bartter Syndrome ◽  
Multicystic Dysplastic Kidney ◽  
Dysplastic Kidney ◽  
Neonatal Bartter Syndrome ◽  
Multicystic Dysplastic Kidney Disease

Metabolic alkalosis decreases bone calcium efflux by suppressing osteoclasts and stimulating osteoblasts

1996 ◽  
Vol 271 (1) ◽  
pp. F216-F222 ◽  
Author(s):  
D. A. Bushinsky
Keyword(s):  
Bone Mineral ◽  
Metabolic Alkalosis ◽  
Collagen Synthesis ◽  
Cell Function ◽  
Urinary Calcium ◽  
Calcium Excretion ◽  
Calcium Efflux ◽  
Medium Ph ◽  
Bone Calcium

In vivo and in vitro evidence indicates that metabolic acidosis, which may occur prior to complete excretion of end products of metabolism, increases urinary calcium excretion. The additional urinary calcium is almost certainly derived from bone mineral. Neutralization of this daily acid load, through the provision of base, decreases calcium excretion, suggesting that alkali may influence bone calcium accretion. To determine whether metabolic alkalosis alters net calcium efflux (JCa+) from bone and bone cell function, we cultured neonatal mouse calvariae for 48 h in either control medium (pH approximately equal to 7.4, [HCO3-] approximately equal to 24), medium simulating mild alkalosis (pH approximately equal to 7.5, [HCO3-] approximately equal to 31), or severe alkalosis (pH approximately equal to 7.6, [HCO3-] approximately equal to 39) and measured JCa+ and the release of osteoclastic beta-glucuronidase and osteoblastic collagen synthesis. Compared with control, metabolic alkalosis caused a progressive decrease in JCa+, which was correlated inversely with initial medium pH (pHi). Alkalosis caused a decrease in osteoclastic beta-glucuronidase release, which was correlated inversely with pHi and directly with JCa+. Alkalosis also caused an increase in osteoblastic collagen synthesis, which was correlated directly with pHi and inversely with JCa+. There was a strong inverse correlation between the effects alkalosis on osteoclastic beta-glucuronidase release and osteoblastic collagen synthesis. Thus metabolic alkalosis decreases JCa+ from bone, at least in part, by decreasing osteoclastic resorption and increasing osteoblastic formation. These results suggest that the provision of base to neutralize endogenous acid production may improve bone mineral accretion.

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