Systematic assessment of bone resorption, collagen synthesis, and calcification in chick embryonic calvaria in vitro: Effects of prostaglandin E2

Bone ◽  
1993 ◽  
Vol 14 (4) ◽  
pp. 655-659 ◽  
Author(s):  
M. Nagai ◽  
Y. Suzuki ◽  
M. Ota
Endocrinology ◽  
1977 ◽  
Vol 100 (3) ◽  
pp. 668-674 ◽  
Author(s):  
ERNESTO M. CANALIS ◽  
JOHN W. DIETRICH ◽  
DONNA M. MAINA ◽  
LAWRENCE G. RAISZ

2009 ◽  
Vol 4 (2) ◽  
pp. 259-268 ◽  
Author(s):  
Richard J. Murrills ◽  
Elizabeth Shane ◽  
Robert Lindsay ◽  
David W. Dempster

1989 ◽  
Vol 257 (3) ◽  
pp. F336-F340
Author(s):  
R. J. Bolterman ◽  
M. D. Bentley ◽  
S. M. Sandberg ◽  
M. J. Fiksen-Olsen ◽  
J. C. Romero

Like arachidonic acid (AA) and bradykinin (BK), the intrarenal administration of atrial natriuretic peptide (ANP) has been shown to increase the urinary excretion of prostaglandin E2 (PGE2). In the present study, the direct in vitro effects of ANP on PGE2 production were compared with those of AA and BK. Canine renal inner medullary slices were preincubated for 30 min and washed in aerated Krebs-Ringer buffer (37 degrees C). During the final incubation period, with the use of varied concentrations of AA, BK, or ANP in Krebs-Ringer buffer, samples were obtained at 0 and 30 min to be used for radioimmunoassay of PGE2. Although the rate of PGE2 production was significantly increased 11-fold with AA and threefold with BK, it was unaffected by four different doses of ANP (10(-5) to 10(-11) M). Furthermore, the production of PGE2 during basal and stimulated (BK or AA) conditions was significantly blocked by indomethacin but not by ANP. These results indicate that ANP had no direct stimulatory or inhibitory effect on the medullary production of PGE2.


1972 ◽  
Vol 136 (6) ◽  
pp. 1329-1343 ◽  
Author(s):  
Armen H. Tashjian ◽  
Edward F. Voelkel ◽  
Lawrence Levine ◽  
Paul Goldhaber

A transplantable mouse fibrosarcoma, HSDM1, produces a potent bone resorption-stimulating factor. The factor can be extracted from the tumor tissue and harvested from the medium of clonal strains of HSDM1 tumor cells growing in monolayer culture. It has several chemical and biological properties of a prostaglandin. Using radioimmunoassay techniques, we have shown that HSDM1 cells synthesize and secrete large quantities of prostaglandin E2 (PGE2). The specific bone resorption-stimulating activity of the HSDM1 factor extracted from the tumor is high and approximately equal to that of PGE2 as measured in a bone tissue culture system in vitro. Indomethacin, a potent inhibitor of PGE2 synthesis in HSDM1 cells, also inhibits production by the cells of the bone resorption-stimulating factor, and has no detectable nonspecific effects on the bone culture assay system. Mice bearing the HSDM1 tumor have higher levels of both calcium and PGE2 in serum than control mice. We conclude that PGE2 is the bone resorption-stimulating factor produced by HSDM1 tumor cells, and that secretion of PGE2 by the tumor in vivo accounts for the relative hypercalcemia observed in tumor-bearing animals. The HSDM1 tumor cell system constitutes a new model for studying the pathogenesis of hypercalcemia associated with certain malignant tumors.


Sign in / Sign up

Export Citation Format

Share Document