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Prostaglandin-stimulated second messenger signaling in bone-derived endothelial cells is dependent on confluency in culture (1994)

Ida, Rodney ; Lee, Austin ; Huang, Jason ; [et al.]

New York, NY [u.a.] : Wiley-Blackwell

Journal of Cellular Physiology 160 (1994), S. 585-595

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ISSN: 0021-9541

Keywords: Life and Medical Sciences ; Cell & Developmental Biology

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Biology , Medicine

Notes: New bone formation is associated with an increase in blood flow by the invasion of capillaries. Endothelial cells that line the capillaries can produce paracrine factors that affect bone growth and development, and in turn, could be affected by products produced by bone cells, in particular the osteoblasts. Since osteoblasts produce prostaglandins E2 and F2α (PGE2, PGF2α), it was investigated if these PGs were agonists to bone-derived endothelial cells (BBE) by assessing changes in cAMP and free cytosolic calcium concentration ([Ca2+]i) second messenger generation. We found that confluent cultures of BBE cells, a clonal endothelial cell line derived from bovine sternal bone, responded to 1 μM PGE2 by an increase in cAMP. PGF2α at the same concentration was less potent in stimulating an increase in cAMP production in confluent BBE cells. Subconfluent cells with a morphology similar to that of fibroblastic cells were not as sensitive to PGE2-stimulated cAMP generation. PGF2α failed to elicit any cAMP production in subconfluent cultures. PGE2 and PGF2α both stimulated an increase in [Ca2+]i concentration in a dose-dependent manner. The potency of PGE2 was similar to that of PGF2α in stimulating an increase in [Ca2+]i. The Ca2+ response was mostly independent of extracellular Ca+, was unchanged even with prior indomethacin treatment, was unaffected by caffeine pretreatment, but was abolished subsequent to thapsigargin pretreatment. The PG-induced increase in [Ca2+]i was also dependent on the confluency of the cells. In a subconfluent state, the responses to PGE2 or PGF2α were either negligible, or only small increases in [Ca2+]i were noted with high concentrations of these two PGs. Consistent, dose-dependent increases in [Ca2+]i were stimulated by these PGs only when the cells were confluent and had a cobblestoned appearance. Since it was previously demonstrated that BBE cells respond to parathyroid hormone (PTH) by the production of cAMP, we tested if bovine PTH(1-34) amide bPTH(1 - 34) also increased [Ca2+]i in these cells. No change in [Ca2+]i was found in response to bPTH (1 - 34), although bPTH (1 - 34) stimulated a nine to tenfold increase in cAMP. We conclude that BBE cells respond to PGE2 and PGF2α but not to bPTH(1 - 34) by an increase in [Ca2+]i probably secondary to stimulation of phospholipase C and that the cAMP and [Ca2+]i second messenger responses in BBE cells are dependent on the state of confluency of the cells. © 1994 Wiley-Liss, Inc.

Additional Material: 9 Ill.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1002/jcp.1041600322

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Dissociation between parathyroid hormone-stimulated cAMP and calcium increase in UMR-106-01 cells (1992)

Merritt, Bradley S. ; Yamaguchi, Dean T. ; Green, Jacob ; [et al.]

New York, NY [u.a.] : Wiley-Blackwell

Journal of Cellular Physiology 152 (1992), S. 520-528

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ISSN: 0021-9541

Keywords: Life and Medical Sciences ; Cell & Developmental Biology

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Biology , Medicine

Notes: We used the osteogenic sarcoma cell line, UMR-106-01, to determine whether the rise in free cytosolic Ca2+ concentration ([Ca2+]i) and cellular cAMP following PTH stimulation are able to be regulated independently. For this purpose, we compared the effect of a PTH antagonist, stimulation of protein kinase C, augmentation by prostaglandins, and the time course of desensitization of the two cellular responses. Two × 10-7 M of the PTH antagonist 8,18Nle 34Tyr-bPTH(3-34) amide ([Nle, Tyr]bPTH(3-34)A) was required to inhibit 10-9 M bPTH(1-34)-stimulated cAMP generation by 50%. 10-7 M bPTH(1-34) completely overcame the inhibition induced by 10-6 M [Nle, Tyr]bPTH(3-34)A. Only 7 × 10-8 M and 2.7 × 10-7 M [Nle, Tyr]bPTH(3-34)A were required to half maximally inhibit the [Ca2+]i increase evoked by 3 × 10-8 and 10-7 M bPTH(1-34), respectively. In addition, dissociation between [Ca2+]i and cAMP signals was observed when modulation by protein kinase C and prostaglandins was tested. Preincubation of the cells with 10 nM TPA for 5 minutes markedly inhibited the PTH-evoked [Ca2+]i increase. Short incubation with PGF2α augmented the PTH-evoked [Ca2+]i increase. Similar pretreatments had no effect on the PTH-stimulated cAMP increase. Finally, preincubation with 1.5 × 10-9 M bPTH(1-34) for 20 minutes almost completely blocked the effect of 10-7 M bPTH(1-34) on [Ca2+]i, while preincubation with 5 × 10-9 M bPTH(1-34) for 4 hours was required to inhibit the effect of 10-8 M bPTH(1-34) on cAMP production by 50%. The differences in the regulation of the two PTH-stimulated cellular signaling systems, in particular, the response to antagonists and the time course of desensitization, could be at the level of the PTH receptor(s) or at a postreceptor domain. © 1992 Wiley-Liss, Inc.

Additional Material: 7 Ill.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1002/jcp.1041520311

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