Effects and Interactions of Parathyroid Hormone and Prostaglandins on Adenosine 3',5'-Monophosphate Concentrations in Isolated Renal Tubules*

Biddulph, David M.; Currie, Mark G.; Wrenn, Robert W.

doi:10.1210/endo-104-4-1164

Cited by 15 publications

(10 citation statements)

References 24 publications

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“…Although trypsinization, under the present conditions, did not alter basal levels of cAMP, the response to PTH was inhibited by 80%. That this effect is relatively specific for PTH is demonstrated by the retention of near-normal responsiveness of these cells to PGEz, an observation consistent with the differential effects of trypsin on responsiveness of target cells to these hormones in other tissues [26,27]. In order to assess the time period required for re-establishment of PTH responsiveness following trypsinization, enzyme-treated cells were subcultured and assayed at various times following trypsin treatment (Fig.…”

Section: Resultsmentioning

confidence: 54%

“…This response, therefore, may represent the development of osteogenic precursors that would normally be present in vivo by this time [7]. Experiments using trypsin treatment established the trypsinsensitive nature of the PTH receptor, as has been extensively documented in established PTH target cells in renal tissue [26,27]. As has been previously demonstrated in renal tissue [26,27], trypsin selectively altered PTH receptors in limb cells while having little effect on PGE2 receptors.…”

Section: Discussionmentioning

confidence: 53%

“…To further assess the role of chondrogenesis in the development of the P T H response, stage 2 4 -2 5 limb cells were grown in the presence of mouse serum (10%) during the last 24 h of the 48 h culture period. As can be seen in Table 1, [26,27]. In order to determine the existence of similar receptors (which are requisite to activation of adenylate cyclase by PTH) in chick limb cells, stage 24-25 limb cells were cultured for 48 h to obtain PTH-sensitive cells.…”

Section: Resultsmentioning

confidence: 99%

“…The validity for this approach is based on the well-documented fact that established target cells for both hormones in a variety of tissues from several species contain adenylate cyclase-coupled receptors [6,13,26]. Hormone: receptor interaction leads to activation of adenylate cyclase [6,13] and increased intracellular concentrations of cAMP [5,13,27], which are thought to mediate a variety of metabolic effects in target cells of both hormone types [11,13,28]. Furthermore, skeletal tissue [5,6] as well as cartilage [4] contain established target cells for both PTH and PGE2.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, the hormone-mediated increase in cAMP levels, utilized in the present study, provides an appropriate means of detecting the presence of both PTH and PGE2-sensitive cell types. When the potent phosphodiesterase inhibitor 1-methyl-3-isobutylxanthine (MIX) [29] is used, the accumulation of cAMP should accurately reflect receptormediated activation of adenylate cyclase by these hormones [27].…”

Section: Discussionmentioning

confidence: 99%

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Development of the cyclic AMP response to parathyroid hormone and prostaglandin E2 in the embryonic chick limb

1981

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The developing chick limb was studied to determine the ability of parathyroid hormone (PTH) and prostaglandin E2 (PGE2) to increase intracellular cyclic AMP (cAMP) during various stages of development. All developmental stages examined (stages 20-21, 24-25, and 26-28) responded to PGE2 when the cells were assayed immediately following the removal of the limbs from the embryos. In contrast, only stage 26-28 limb cells responded to PTH when assayed in a similar manner. The response to PTH was temporally correlated with the appearance of cartilage matrix in vivo. Undifferentiated limb cells were also cultured and assayed at various times for hormone responsiveness. Stage 24-25 high-density cell cultures responded initially to PGE2 but not to PTH. However, by 36 h and in all subsequent time intervals tested, the response to PTH was significantly greater than that to PGE2. The PTH receptor, in contrast to that of PGE2, was shown to be sensitive to trypsin treatment, but could be generated during subsequent cell culture. The majority of the hormone-responsive cells were found in cartilaginous regions of the limb, and were shown to respond to both hormones in a dose-dependent manner. The PTH-induced cAMP response was affected by low cell density and mouse serum, both of which significantly inhibit the chondrogenic potential of cultured limb cells. These findings are consistent with a temporal correlation between the development of the PTH response and chondrogenesis in vivo.

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Section: Resultsmentioning

confidence: 54%

Section: Discussionmentioning

confidence: 53%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Development of the cyclic AMP response to parathyroid hormone and prostaglandin E2 in the embryonic chick limb

1981

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Parathyroid Hormone and Calcitonin

Kleeman¹

1985

Contemporary Endocrinology

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Development of PTH-responsive adenylate cyclase activity during chondrogenesis in cultured mesenchyme from chick limb buds

Capehart

Biddulph

1991

Calcif Tissue Int

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The present study investigated the development of parathyroid hormone (PTH)-responsive adenylate cyclase (AC) activity in chondrogenic cells differentiating from chick limb mesenchyme in culture. Mesenchyme from stage 25 chick embryos was removed from the distal tip (0.3 mm) of limb buds and cultured for a 6 day period in high density micromass cultures. Under these conditions, initial appearance of cartilage matrix and chondroblasts occurred on day 3 of culture and rapidly progressed over the next 3 days to produce, by day 6, a highly confluent and homogeneous layer of cartilage matrix and chondrocytes. Cells initially dissociated from limb mesenchyme on day 0 were essentially unresponsive to PTH, but development of AC-coupled, PTH receptors occurred rapidly during the initial 24 hours of culture. Based on data from dose-response experiments, prechondrogenic cells on day 1 of culture had synthesized their full complement of these receptors relative to fully differentiated chondrocytes in cultures at day 6. Inhibition of chondrocyte differentiation by retinoic acid did not significantly affect the initial development of AC-coupled, PTH receptors but it almost completely prevented synthesis of cartilage matrix. The results indicate that development of AC-coupled PTH receptors during chondrogenesis precedes, by at least 48 hours, overt differentiation of chondrocytes and the accumulation of cartilage-specific extracellular matrix and appears to represent one of the earliest reported events in chondrocyte differentiation. The lack of effect of retinoids on development of these receptors indicates that the inhibitory effects of retinoids on differentiating cartilage are at least somewhat specific for genes regulating synthesis of extracellular matrix molecules.

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Effects and Interactions of Parathyroid Hormone and Prostaglandins on Adenosine 3',5'-Monophosphate Concentrations in Isolated Renal Tubules*

Cited by 15 publications

References 24 publications

Development of the cyclic AMP response to parathyroid hormone and prostaglandin E2 in the embryonic chick limb

Development of the cyclic AMP response to parathyroid hormone and prostaglandin E2 in the embryonic chick limb

Parathyroid Hormone and Calcitonin

Development of PTH-responsive adenylate cyclase activity during chondrogenesis in cultured mesenchyme from chick limb buds

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