Alterations in hormone-sensitive adenylate cyclase of cloned rat osteosarcoma cells during long-term culture

Gutiérrez, Gloria; Mundy, Gregory R.; Katz, Michael

doi:10.1002/jbmr.5650010404

Cited by 14 publications

(1 citation statement)

References 23 publications

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“…Our data describe similar initial attachment to smooth and roughened titanium surfaces but a distinct reduction in attachment to NCPIT surfaces by osteoblasts (similar to other studies), whereas osteosarcoma (UMR‐106 cells) displayed a pronounced increase in migration. Although UMR‐106 cells have been used for years as a model system for osteoblast differentiation, 33‐36 our data indicate that the UMR cells do not represent a good model system for examining osteoblast interaction with titanium surfaces.…”

Section: Discussionmentioning

confidence: 83%

Altered Cell Motility and Attachment With Titanium Surface Modifications

Palaiologou

Stoute

Fan

et al. 2012

Journal of Periodontology

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Section: Discussionmentioning

confidence: 83%

Altered Cell Motility and Attachment With Titanium Surface Modifications

Palaiologou

Stoute

Fan

et al. 2012

Journal of Periodontology

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Consistent patterns of changing hormone responsiveness during continuous culture of cloned rat calvaria cells

Aubin

Tertinegg²,

Ber³

et al. 1988

Journal of Bone and Mineral Research

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The loss of responsiveness to hormones in cell populations is a fundamental problem in cell biology and aging. We have studied this process in cloned rat calvaria (RC) bone cell populations maintained in exponential growth in long-term culture in alpha-minimal essential medium supplemented with fetal bovine serum. At various times after cloning, the populations were tested for their ability to respond to parathyroid hormone (PTH), prostaglandin E2 (PGE2), and L-isoproterenol (IPT) with an increase in intracellular cAMP. Clone RCB 2.2, which was originally responsive to PTH but not PGE2, maintained this characteristic throughout 14 mo of culture, after which PTH responsiveness was gradually lost and a concomitant increase in responsiveness to PGE2 was observed. Subsequently, PGE2 responsiveness was also lost; however, continued response to IPT indicated the presence of a hormone-sensitive adenylate cyclase. A similar pattern of hormone responsiveness was observed when a number of frozen stocks of RCB 2.2 cells were thawed and the cells were again maintained in continuous culture. That this pattern of phenotypic change was not unique to clone RCB 2.2 was verified by assessing the hormone responses in other independently selected clones. Although the precise time sequence for hormone response changes was not constant, in all cases the pattern of hormone response changes was similar: i.e., PTH response was always lost and PGE2 response often first increased and then also was lost, despite the maintenance of response to IPT. These data indicate that clonal hormone-responsive populations can reproducibly give rise to unresponsive populations in an ordered series of phenotypic changes.(ABSTRACT TRUNCATED AT 250 WORDS)

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Transforming growth factor β enhances parathyroid hormone stimulation of adenylate cyclase in clonal osteoblast‐like cells

Gutiérrez

Mundy

Manning

et al. 1990

Journal Cellular Physiology

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The effects of transforming growth factor beta (TGF beta) on parathyroid hormone (PTH)-responsive adenylate cyclase were examined in clonal rat osteosarcoma cells (UMR-106) with the osteoblast phenotype. Purified TGF beta incubated with UMR-106 cells for 48 hr produced a concentration-dependent increase in PTH stimulation of adenylate cyclase, with maximal increase in PTH response (37%) occurring at 1 ng/ml TGF beta. TGF beta also enhanced receptor-mediated activation of adenylate cyclase by isoproterenol and prostaglandin E2 (PGE2) and nonreceptor-mediated enzyme activation by cholera toxin and forskolin. In cells in which PTH-stimulated adenylate cyclase activity was augmented by treatment with pertussis toxin, the incremental increase in PTH response produced by TGF beta was reduced by 33%. However, TGF beta neither mimicked nor altered the ability of pertussis toxin to catalyze the ADP-ribosylation of a 41,000-Da protein, presumably the alpha subunit of the inhibitory guanine nucleotide-binding regulatory component (Gi) of adenylate cyclase, in cholate-extracted UMR-106 cell membranes. TGF beta also had no effect on the levels of alpha or beta subunits of Gi, as assessed by immunotransfer blotting. In time course studies, brief (less than or equal to 30 min) exposure of cells to TGF beta during early culture was sufficient to increase PTH response but only after exposed cells were subsequently allowed to grow for prolonged periods. TGF beta enhancement of PTH and isoproterenol responses was blocked by prior treatment of cells with cycloheximide but not indomethacin. The results suggest that TGF beta enhances PTH response in osteoblast-like cells by action(s) exerted at nonreceptor components of adenylate cyclase. The effect of TGF beta may involve Gi, although in a manner unrelated to either pertussis toxin-catalyzed ADP-ribosylation of the alpha subunit of Gi or changes in levels of Gi subunits. The regulatory action of TGF beta on adenylate cyclase is likely to be mediated by the rapid generation of cellular signals excluding prostaglandins, followed by a prolonged sequence of events involving protein synthesis. These observations suggest a mechanism by which TGF beta may regulate osteoblast responses to systemic hormones.

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Alterations in hormone-sensitive adenylate cyclase of cloned rat osteosarcoma cells during long-term culture

Cited by 14 publications

References 23 publications

Altered Cell Motility and Attachment With Titanium Surface Modifications

Altered Cell Motility and Attachment With Titanium Surface Modifications

Consistent patterns of changing hormone responsiveness during continuous culture of cloned rat calvaria cells

Transforming growth factor β enhances parathyroid hormone stimulation of adenylate cyclase in clonal osteoblast‐like cells

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