Parathyroid Hormone and Adenosine-3′,5′-Monophosphate Acutely Increase Phospholipids of the Phosphatidate-Polyphosphoinositide Pathway in Rabbit Kidney Cortex Tubules<i>in Vitro</i>by a Cycloheximide-Sensitive Process*

Bidot-López, P; Farese, Robert V.; Sabir, Mohammad A.

doi:10.1210/endo-108-6-2078

Cited by 52 publications

(9 citation statements)

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“…These results are of interest in relation to the reports by Budot-Lopez et al [14] and Farese et al [15]. They showed that PTH and dibutyryl cAMP acutely increased phos pholipids, i.e.…”

Section: Discussionsupporting

confidence: 76%

“…They showed that PTH and dibutyryl cAMP acutely increased phos pholipids, i.e. phosphatidic acid, phosphatidyinositol, phosphatidylinositol 4'-monophosphate and phosphati dylinositol 4',5'-bisphosphate, in rabbit kidney cortical tubules both in vivo and in vitro [14,15]. These anionic phospholipids are important brush-border gentamicin binding sites [16].…”

Section: Discussionmentioning

confidence: 99%

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Parathyroid Hormone Enhances Gentamicin Uptake by Opposum Kidney Cells but Not by LLC-PK1 Cells

Nakahama¹,

Kakihara²,

Fukuhara³

et al. 1991

Nephron

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Parathyroidectomy is proposed to be protective against gentamicin nephrotoxicity in rats. In the present study, we evaluated the effects of bovine PTH(1-34) on gentamicin accumulation in cultured kidney epithelial cell lines, oppossum kidney (OK) cells which possess PTH receptors and LLC-PK1 cells which are devoid of PTH receptors. Ten days after seeding, the culture medium was exchanged for medium containing 1 mM gentamicin and bovine PTH. The cell gentamicin concentration was measured by a substrate-labeled fluorescence immunoassay (TDA gentamicin kit). Gentamicin uptake was accelerated by bovine PTH in OK cells but not in LLC-PK1 cells. The enhancing effect of bovine PTH seems to be mediated by a cAMP-dependent process. The results suggest that PTH accelerates gentamicin accumulation in renal tissues and potentiates gentamicin nephrotoxicity.

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“…These results are of interest in relation to the reports by Budot-Lopez et al [14] and Farese et al [15]. They showed that PTH and dibutyryl cAMP acutely increased phos pholipids, i.e.…”

Section: Discussionsupporting

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Parathyroid Hormone Enhances Gentamicin Uptake by Opposum Kidney Cells but Not by LLC-PK1 Cells

Nakahama¹,

Kakihara²,

Fukuhara³

et al. 1991

Nephron

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“…Several investigators (18)(19)(20)(21) have shown an effect of PTH on renal tubular phosphoinositide metabolism, and one report shows the effect was present in the apical membrane of the proximal renal tubule (18). Some have reported that the stimulation of phosphoinositide metabolism by PTH was cyclic AMP dependent (19). This would remove it from a mechanism of cell activation, and place it in the realm of a biologic response.…”

Section: Introductionmentioning

confidence: 99%

Stimulation of inositol trisphosphate and diacylglycerol production in renal tubular cells by parathyroid hormone.

Hruska¹,

Moskowitz²,

Esbrit³

et al. 1987

J. Clin. Invest.

232

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“…Effects of hormones have been reported on membrane phospholipase A2, arachidonic acid, saturation of phospholipid acyl groups, phosphatidic acid, phosphoinositides, phosphatidylglycerol, and N-methyl transferases (16)(17)(18)(19)(20)(21). The changes in lipids shown to occur in plasma membranes by these hormones have been small, but small changes may produce significant effects through association with receptors or as annulus lipids for membrane proteins (22,23).…”

Section: Discussionmentioning

confidence: 99%

Dexamethasone increases the synthesis of sphingomyelin in 3T3-L1 cell membranes.

Nelson¹,

Murray²

1982

Proc. Natl. Acad. Sci. U.S.A.

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An acute increase in the sphingomyelin content of a plasma membrane-enriched fraction of 3T3-LI cells was produced by incubation of the cells with 0.1 FLM dexamethasone for 4 hr. Dexamethasone also stimulated the activity of the pathway of sphingomyelin synthesis by utilizing the phosphorylcholine of phosphatidylcholine as a donor to ceramide to synthesize the phospholipid (phosphatidylcholine:ceramide cholinephosphotransferase). Dexamethasone-stimulated increase in the utilization of 14C-labeled choline of phosphatidylcholine for the synthesis of sphingomyelin was inhibited by the addition of cycloheximide to the incubation. Therefore, it appears that corticosteroid stimulation of new protein synthesis was required to produce the effect. An increase in the enzymatic pathway by 83% and of the sphingomyelin content of the plasma membrane-enriched fraction by 50% after incubation with dexamethasone for 4 hr demonstrates the rapidity with which the hormone can produce considerable remodeling of the membrane. The increase in the synthetic pathway in the plasma membrane-enriched fraction was sufficient to account for the measured increase in sphingomyelin. It appears likely that the large increase in membrane sphingomyelin could contribute significantly to the many demonstrated effects of corticosteroids upon membrane processes, including transport, receptors, and enzymatic activity.Corticosteroids have widespread effects on the function ofmost cells (1, 2). In the whole animal, deficiency or chronic excess is incompatible with survival. Glucocorticoids are essential for the growth of many cells in culture and have effects upon receptors, enzyme activity, and membrane transport. Most of these effects are thought to be secondary to steroid-receptor interactions influencing protein synthesis, but the proteins or enzymes involved have been identified in only a few instances.We have previously demonstrated an effect of dexamethasone and adrenalectomy upon the sphingomyelin content of human leukocytes and ghosts of rat epididymal fat cells (3-5).These effects have been seen both in vitro and in vivo, and cells obtained from adrenalectomized and intact animals have responded to the hormones. Fat cell ghosts from the adrenalectomized animals contain less sphingomyelin than those obtained from intact animals and undergo a greater increase when exposed to the corticosteroid. Studies of this action of corticosteroids and the mechanism by which it is produced were undertaken with 3T3-L1 cells in culture. METHODS3T3-L1 fibroblasts, obtained from the American Type Culture Collection (Rockville, MD), were cultured in Dulbecco's modified Eagle's medium with 10% fetal calf serum in the presence of 5% CO2 in air. After cells became confluent, they were incubated in media and 10% calf serum at 370C with and without 0.1 AM dexamethasone for 4 hr. When cycloheximide was added to the incubations it was at a concentration of 2 jig/ml.At the end of the incubation period, cells (=7 X 106) were washed with Hanks' balanced salt solut...

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Parathyroid Hormone and Adenosine-3′,5′-Monophosphate Acutely Increase Phospholipids of the Phosphatidate-Polyphosphoinositide Pathway in Rabbit Kidney Cortex Tubulesin Vitroby a Cycloheximide-Sensitive Process*

Cited by 52 publications

References 0 publications

Parathyroid Hormone Enhances Gentamicin Uptake by Opposum Kidney Cells but Not by LLC-PK1 Cells

Parathyroid Hormone Enhances Gentamicin Uptake by Opposum Kidney Cells but Not by LLC-PK1 Cells

Stimulation of inositol trisphosphate and diacylglycerol production in renal tubular cells by parathyroid hormone.

Dexamethasone increases the synthesis of sphingomyelin in 3T3-L1 cell membranes.

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