Parathyroid hormone acutely increases polyphosphoinositides of the rabbit kidney cortex by a cycloheximide-sensitive process.

Farese, Robert V.; Bidot-López, P; Sabir, Ayub M.; Smith, Jacqueline; B, Schinbeckler; Larson, Ronald E.

doi:10.1172/jci109818

Cited by 56 publications

(12 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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%

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

Nakahama¹,

Kakihara²,

Fukuhara³

et al. 1991

Nephron

View full text Add to dashboard Cite

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.

show abstract

“…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%

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

Nakahama¹,

Kakihara²,

Fukuhara³

et al. 1991

Nephron

View full text Add to dashboard Cite

show abstract

“…OK cells are PTH responsive, and PTH has been shown to acutely increase production of phos phatidylinositols in rabbit proximal tubules [134]. 'Toxic' effects of PTH could be mediated by changes in intracel- 392 Thomas/Schreiner Proteinuria and Progressive Renal Injury lular lipids, including lipid second messengers.…”

Section: Resultsmentioning

confidence: 99%

“…Farese et al [134] showed that PTH increases phosphatidylinositols in rab bit kidney tubules. This effect of PTH peaked at 20 min and then declined.…”

Section: Concluding Discussionmentioning

confidence: 99%

Contribution of Proteinuria to Progressive Renal Injury: Consequences of Tubular Uptake of Fatty Acid Bearing Albumin

Thomas

Schreiner²

1993

Am J Nephrol

112

View full text Add to dashboard Cite

Proteinuria is a marker of a poor prognosis in the glomerulonephritides and progressive renal disease. Recent animal studies have directly implicated proteinuria in inflammatory tubulointerstitial injury. The proximal tubule takes up significant amounts of lipid in the human nephrotic syndrome. We propose that proximal tubular uptake and metabolism of lipids, notably fatty acid bearing albumin, contributes to the chronic tubulointerstitial infiltration and injury associated with heavy proteinuria. Work in our laboratory has shown that a novel nonpolar lipid released by proximal tubules endocytosing fatty acid-bearing albumin is a potent macrophage chemoattractant. We have also studied the metabolic destiny of fatty acids liberated upon proximal tubular catabolism of albumin. Palmitate was preferentially metabolized to phosphatidylcholines, phosphatidylinositols and diglycerides. Oleate and linoleate were metabolized to triglycerides. Palmitate was profoundly inhibitory to OK cell growth, whilst oleate was stimulatory. In nephrosis, faced with an unregulated influx of fatty acids on albumin, the proximal tubule metabolizes them to a variety of lipids, some of which have pathological effects. Thus, the metabolism of albumin-bound fatty acids by the proximal tubule during heavy proteinuria may directly underlie subsequent tubulointerstitial inflammation and altered response to injury.

show abstract

“…A decline in circulating parathyroid hormone (PTH) levels may also participate in the effect. PTH has been shown to increase the levels of acidic phospholipids in the renal cortex (46,47). Suppression of PTH release by oral calcium loading may result in a decline in the number of high affinity binding sites in the renal tubular cell, diminish gentamicinmembrane interactions, and reduce the toxic potential of the antibiotic.…”

Section: Discussionmentioning

confidence: 99%

Calcium is a competitive inhibitor of gentamicin-renal membrane binding interactions and dietary calcium supplementation protects against gentamicin nephrotoxicity.

Humes¹,

Sastrasinh²,

Weinberg³

1984

J. Clin. Invest.

126

View full text Add to dashboard Cite

Parathyroid hormone acutely increases polyphosphoinositides of the rabbit kidney cortex by a cycloheximide-sensitive process.

Cited by 56 publications

References 22 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

Contribution of Proteinuria to Progressive Renal Injury: Consequences of Tubular Uptake of Fatty Acid Bearing Albumin

Calcium is a competitive inhibitor of gentamicin-renal membrane binding interactions and dietary calcium supplementation protects against gentamicin nephrotoxicity.

Contact Info

Product

Resources

About