ArticleThe Journal of clinical investigation1992
Role of protein kinase C in parathyroid hormone stimulation of renal 1,25-dihydroxyvitamin D3 secretion.
Article in The Journal of clinical investigation, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 41 citations in OpenAlex.
- Intermittent Administration of Parathyroid Hormone 1-34 Enhances Osteogenesis of Human Mesenchymal Stem Cells by Regulating Protein Kinase Cδ.International journal of molecular sciences · 2017Article
- Heterotrimeric G proteins in the control of parathyroid hormone actions.Journal of molecular endocrinology · 2017Review
- Article
- Chondrogenic differentiation of clonal mouse embryonic cell line ATDC5 in vitro: differentiation-dependent gene expression of parathyroid hormone (PTH)/PTH-related peptide receptor.The Journal of cell biology · 1996Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
PTH is a major regulator of renal proximal tubule 1,25(OH)2D3 biosynthesis. However, the intracellular pathways involved in PTH activation of the mitochondrial 25-hydroxyvitamin D3-1 alpha-hydroxylase (1-OHase) remain unknown. PTH can activate both the adenylate cyclase/protein kinase A (PKA) and the plasma membrane phospholipase C/protein kinase C (PKC) pathways. The present study was undertaken to determine whether PKC may mediate PTH activation of renal 25-hydroxyvitamin D3-1 alpha-hydroxylase activity. Rat PTH 1-34 fragment in vitro translocated PKC activity from cytosolic to soluble membrane fraction from freshly prepared rat proximal tubules. Physiologic concentrations (10(-11)-10(-10) M) of rat PTH 1-34 fragment increased PKC translocation three- to fourfold while PKA activity ratio increased at PTH 10(-7) M. PTH stimulation of PKC and PKA was reduced in the presence of staurosporine (10 nM) by 41 and 29%, respectively. Sangivamycin (10 and 50 microM) also reduced PTH-stimulated PKC translocation, but did not alter PKA activity ratio. In vitro perifusion of renal proximal tubules with PTH (10(-11) M) increased 1,25(OH)2D3 steady-state secretion two- to fourfold. Sangivamycin at the same concentration that inhibited PKC translocation by 52% completely inhibited PTH-stimulated 1,25(OH)2D3 secretion. The present studies indicate that the phospholipase C/PKC pathway may mediate PTH stimulation of mammalian renal proximal tubule 1,25(OH)2D3 secretion.
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Registered trials
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