ArticleJournal of the American Society of Nephrology : JASN2016
Phosphorylation of Ribosomal Protein S6 Mediates Mammalian Target of Rapamycin Complex 1-Induced Parathyroid Cell Proliferation in Secondary Hyperparathyroidism.
Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 37 citations in OpenAlex.
- Serum-free culture with PVP enables maintenance of primary culture of parathyroid cells in vitro.Bioscience reports · 2026Article
- The roles of mTORC1 in parathyroid gland function in chronic kidney disease-induced secondary hyperparathyroidism: Evidence from male genetic mouse models and clinical data.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Dicer-Mediated mTORC1 Signaling and Parathyroid Gland Integrity and Function.Journal of the American Society of Nephrology : JASN · 2024Article
- Article
- Role of Calcimimetics in Treating Bone and Mineral Disorders Related to Chronic Kidney Disease.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Molecular Mechanisms of Parathyroid Disorders in Chronic Kidney Disease.Metabolites · 2022Review
- Mechanism of calcitriol regulating parathyroid cells in secondary hyperparathyroidism.Frontiers in pharmacology · 2022Review
- Increasing mTORC1 Pathway Activity or Methionine Supplementation during Pregnancy Reverses the Negative Effect of Maternal Malnutrition on the Developing Kidney.Journal of the American Society of Nephrology : JASN · 2021Article
- Rapamycin and dexamethasone during pregnancy prevent tuberous sclerosis complex-associated cystic kidney disease.JCI insight · 2020Article
- Circadian rhythms of mineral metabolism in chronic kidney disease-mineral bone disorder.Current opinion in nephrology and hypertension · 2020Review
- Parathyroid Cell Proliferation in Secondary Hyperparathyroidism of Chronic Kidney Disease.International journal of molecular sciences · 2020Review
- Towards minimally-invasive, quantitative assessment of chronic kidney disease using optical spectroscopy.Scientific reports · 2019Article
- Novel insights into parathyroid hormone: report of The Parathyroid Day in Chronic Kidney Disease.Clinical kidney journal · 2019Article
- Prenatal Exposure to Methamphetamine: Up-Regulation of Brain Receptor Genes.Frontiers in neuroscience · 2019Article
- Article
- Article
- Proteome-Wide Effect of 17-β-Estradiol and Lipoxin A4 in an Endometriotic Epithelial Cell Line.Frontiers in endocrinology · 2015Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Secondary hyperparathyroidism is characterized by increased serum parathyroid hormone (PTH) level and parathyroid cell proliferation. However, the molecular pathways mediating the increased parathyroid cell proliferation remain undefined. Here, we found that the mTOR pathway was activated in the parathyroid of rats with secondary hyperparathyroidism induced by either chronic hypocalcemia or uremia, which was measured by increased phosphorylation of ribosomal protein S6 (rpS6), a downstream target of the mTOR pathway. This activation correlated with increased parathyroid cell proliferation. Inhibition of mTOR complex 1 by rapamycin decreased or prevented parathyroid cell proliferation in secondary hyperparathyroidism rats and in vitro in uremic rat parathyroid glands in organ culture. Knockin rpS6(p-/-) mice, in which rpS6 cannot be phosphorylated because of substitution of all five phosphorylatable serines with alanines, had impaired PTH secretion after experimental uremia- or folic acid-induced AKI. Uremic rpS6(p-/-) mice had no increase in parathyroid cell proliferation compared with a marked increase in uremic wild-type mice. These results underscore the importance of mTOR activation and rpS6 phosphorylation for the pathogenesis of secondary hyperparathyroidism and indicate that mTORC1 is a significant regulator of parathyroid cell proliferation through rpS6.
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