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• W2023345060 abstract "The parathyroid glands belong to the class of low turnover, discontinuously replicating tissues composed of cells with a long life span, as is the case with most hormonally active tissues. This makes the analysis of normal growth characteristics difficult, all the more so when considering that no adequate cell culture model is available to study the regulation of parathyroid cell proliferation and death under physiological conditions in vitro. Fortunately, techniques using the expression of cell cycle–associated antigens presently allow a relatively precise measurement of the proliferation rate of parathyroid cells in gland tissues ex vivo1Drüeke T.B. Cell biology of parathyroid gland hyperplasia in chronic renal failure.J Am Soc Nephrol. 2000; 11: 1141-1152PubMed Google Scholar. In contrast, the determination of parathyroid apoptosis remains a technically difficult task. Three groups have failed to detect apoptosis in normal rat parathyroid, whereas others have recently been able to measure apoptosis in normal dog2Canalejo A. Almadén Y. Torregrosa V. The in vitro effect of calcitriol on parathyroid cell proliferation and apoptosis.J Am Soc Nephrol. 2000; 11: 1865-1872PubMed Google Scholar, as well as in normal and pathologic human glands2Canalejo A. Almadén Y. Torregrosa V. The in vitro effect of calcitriol on parathyroid cell proliferation and apoptosis.J Am Soc Nephrol. 2000; 11: 1865-1872PubMed Google Scholar, 3Zhang P. Duchambon P. Gogusev J. Apoptosis in parathyroid hyperplasia of patients with primary or secondary uremic hyperparathyroidism.Kidney Int. 2000; 57: 437-445Abstract Full Text Full Text PDF PubMed Scopus (34) Google Scholar. The hyperplasia of parathyroid tissue in chronic renal failure is primarily the result of an increase in parathyroid cell proliferation. Cell hypertrophy is only of minor importance. Whether the rate of apoptosis is also modified is still a matter of debate1Drüeke T.B. Cell biology of parathyroid gland hyperplasia in chronic renal failure.J Am Soc Nephrol. 2000; 11: 1141-1152PubMed Google Scholar. Our group actually found an increase in parathyroid gland apoptosis in dialysis patients with severe secondary hyperparathyroidism3Zhang P. Duchambon P. Gogusev J. Apoptosis in parathyroid hyperplasia of patients with primary or secondary uremic hyperparathyroidism.Kidney Int. 2000; 57: 437-445Abstract Full Text Full Text PDF PubMed Scopus (34) Google Scholar, possibly as a compensatory reaction to hyperplasia. The mechanisms involved in the pathogenesis of parathyroid hyperplasia in patients with chronic renal failure are still incompletely understood. At least two different types of growth can be distinguished. After an initial stage of polyclonal growth, probably in response to uremia-related metabolic disturbances, clonal proliferation is observed in patients with long-standing, severe hyperparathyroidism1Drüeke T.B. Cell biology of parathyroid gland hyperplasia in chronic renal failure.J Am Soc Nephrol. 2000; 11: 1141-1152PubMed Google Scholar. The latter is almost certainly the result of a number of acquired, somatic gene mutations. It is known that chronic calcium depletion and vitamin D deficiency lead to secondary hyperparathyroidism, presumably the polyclonal type. Since renal failure is frequently associated with disturbances of calcium and vitamin D metabolism, a major role of calcium and calcitriol deficiency in initiating uremic hyperparathyroidism is widely recognized. How a calcium deficiency precisely stimulates parathyroid cell proliferation is actually unknown. It is commonly believed that low extracellular calcium directly induces parathyroid hyperplasia. However, our in vitro studies using uremic parathyroid cells in long-term culture showed evidence for the opposite, specifically, a stimulation of parathyroid cell proliferation in response to a high calcium concentration4Roussane M.-C. Lieberherr M. Souberbielle J.-C. Human parathyroid cell proliferation in response to calcium, NPS R-467, calcitriol and phosphate.Eur J Clin Invest. in press. 2001Crossref Scopus (60) Google Scholar. It is possible that the response of pathologically transformed, primarily clonal cells to extracellular calcium is different from that of normal cells. However, it is of note that a similar direct stimulation by calcium has been observed in many other cell types. The recently reported inverse relation between parathyroid calcium-sensing receptor (CaR) expression and proliferative activity of parathyroid tissue sampled from uremic patients might be interpreted to reflect an inverse relationship between extracellular calcium and proliferation5Yano S. Sugimoto T. Chihara K. Association of decreased calcium-sensing receptor expression with proliferation of parathyroid cells in secondary hyperparathyroidism.Kidney Int. 2000; 58: 1980-1986Abstract Full Text Full Text PDF PubMed Google Scholar. In our opinion, however, the CaR down-regulation observed in severe uremic hyperparathyroidism probably reflects secondary changes caused by clonal growth, rather than primary changes. This conclusion is in line with the failure to identify mutations of the CaR gene in this condition. Calcitriol reduces parathyroid cell proliferation by decreasing the expression of the early gene, c-myc. This gene modulates the progression from G1 to S phase in the cell cycle. A decrease in plasma calcitriol and/or a disturbance of its action at the level of the parathyroid cell, which are both frequently observed in uremic patients, may cause progression into the cell cycle and a disinhibition of c-myc expression. Calcitriol also induces the differential expression of the cyclin kinase inhibitor p21WAF1,C1P1 in the myelomonocytic cell line U937 and activates the p21 gene transcriptionally in a VDR-dependent, but p53-independent, manner6Liu M. Lee M.H. Cohen M. Transcriptional activation of the Cdk inhibitor p21 by vitamin D3 leads to the induced differentiation of the myelomonocytic cell line U937.Genes Dev. 1996; 10: 142-153Crossref PubMed Scopus (805) Google Scholar. This finding indicates another possible mechanism by which calcitriol may regulate the proliferation of parathyroid cells. How phosphate controls parathyroid function remains a mystery. It was initially thought that the stimulation of parathyroid hormone secretion by hyperphosphatemia was indirect. However, recent in vitro studies provide convincing evidence for a direct effect, involving post-transcriptional regulation of parathyroid hormone mRNA stability through the specific nuclear protein, AUF17Sela Brown A. Silver J. Brewer G. Naveh Many T. Identification of AUF1 as a parathyroid hormone mRNA 3′-untranslated region-binding protein that determines parathyroid hormone mRNA stability.J Biol Chem. 2000; 275: 7424-7429Crossref Scopus (121) Google Scholar. It is as yet unclear how the parathyroid cell senses extracellular phosphate. Similarly, it is unclear how a phosphate-rich diet and hyperphosphatemia induce parathyroid hyperplasia, and conversely how a phosphate-poor diet inhibits parathyroid tissue growth. In this issue of Kidney International, Dusso et al made an important step forward with respect to this issue8Dusso A.S. Pavlopoulos T. Naumovich L. p21WAF1 and transforming growth factor-α mediate dietary phosphate regulation of parathyroid cell growth.Kidney Int. 2001; 59: 855-865Abstract Full Text Full Text PDF PubMed Scopus (100) Google Scholar. They reasoned that in vivo, the phosphate effect on parathyroid cell proliferation might be indirect, via changes in plasma calcitriol and a subsequent inhibition or induction of p21, respectively. However, they observed in a first experiment that feeding a low phosphate diet to uremic rats increased p21 mRNA and protein expression in the absence of changes in plasma calcitriol. The concomitant reduction of parathyroid cell proliferation must therefore be ascribed to a vitamin D–independent mechanism. In a second experiment they administered a high phosphate diet to uremic rats, known to induce parathyroid hyperplasia. In this case, they did not observe the expected mirror image of reduced p21 expression. Actually, the level of this growth inhibitor was the same as in control animals. Therefore, they tested the hypothesis of a possible induction by high dietary phosphate of transforming growth factor-α (TGF-α) in rat parathyroid glands, based on our previous observation of de novo TGF-α expression in severely hyperplastic parathyroid tissue of uremic patients9Gogusev J. Duchambon P. Stoermann-Chopard C. De novo expression of transforming growth factor-α in parathyroid gland tissue of patients with primary or secondary uraemic hyperparathyroidism.Nephrol Dial Transplant. 1996; 11: 2155-2162Crossref PubMed Scopus (66) Google Scholar. Dusso et al. were able to demonstrate an increase in TGF-α protein in uremic rats, compared with normal rats, and observed a further increment in response to a high phosphate diet. Moreover, a secondary decrease of TGF-α was seen when switching the animals from a high to a low phosphate diet. Finally, the rate of cellular proliferation correlated directly with TGF-α and inversely with p21 expression. Although these findings provide additional insights into the pathways by which changes in phosphate intake and, ultimately, variations in plasma phosphate control parathyroid tissue growth, the exciting question of the transmembrane signal transduction mechanism and subsequent nuclear events triggered by phosphate remains to be answered. In addition to p21 and TGF-α, a number of other growth factors and inhibitors may be involved in polyclonal parathyroid hyperplasia. Thus, parathyroid hormone-related protein has also been proposed as a possible growth suppressor in the human parathyroid10Matsushita H. Hara M. Endo Y. Proliferation of parathyroid cells negatively correlates with expression of parathyroid hormone-related protein in secondary parathyroid hyperplasia.Kidney Int. 1999; 55: 130-138Abstract Full Text Full Text PDF PubMed Scopus (33) Google Scholar. It will be particularly interesting to see whether the recently identified, parathyroid-specific transcription factor, Gcm2, which specifically controls the embryonic differentiation of parathyroid precursor cells into parathyroid tissue11Günther T. Chen Z.F. Kim J. Genetic ablation of parathyroid glands reveals another source of parathyroid hormone.Nature. 2000; 406: 199-203Crossref PubMed Scopus (287) Google Scholar, is also involved in normal or pathologic parathyroid cell proliferation and whether Gcm2 itself is submitted to regulation by other factors such as vitamin D, calcium, or phosphate." @default.
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