Differential Gene Expression by Oxyphil and Chief Cells of Human Parathyroid Glands

Ritter, Cynthia S.; Haughey, Bruce H.; Miller, Bradley R.; Brown, Alex

doi:10.1210/jc.2011-3366

Cited by 71 publications

(87 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Baseline PTH production under normocalcemic conditions (1.25 mM) in individual patientmatched pairs of chief and oxyphil cells was significantly higher in oxyphil cells relative to the chief cells. The enhanced calcium sensitivity and increased PTH production we observed in oxyphil cells relative to chief cells is consistent with a recent report that used immunohistochemistry to compare oxyphil and chief cell gene expression in hyperplastic parathyroid tissue from patients with hyperparathyroidism secondary to chronic kidney disease (23). In their study, Ritter et al (23) demonstrated elevated expression of parathyroid-relevant genes including PTH and PTHrP in oxyphil cells relative to chief cells.…”

Section: Discussionsupporting

confidence: 91%

Functional and genetic studies of isolated cells from parathyroid tumors reveal the complex pathogenesis of parathyroid neoplasia

Shi

Hogue

Dixit

et al. 2014

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

View full text Add to dashboard Cite

Significance Parathyroid adenomas, the main cause of primary hyperparathyroidism (PHPT), are thought to result from clonal expansion of tumor cells and to be insensitive to normal calcium feedback due to the loss of the calcium-sensing receptor (CASR). Utilizing flow cytometric analysis to isolate and individually study oxyphil cells, chief cells, and lymphocytes from resected parathyroid tumors and glands, we now report previously unrecognized heterogeneity in these tissues with respect to calcium responsiveness, CASR expression, and clonal origin of parathyroid tumors. Such heterogeneity of parathyroid adenomas likely reflects the complex etiopathogenesis and clinical heterogeneity of PHPT.

show abstract

Section: Discussionsupporting

confidence: 91%

Functional and genetic studies of isolated cells from parathyroid tumors reveal the complex pathogenesis of parathyroid neoplasia

Shi

Hogue

Dixit

et al. 2014

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

View full text Add to dashboard Cite

show abstract

“…Indeed, data on the effect of cinacalcet on the pathology of human PTG in HP with SHPT are very few (33,34,36). Lomonte et al did not find significant differences in the number, weight, and percentage of NH in the PTG of patients who received calcitriol and cinacalcet with respect to those who received calcitriol only.…”

Section: Discussionmentioning

confidence: 96%

“…However, the increase in the OC:CC ratio observed after short-or long-term cinacalcet therapy did not translate into pharmacological control of SHPT. Certainly, the OC are not simply deactivated CC (36,37,38,39,40,41). However, additional studies are required to define the effects of vitamin D and cinacalcet on the expression and role of the OC in the pathophysiology of PTG.…”

Section: Discussionmentioning

confidence: 99%

Histology and immunohistochemistry of the parathyroid glands in renal secondary hyperparathyroidism refractory to vitamin D or cinacalcet therapy

Vulpio

Bossola

Stasio

et al. 2013

European Journal of Endocrinology

View full text Add to dashboard Cite

Background: Cinacalcet is a new effective treatment of secondary hyperparathyroidism (SHPT) in hemodialysis patients (HP), but the alterations of parathyroid gland (PTG) hyperplasia determined by cinacalcet and vitamin D have not been extensively investigated in humans. Methods: We performed histological analyses of 94 PTGs removed from 25 HP who underwent parathyroidectomy (PTx) because of SHPT refractory to therapy with vitamin D alone (group AZ13 HP and 46 PTGs) or associated with cinacalcet (group BZ12 HP and 48 PTGs). The number, weight, the macroscopic cystic/hemorrhagic changes, and type of hyperplasia of PTG (nodularZNH, diffuseZDH) were assessed. In randomly selected HP of group A (4 HP and 14 PTGs) and group B (4 HP and 15 PTGs), the labeling index of cells positive to Ki-67 and TUNEL and the semiquantitative score of immunohistochemistry staining of vitamin D receptor, calcium-sensing receptor, and vascular endothelial growth factor-a (VEGF-a) were measured in the entire PTGs and in the areas with DH or NH. Results: The number and weight of single and total PTG of each HP were similar in the two groups as well as the number of PTG with macroscopic cystic/hemorrhagic areas. TUNEL, Ki-67, and VEGF-a scores were higher in NH than in DH areas. Conclusion: This observational study of a highly selected population of HP, submitted to PTx because SHPT refractory to therapy, shows that the macroscopic, microscopic, and immunochemistry characteristics of PTG in HP who received or did not receive cinacalcet before PTx did not differ significantly.

show abstract

“…Expression of PTHrP has not been sought in human fetal parathyroids, but PTHrP mRNA and protein have been detected in the oxyphil cells of adult normal, hyperplastic, and adenomatous parathyroids by a variety of methods (28,137,157,277,313,314,424,552). Since adult parathyroids express PTHrP, it is conceivable that the fetal parathyroids do as well.…”

Section: Human Datamentioning

confidence: 99%

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Kovacs

2014

Physiological Reviews

197

188

View full text Add to dashboard Cite

Mineral and bone metabolism are regulated differently in utero compared with the adult. The fetal kidneys, intestines, and skeleton are not dominant sources of mineral supply for the fetus. Instead, the placenta meets the fetal need for mineral by actively transporting calcium, phosphorus, and magnesium from the maternal circulation. These minerals are maintained in the fetal circulation at higher concentrations than in the mother and normal adult, and such high levels appear necessary for the developing skeleton to accrete a normal amount of mineral by term. Parathyroid hormone (PTH) and calcitriol circulate at low concentrations in the fetal circulation. Fetal bone development and the regulation of serum minerals are critically dependent on PTH and PTH-related protein, but not vitamin D/calcitriol, fibroblast growth factor-23, calcitonin, or the sex steroids. After birth, the serum calcium falls and phosphorus rises before gradually reaching adult values over the subsequent 24 -48 h. The intestines are the main source of mineral for the neonate, while the kidneys reabsorb mineral, and bone turnover contributes mineral to the circulation. This switch in the regulation of mineral homeostasis is triggered by loss of the placenta and a postnatal fall in serum calcium, and is followed in sequence by a rise in PTH and then an increase in calcitriol. Intestinal calcium absorption is initially a passive process facilitated by lactose, but later becomes active and calcitriol-dependent. However, calcitriol's role can be bypassed by increasing the calcium content of the diet, or by parenteral administration of calcium.

show abstract

Differential Gene Expression by Oxyphil and Chief Cells of Human Parathyroid Glands

Cited by 71 publications

References 31 publications

Functional and genetic studies of isolated cells from parathyroid tumors reveal the complex pathogenesis of parathyroid neoplasia

Functional and genetic studies of isolated cells from parathyroid tumors reveal the complex pathogenesis of parathyroid neoplasia

Histology and immunohistochemistry of the parathyroid glands in renal secondary hyperparathyroidism refractory to vitamin D or cinacalcet therapy

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Contact Info

Product

Resources

About