Estrogen receptors and biologic response in rat parathyroid tissue and C cells.

Naveh-Many, Tally; Almogi, Gideon; Livni, Nelly; Silver, Justin

doi:10.1172/jci116134

Cited by 95 publications

(51 citation statements)

References 43 publications

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“…The stimuli which lead to increased PTH gene expression, translation and secretion are well characterized. In vivo, these include low calcium, high phosphate and estrogens (2)(3)(4). The factors which lead to decreased PTH gene expression in vivo are 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) (5) and low phosphate (3).…”

Section: Introductionmentioning

confidence: 99%

“…The integrity of the RNA and the uniformity of RNA transfer to the membrane were determined by UV visualization of the ribosomal RNA bands of the gels and the filters. The filters were fixed by UV cross-linking and hybridized as previously described (4,5). Hybridization was to a random primed rat PTH cDNA (a gift of H. Meyer, GBF, Braunschweig, Germany) and 18S RNA (gift of M. A. Levine, Baltimore, MD).…”

Section: Introductionmentioning

confidence: 99%

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Parathyroid cell proliferation in normal and chronic renal failure rats. The effects of calcium, phosphate, and vitamin D.

Naveh-Many

Rahamimov²,

Livni³

et al. 1995

J. Clin. Invest.

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372

210

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Secondary hyperparathyroidism is characterized by an increase in parathyroid (PT) cell number, and parathyroid hormone (PTH) synthesis and secretion. It is still unknown as to what stimuli regulate PT cell proliferation and how they do this. We have studied rats with dietary-induced secondary hyper-and hypoparathyroidism, rats given 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) and rats after 5/6 nephrectomy for the presence of PT cell proliferation and apoptosis. PT cell proliferation has been measured by staining for proliferating cell nuclear antigen (PCNA) and apoptosis by in situ detection of nuclear DNA fragmentation and correlated with serum biochemistry and PTH mRNA levels. A low calcium diet led to increased levels of PTH mRNA and a 10-fold increase in PT cell proliferation. A low phosphate diet led to decreased levels of PTH mRNA and the complete absence of PT cell proliferation. 1,25(OH)2D3 (25 pmol/d x 3) led to a decrease in PTH mRNA levels and unlike the hypophosphatemic rats there was no decrease in cell proliferation. There were no cells undergoing apoptosis in any of the experimental conditions. The secondary hyperparathyroidism of 5/6 nephrectomized rats was characterized by an increase in PTH mRNA levels and PT cell proliferation which were both markedly decreased by a low phosphate diet. The number of PCNA positive cells was increased by a high phosphate diet. Therefore hypocalcemia, hyperphosphatemia and uremia lead to PT cell proliferation, and hypophosphatemia completely abolishes this effect. Injected 1,25(OH)2D3 had no effect.These findings emphasize the importance of a normal phosphate and calcium in the prevention of PT cell hyperplasia. (J. Clin. Invest. 1995. 96:1786-1793.) Key words: parathyroid hormone * apoptosis* hyperplasia * 1,25(OH)2D3 chronic renal failure.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Parathyroid cell proliferation in normal and chronic renal failure rats. The effects of calcium, phosphate, and vitamin D.

Naveh-Many

Rahamimov²,

Livni³

et al. 1995

J. Clin. Invest.

Self Cite

372

210

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“…Parafollicular C cells secrete a polypeptide hormone, calcitonin. Previously, it has been demonstrated that calcitonin gene expression is elevated in response to estrogen, suggesting the presence of an estrogen receptor (ER; Naveh-Many et al 1992). Immunohistochemical studies using monoclonal antibody revealed that ERb, but not ERa, was detected in normal human thyroid follicular and parafollicular C cells (Taylor & Al-Azzawi 2000).…”

Section: Introductionmentioning

confidence: 99%

Expression and role of estrogen receptor α and β in medullary thyroid carcinoma: different roles in cancer growth and apoptosis

Cho¹,

Nam²,

Chung³

et al. 2007

Journal of Endocrinology

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Medullary thyroid carcinoma (MTC) originates from parafollicular C cells. Estrogen receptor b (ERb) expression was detected in normal parafollicular C cells and MTC tumor tissue, but ERa expression in MTC tumors still remains undetermined. The appearance and loss of ERa or ERb expression has been known to play a role in the development and progression of many human cancers. We performed immunohistochemical studies of ERa, ERb, and Ki67, a mitotic index, in 11 human MTC tissue samples. ERa was detected in 10 cases (91%), and ERb expression was observed in 8 cases (72 . 7%). A majority (8/10) of ERa-positive tumors showing ERb Ki67 expression was detected in three cases (27 . 3%). Neither clinical parameters nor tumor node metastasis (TNM) tumor staging was correlated with the positivity for ERs or Ki67. To investigate the biological role of each ER, we used ER-negative MTC TT cells and adenoviral vectors carrying ERa (Ad-ERa), ERb (Ad-ERb), estrogen response element (ERE)-Luc (Ad-ERE-Luc), and activator protein 1 (AP1)-Luc (Ad-AP1-Luc). Estrogen stimulated and anti-estrogen, ICI 182 780, suppressed ERE reporter activity in TT cells expressing ERa or ERb, suggesting that both ERs use the same classical ERE-mediated pathway. Ad-ERa infection stimulated TT cell growth; in contrast, Ad-ERb infection suppressed their growth. Apoptosis was detected in Ad-ERb-infected TT cells. Estrogen and antiestrogen suppressed AP1 activity in Ad-ERa-infected cells, whereas upon Ad-ERb infection estrogen further stimulated AP1 activity which in turn is suppressed by anti-estrogen, suggesting that each ER acts differently through a non-EREmediated pathway. Our results suggest that ERa and ERb may play different roles in MTC tumor growth and progression.

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“…Because estrogen does not affect intestinal VDR content (169), these data support the hypothesis for a vitamin D-independent action of estrogen on intestinal Ca absorption (168). Estrogen receptors are present in parathyroid tissue and thyroid C cells, and treatment of ovariectomized rats with 17|3-esti*adiol stimulates expression of the mRNAs for PTH and CT (170). The combined anabolic effects of PTH and CT on bone provide an indirect pathway for estrogen action in prevention of bone loss (170).…”

Section: Gender and Sex Hormone Effects On Factors Involved In Regulamentioning

confidence: 68%

“…Estrogen receptors are present in parathyroid tissue and thyroid C cells, and treatment of ovariectomized rats with 17|3-esti*adiol stimulates expression of the mRNAs for PTH and CT (170). The combined anabolic effects of PTH and CT on bone provide an indirect pathway for estrogen action in prevention of bone loss (170).…”

Section: Gender and Sex Hormone Effects On Factors Involved In Regulamentioning

confidence: 99%

Age, gender and diet effects on gene expression regulated by 1,25-dihydroxyvitamin D3

Johnson

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This manuscript has been reproduced from the microfilm master. UMI films the text directly from the original or copy submitted. Thus, some thesis and dissertation copies are in typewriter face, while others may be from any type of computer printer.The quality of this reproduction is dependent upon the quality of the copy submitted. Broken or indistinct print, colored or poor quality illustrations and photographs, print bleedthrough, substandard margins, and improper alignment can adversely affect reproduction.In the unlikely event that the author did not send UMI a complete manuscript and there are missing pages, these will be noted. Also, if unauthorized copyright material had to be removed, a note will indicate the deletion.Oversize materials (e.g., maps, drawings, charts) are reproduced by sectioning the original, beginning at the upper left-hand comer and continuing from left to right in equal sections with small overlaps. Each original is also photographed in one exposure and is included in reduced form at the back of the book.

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Estrogen receptors and biologic response in rat parathyroid tissue and C cells.

Abstract: The expression of the PTH and calcitonin genes is dramatically decreased by 1,25(OH)2D3 in vivo, and the PTH gene expression is increased by hypocalcemia. We have now studied the effect of estrogens on the expression of these genes in vivo.

Cited by 95 publications

References 43 publications

Parathyroid cell proliferation in normal and chronic renal failure rats. The effects of calcium, phosphate, and vitamin D.

Parathyroid cell proliferation in normal and chronic renal failure rats. The effects of calcium, phosphate, and vitamin D.

Expression and role of estrogen receptor α and β in medullary thyroid carcinoma: different roles in cancer growth and apoptosis

Age, gender and diet effects on gene expression regulated by 1,25-dihydroxyvitamin D3

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