Thyroid origin of Calcitonin

Foster, G. V.; Baghdiantz, A; Kumar, M. Sunil; Slack, Ella; Soliman, Hanan A.; MacIntyre, I.

doi:10.1038/2021303a0

Cited by 269 publications

(61 citation statements)

References 6 publications

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“…CT was discovered as an acute hypocalcaemic hormone released from the parathyroid glands (Copp & Cheney 1962), but shortly thereafter shown to be secreted by thyroid C-cells (Foster et al 1964, Zaidi et al 2002. The hypocalcaemic response is mainly due to inhibition of bone resorption (Friedman & Raisz 1965), caused by activation of CT receptors (CTRs) in mature osteoclasts leading to contraction, ceased motility and decreased bone-resorbing activity (Chambers et al 1984).…”

Section: Introductionmentioning

confidence: 99%

Calcitonin inhibits osteoclast formation in mouse haematopoetic cells independently of transcriptional regulation by receptor activator of NF-κB and c-Fms

Granholm

Lundberg²,

Lerner

2007

Journal of Endocrinology

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The effects of calcitonin (CT) on osteoclast formation and gene expression have been studied in cultured mouse spleen cells and mouse bone marrow macrophages (BMMs). CT inhibited the formation of multinucleated osteoclasts and resorption pits in spleen cell cultures and BMM as well as in CD115 C CD3 K CD45RK sorted BMM cultures, incubated in the presence of macrophage colony-stimulating factor and receptor activator of NF-kB ligand (RANKL). No effect on apoptosis by CT was observed. CT did not affect the mRNA expressions of RANK and c-Fms, or the mRNA expressions of a wide variety of transcription factors and genes important for osteoclast differentiation and activity. CT induced inhibition of tartrateresistant acid phosphatase (TRAP), positive multinucleated osteoclast formation was not associated with any decrease of total TRAP activity, resulting in a large number of TRAP C mononucleated cells in CT-treated cultures. CT did not affect the mRNA expression of dendritic cell-specific transmembrane protein, d2 isoform of vacuolar (H C ) ATPase v o domain, a disintegrin and metalloproteinase domain 8 (ADAM8), ADAM12, DNAX-activating protein or Fc receptor common g chain suggested to be involved in fusion of mononucleated osteoclast progenitor cells. The inhibitory effect by CT was mimicked not only by compounds activating cAMP and protein kinase A (PKA) but also by a cAMP analogue activating the exchange protein directly activated by cAMP (Epac) pathway. It is concluded that CT, through cAMP/PKA/Epac cascades, inhibits osteoclast formation and that this effect is not associated with decreased transcription of genes known to be important for osteoclast progenitor cell differentiation, fusion or function.

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Section: Introductionmentioning

confidence: 99%

Calcitonin inhibits osteoclast formation in mouse haematopoetic cells independently of transcriptional regulation by receptor activator of NF-κB and c-Fms

Granholm

Lundberg²,

Lerner

2007

Journal of Endocrinology

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“…Calcitonin (CT) is a hypocalcaemic and hypophosphataemic hormone produced by the parafollicular cells of the thyroid gland (Foster et al 1964). A major physiological effect of CT is to inhibit bone resorption, while it is unclear whether the hormone also enhances bone formation (Rasmussen & Bordier 1974, Talmage & Cooper 1979.…”

mentioning

confidence: 99%

Increase in Plasma Calcitonin Following Femoral Fracture in Rats

Ekeland¹,

Gautvik²,

Myhre

1981

Acta Orthopaedica Scandinavica

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“…Calcitonin is predominantly synthesized and released from thyroid C-cells [15]. An important stimulator of calcitonin secretion is an increase in the extracellular calcium concentration [36].…”

Section: Summary Calcitonin Gene-related Peptide (Cgrp)mentioning

confidence: 99%

“…As a result, distinct receptors for calcitonin and CGRP have been identified [7,11,33,42]. Human CGRP-I and -II, due to their high homology, crossreact almost completely, but subtle differences in the distribution of human CGRP-I and -II binding sites have been observed on receptor autoradiography of the human brain [22].Calcitonin is predominantly synthesized and released from thyroid C-cells [15]. An important stimulator of calcitonin secretion is an increase in the extracellular calcium concentration [36].…”

mentioning

confidence: 99%

Calcitonin gene products and the kidney

1989

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Summary. Calcitonin gene-related peptide (CGRP) is localized in capsaicin-sensitive nerve fibres in the kidney and urogenital tract whereas calcitonin reaches the kidney through the general circulation. Systemic infusion of CGRP and perfusion of isolated rat kidney reduces vascular resistance, and increases renal blood flow and glomerular filtration. CGRP stimulates renin secretion in vivo and in vitro and inhibits contraction of isolated rat mesangial cells by angiotensin II. Calcitonin does not affect vascular resistance, renal blood flow and glomerular filtration, and is tess potent in stimulating renin secretion, and does not alter contraction of isolated rat mesangial cells by angiotensin II. CGRP also exerts renal tubular effects brought about probably through interaction with calcitonin receptors. To this end, increased excretion of sodium and chloride, and stimulation of urinary flow are less pronounced with CGRP than with calcitonin. Calcitonin, moreover, stimulates the fractional urinary excretion of calcium and phosphate.Key words: Calcitonin -Calcitonin gene-related peptide -Renovascular effects -Renotubular effects -Renin secretion Alternative splicing of the initial calcitonin gene transcript results in the formation of two distinct messenger RNAs encoding the precursors of calcitonin and of calcitonin gene-related peptide (CGRP) [2,26]. In man and rat two calcitonin/ CGRP genes have been recognized [3,40]. A pseudogene encoding a second calcitonin-like structure appears not to be expressed in man [40]. But CGRP-I (or 7) and -II (or fl) have been identified in man and rat at the mRNA and peptide levels [3, 23, 341. Calcitonin and CGRP are single chain polypeptides consisting of 32 and 37 amino acids, respectively. They have in common amino-terminal ring structures linked by disulfide bridges and the carboxyltermini are amidated. In man, CGRP shares 16% structural homology with calcitonin whereas the homology between CGRP-I and -II is 92% [13]. As a result, distinct receptors for calcitonin and CGRP have been identified [7,11,33,42]. Human CGRP-I and -II, due to their high homology, crossreact almost completely, but subtle differences in the distribution of human CGRP-I and -II binding sites have been observed on receptor autoradiography of the human brain [22].Calcitonin is predominantly synthesized and released from thyroid C-cells [15]. An important stimulator of calcitonin secretion is an increase in the extracellular calcium concentration [36]. Calcitonin can be considered as a hormone that reaches its target tissues via the circulation. Calcitonin lowers serum calcium levels through inhibition of bone resorption [37]. In the kidney, calcitonin stimulates the urinary excretion of calcium, phosphate, sodium, potassium and chloride, and enhances 1,25-dihydroxycholecalciferol production [5,20,25,32].CGRP is predominantly synthesized in the nervous system and is frequently found in peripheral nerves associated with blood vessels, but CGRP has also been identified in the normal human thyroid glan...

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Thyroid origin of Calcitonin

Cited by 269 publications

References 6 publications

Calcitonin inhibits osteoclast formation in mouse haematopoetic cells independently of transcriptional regulation by receptor activator of NF-κB and c-Fms

Calcitonin inhibits osteoclast formation in mouse haematopoetic cells independently of transcriptional regulation by receptor activator of NF-κB and c-Fms

Increase in Plasma Calcitonin Following Femoral Fracture in Rats

Calcitonin gene products and the kidney

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