scholarly journals Overexpression of the Transcriptional Factor Runx2 in Osteoblasts Abolishes the Anabolic Effect of Parathyroid Hormone in Vivo

2007 ◽  
Vol 170 (5) ◽  
pp. 1676-1685 ◽  
Author(s):  
Didier Merciris ◽  
Caroline Marty ◽  
Corinne Collet ◽  
Marie-Christine de Vernejoul ◽  
Valerie Geoffroy
Keyword(s):  
Parathyroid Hormone ◽  
Transcriptional Factor ◽  
Anabolic Effect

scholarly journals Development and in vivo evaluation of intranasal formulations of parathyroid hormone (1-34)

Drug Delivery ◽  
2021 ◽  
Vol 28 (1) ◽  
pp. 487-498
Author(s):  
Dan Wang ◽  
Yimeng Du ◽  
Wenpeng Zhang ◽  
Xiaolu Han ◽  
Hui Zhang ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
In Vivo Evaluation

Exogenous parathyroid hormone attenuates ovariectomy-induced skeletal muscle weakness in vivo

Bone ◽  
2021 ◽  
pp. 116029
Author(s):  
Taro Fujimaki ◽  
Takashi Ando ◽  
Takanori Hata ◽  
Yoshihiro Takayama ◽  
Tetsuro Ohba ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Parathyroid Hormone ◽  
Muscle Weakness ◽  
Skeletal Muscle Weakness

scholarly journals Extracellular vesicles-released parathyroid hormone-related protein from Lewis lung carcinoma induces lipolysis and adipose tissue browning in cancer cachexia

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Wenjun Hu ◽  
Hairong Xiong ◽  
Zeyuan Ru ◽  
Yan Zhao ◽  
Yali Zhou ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Parathyroid Hormone ◽  
Lung Carcinoma ◽  
Lewis Lung Carcinoma ◽  
Cancer Cachexia ◽  
Lewis Lung ◽  
Related Protein ◽  
Parathyroid Hormone Related Protein ◽  
Tissue Browning

AbstractCancer cachexia is a metabolic disorder characterized by skeletal muscle wasting and white adipose tissue browning. Specific functions of several hormones, growth factors, and cytokines derived from tumors can trigger cachexia. Moreover, adipose tissue lipolysis might explain weight loss that occurs owing to cachexia. Extracellular vesicles (EVs) are involved in intercellular communication. However, whether EVs participate in lipolysis induced by cancer cachexia has not been thoroughly investigated. Using Lewis lung carcinoma (LLC) cell culture, we tested whether LLC cell-derived EVs can induce lipolysis in 3T3-L1 adipocytes. EVs derived from LLC cells were isolated and characterized biochemically and biophysically. Western blotting and glycerol assay were used to study lipolysis. LLC cell-derived EVs induced lipolysis in vivo and vitro. EVs fused directly with target 3T3-L1 adipocytes and transferred parathyroid hormone-related protein (PTHrP), activating the PKA signaling pathway in 3T3-L1 adipocytes. Blocking PTHrP activity in LLC-EVs using a neutralizing antibody and by knocking down PTHR expression prevented lipolysis in adipocytes. Inhibiting the PKA signaling pathway also prevents the lipolytic effects of EVs. In vivo, suppression of LLC-EVs release by knocking down Rab27A alleviated white adipose tissue browning and lipolysis. Our data showed that LLC cell-derived EVs induced adipocyte lipolysis via the extracellular PTHrP-mediated PKA pathway. Our data demonstrate that LLC-EVs induce lipolysis in vitro and vivo by delivering PTHrP, which interacts with PTHR. The lipolytic effect of LLC-EVs was abrogated by PTHR knockdown and treatment with a neutralizing anti-PTHrP antibody. Together, these data show that LLC-EV-induced lipolysis is mediated by extracellular PTHrP. These findings suggest a novel mechanism of lipid droplet loss and identify a potential therapeutic strategy for cancer cachexia.

scholarly journals Suppression of parathyroid hormone production in vitro and in vivo by RNA interference

2009 ◽  
Vol 75 (5) ◽  
pp. 490-498 ◽  
Author(s):  
Genta Kanai ◽  
Takatoshi Kakuta ◽  
Kaichiro Sawada ◽  
Tun A. Yokoyama ◽  
Reika Tanaka ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Rna Interference ◽  
Hormone Production

Cooperative interactions between extracellular matrix, integrins and parathyroid hormone-related peptide regulate parietal endoderm differentiation in mouse embryos

Development ◽  
1995 ◽  
Vol 121 (12) ◽  
pp. 4137-4148 ◽  
Author(s):  
O. Behrendtsen ◽  
C.M. Alexander ◽  
Z. Werb
Keyword(s):  
Extracellular Matrix ◽  
Parathyroid Hormone ◽  
Mouse Embryos ◽  
Collagen Type Iv ◽  
Related Peptide ◽  
Parathyroid Hormone Related Peptide ◽  
Parietal Endoderm ◽  
Alpha V Beta 3 ◽  
Endodermal Cells

The outgrowth of parietal endoderm (PE) cells from precursor endodermal cells is one of the first differentiation events that occur in mouse embryos. We have analyzed the molecular determinants of this process by placing isolated inner cell masses (ICMs) on defined extracellular matrix substrata in microdrop cultures. Differentiation and outgrowth of PE required a fibronectin substratum. Laminin supported the adhesion and outgrowth of visceral endoderm (VE) and actively suppressed the differentiation of PE in mixtures of fibronectin and laminin. Collagen type IV, gelatin, vitronectin or entactin supported little or no endodermal outgrowth. Trophectoderm (TE) cells have been implied to be important in PE induction in vivo. We found that recombination of ICMs in culture with TE cells, or with medium conditioned by TE cells, greatly increased the differentiation of PE. TE cells stimulated PE outgrowth on substrata other than fibronectin. One cytokine secreted by trophoblast and endodermal cells, parathyroid hormone-related peptide (PTHrP), was critical for outgrowth on any substratum. A function-perturbing antibody to PTHrP reduced the number of PE cells, whereas the addition of PTHrP increased that number. Furthermore, addition of PTHrP changed the substratum requirements for outgrowth, making laminin, vitronectin and low concentrations of fibronectin permissive for PE outgrowth. Immunostaining with anti-integrin antibodies showed that fully differentiated PE cells outgrowing on fibronectin expressed alpha 5, alpha 6 and alpha v beta 3 integrins. However, analysis of outgrowths in the presence of function-perturbing antibodies to alpha 5, alpha 6 and alpha v beta 3 integrins showed that these integrins directed PE outgrowth only on fibronectin, laminin and vitronectin substrata, respectively. We have shown that there is a cooperative interplay of extracellular matrix, integrins and PTHrP that modulates PE outgrowth.

scholarly journals The interplay of osteogenesis and hematopoiesis

2004 ◽  
Vol 167 (6) ◽  
pp. 1113-1122 ◽  
Author(s):  
Sergei A. Kuznetsov ◽  
Mara Riminucci ◽  
Navid Ziran ◽  
Takeo W. Tsutsui ◽  
Alessandro Corsi ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Parathyroid Hormone ◽  
Ex Vivo ◽  
Cell Types ◽  
Heterotopic Bone ◽  
Stromal Compartment ◽  
Marrow Space ◽  
Stromal Tissue

The ontogeny of bone marrow and its stromal compartment, which is generated from skeletal stem/progenitor cells, was investigated in vivo and ex vivo in mice expressing constitutively active parathyroid hormone/parathyroid hormone–related peptide receptor (PTH/PTHrP; caPPR) under the control of the 2.3-kb bone-specific mouse Col1A1 promoter/enhancer. The transgene promoted increased bone formation within prospective marrow space, but delayed the transition from bone to bone marrow during growth, the formation of marrow cavities, and the appearance of stromal cell types such as marrow adipocytes and cells supporting hematopoiesis. This phenotype resolved spontaneously over time, leading to the establishment of marrow containing a greatly reduced number of clonogenic stromal cells. Proliferative osteoprogenitors, but not multipotent skeletal stem cells (mesenchymal stem cells), capable of generating a complete heterotopic bone organ upon in vivo transplantation were assayable in the bone marrow of caPPR mice. Thus, PTH/PTHrP signaling is a major regulator of the ontogeny of the bone marrow and its stromal tissue, and of the skeletal stem cell compartment.

scholarly journals Inhibition of the in vivo parathyroid hormone-mediated calcemic response in rats by a synthetic hormone antagonist.

1986 ◽  
Vol 83 (19) ◽  
pp. 7557-7560 ◽  
Author(s):  
S. H. Doppelt ◽  
R. M. Neer ◽  
S. R. Nussbaum ◽  
P. Federico ◽  
J. T. Potts ◽  
...  
Keyword(s):  
Parathyroid Hormone

Comparison of the feedback effect of magnesium and calcium on parathyroid hormone secretion in man

1987 ◽  
Vol 113 (1) ◽  
pp. 117-122 ◽  
Author(s):  
O. Ferment ◽  
P. E. Garnier ◽  
Y. Touitou
Keyword(s):  
Parathyroid Hormone ◽  
Urinary Excretion ◽  
Hormone Secretion ◽  
Plasma Concentrations ◽  
Magnesium Salt ◽  
Saline Injection ◽  
Molar Basis ◽  
Magnesium Salts ◽  
High Doses

ABSTRACT Administration of high doses of magnesium is known to produce a decrease in parathyroid hormone (PTH) secretion in human patients but the effect of magnesium on the secretion of PTH in healthy man is not known. We have looked at the effect of a relatively moderate i.v. dose of magnesium (7·08 mmol) in seven healthy men. In addition and for comparison the effect of calcium (4·25 mmol) was studied. Two magnesium salts were considered, magnesium sulphate (MgSO4) and magnesium pyrrolidone carboxylate (MgPC). Four i.v. injections were given at 08.00 h (MgPC, NaCl (control), MgSO4 and Ca gluconate), with an interval of 1 week between each injection. Whatever the magnesium salt the variations in plasma concentrations of magnesium were the same whereas no change in erythrocyte magnesium was observed. Plasma concentration of C-terminal PTH did not show significant variations after MgPC or saline injection. Both MgSO4 and Ca gluconate produced a statistically significant 30% decrease in plasma PTH levels 45 min after the injection. The effect was more sustained with calcium (2 h) than with magnesium (45 min). The urinary excretion of magnesium was significantly higher after injection of MgSO4 than after MgPC. These results suggest (1) that magnesium was, on a molar basis, less potent than calcium in regulating PTH secretion in vivo, (2) that the nature of the magnesium salt used must be kept in mind for the interpretation of the effect of magnesium on PTH secretion in vivo and (3) that the decrease in plasma PTH can partly explain the larger urinary excretion of magnesium after MgSO4 than after MgPC. J. Endocr. (1987) 113, 117–122

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