Prolactin decreases expression of Runx2, osteoprotegerin, and RANKL in primary osteoblasts derived from tibiae of adult female rats
Hyperprolactinemia caused by physiological or pathological conditions, such as those occurring during lactation and prolactinoma, respectively, results in progressive osteopenia. The underlying mechanisms, however, are controversial. Prolactin (PRL) may directly attenuate the functions of osteoblast...
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th-mahidol.189242018-07-12T09:50:56Z Prolactin decreases expression of Runx2, osteoprotegerin, and RANKL in primary osteoblasts derived from tibiae of adult female rats Narattaphol Charoenphandhu Jarinthorn Teerapornpuntakit Methajit Methawasin Kannikar Wongdee Kanogwun Thongchote Nateetip Krishnamra Mahidol University Biochemistry, Genetics and Molecular Biology Pharmacology, Toxicology and Pharmaceutics Hyperprolactinemia caused by physiological or pathological conditions, such as those occurring during lactation and prolactinoma, respectively, results in progressive osteopenia. The underlying mechanisms, however, are controversial. Prolactin (PRL) may directly attenuate the functions of osteoblasts, since these bone cells express PRL receptors. The present study therefore aimed to investigate the effects of PRL on the expression of genes related to the osteoblast functions by using quantitative real-time PCR technique. Herein, we used primary osteoblasts that were derived from the tibiae of adult rats and displayed characteristics of differentiated osteoblasts, including in vitro mineralization. Osteoblasts exposed for 48 h to 1000 ng/mL PRL, but not to 10 or 100 ng/mL PRL, showed decreases in the mRNA expression of Runx2, osteoprotegerin (OPG), and receptor activator of nuclear factor κB ligand (RANKL) by 60.49%, 72.74%, and 87.51%, respectively. Nevertheless, PRL did not change the RANKL/OPG ratio, since expression of OPG and RANKL were proportionally decreased. These concentrations of PRL had no effect on the mRNA expression of osteocalcin and osteopontin, nor on mineralization. High pathologic concentrations of PRL (1000 ng/mL) may downregulate expression of genes that are essential for osteoblast differentiation and functions. The present results explained the clinical findings of hyperprolactinemia-induced bone loss. © 2008 NRC. 2018-07-12T02:18:46Z 2018-07-12T02:18:46Z 2008-05-01 Article Canadian Journal of Physiology and Pharmacology. Vol.86, No.5 (2008), 240-248 10.1139/Y08-037 00084212 2-s2.0-43949092075 https://repository.li.mahidol.ac.th/handle/123456789/18924 Mahidol University SCOPUS https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=43949092075&origin=inward |
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Biochemistry, Genetics and Molecular Biology Pharmacology, Toxicology and Pharmaceutics Narattaphol Charoenphandhu Jarinthorn Teerapornpuntakit Methajit Methawasin Kannikar Wongdee Kanogwun Thongchote Nateetip Krishnamra Prolactin decreases expression of Runx2, osteoprotegerin, and RANKL in primary osteoblasts derived from tibiae of adult female rats |
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Hyperprolactinemia caused by physiological or pathological conditions, such as those occurring during lactation and prolactinoma, respectively, results in progressive osteopenia. The underlying mechanisms, however, are controversial. Prolactin (PRL) may directly attenuate the functions of osteoblasts, since these bone cells express PRL receptors. The present study therefore aimed to investigate the effects of PRL on the expression of genes related to the osteoblast functions by using quantitative real-time PCR technique. Herein, we used primary osteoblasts that were derived from the tibiae of adult rats and displayed characteristics of differentiated osteoblasts, including in vitro mineralization. Osteoblasts exposed for 48 h to 1000 ng/mL PRL, but not to 10 or 100 ng/mL PRL, showed decreases in the mRNA expression of Runx2, osteoprotegerin (OPG), and receptor activator of nuclear factor κB ligand (RANKL) by 60.49%, 72.74%, and 87.51%, respectively. Nevertheless, PRL did not change the RANKL/OPG ratio, since expression of OPG and RANKL were proportionally decreased. These concentrations of PRL had no effect on the mRNA expression of osteocalcin and osteopontin, nor on mineralization. High pathologic concentrations of PRL (1000 ng/mL) may downregulate expression of genes that are essential for osteoblast differentiation and functions. The present results explained the clinical findings of hyperprolactinemia-induced bone loss. © 2008 NRC. |
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Mahidol University |
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Mahidol University Narattaphol Charoenphandhu Jarinthorn Teerapornpuntakit Methajit Methawasin Kannikar Wongdee Kanogwun Thongchote Nateetip Krishnamra |
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Article |
author |
Narattaphol Charoenphandhu Jarinthorn Teerapornpuntakit Methajit Methawasin Kannikar Wongdee Kanogwun Thongchote Nateetip Krishnamra |
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Narattaphol Charoenphandhu |
title |
Prolactin decreases expression of Runx2, osteoprotegerin, and RANKL in primary osteoblasts derived from tibiae of adult female rats |
title_short |
Prolactin decreases expression of Runx2, osteoprotegerin, and RANKL in primary osteoblasts derived from tibiae of adult female rats |
title_full |
Prolactin decreases expression of Runx2, osteoprotegerin, and RANKL in primary osteoblasts derived from tibiae of adult female rats |
title_fullStr |
Prolactin decreases expression of Runx2, osteoprotegerin, and RANKL in primary osteoblasts derived from tibiae of adult female rats |
title_full_unstemmed |
Prolactin decreases expression of Runx2, osteoprotegerin, and RANKL in primary osteoblasts derived from tibiae of adult female rats |
title_sort |
prolactin decreases expression of runx2, osteoprotegerin, and rankl in primary osteoblasts derived from tibiae of adult female rats |
publishDate |
2018 |
url |
https://repository.li.mahidol.ac.th/handle/123456789/18924 |
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1763489435180072960 |