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Parathyroid Hormone Signaling in Osteocytes

Osteocytes are the most abundant cell type in bone and play a central role in orchestrating skeletal remodeling, in part by producing paracrine‐acting factors that in turn influence osteoblast and osteoclast activity. Recent evidence has indicated that osteocytes are crucial cellular targets of para...

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Detalles Bibliográficos
Autor principal: Wein, Marc N
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6124166/
https://www.ncbi.nlm.nih.gov/pubmed/30283888
http://dx.doi.org/10.1002/jbm4.10021
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author Wein, Marc N
author_facet Wein, Marc N
author_sort Wein, Marc N
collection PubMed
description Osteocytes are the most abundant cell type in bone and play a central role in orchestrating skeletal remodeling, in part by producing paracrine‐acting factors that in turn influence osteoblast and osteoclast activity. Recent evidence has indicated that osteocytes are crucial cellular targets of parathyroid hormone (PTH). Here, we will review the cellular and molecular mechanisms through which PTH influences osteocyte function. Two well‐studied PTH target genes in osteocytes are SOST and receptor activator of NF‐κB ligand (RANKL). The molecular mechanisms through which PTH regulates expression of these two crucial target genes will be discussed. Beyond SOST and RANKL, PTH/PTH‐related peptide (PTHrP) signaling in osteocytes may directly influence the way osteocytes remodel their perilacunar environment to influence bone homeostasis in a cell‐autonomous manner. Here, I will highlight novel, additional mechanisms used by PTH and PTHrP to modulate bone homeostasis through effects in osteocytes. © 2017 The Authors. JBMR Plus is published by Wiley Periodicals, Inc. on behalf of the American Society for Bone and Mineral Research.
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spelling pubmed-61241662018-10-03 Parathyroid Hormone Signaling in Osteocytes Wein, Marc N JBMR Plus Review Osteocytes are the most abundant cell type in bone and play a central role in orchestrating skeletal remodeling, in part by producing paracrine‐acting factors that in turn influence osteoblast and osteoclast activity. Recent evidence has indicated that osteocytes are crucial cellular targets of parathyroid hormone (PTH). Here, we will review the cellular and molecular mechanisms through which PTH influences osteocyte function. Two well‐studied PTH target genes in osteocytes are SOST and receptor activator of NF‐κB ligand (RANKL). The molecular mechanisms through which PTH regulates expression of these two crucial target genes will be discussed. Beyond SOST and RANKL, PTH/PTH‐related peptide (PTHrP) signaling in osteocytes may directly influence the way osteocytes remodel their perilacunar environment to influence bone homeostasis in a cell‐autonomous manner. Here, I will highlight novel, additional mechanisms used by PTH and PTHrP to modulate bone homeostasis through effects in osteocytes. © 2017 The Authors. JBMR Plus is published by Wiley Periodicals, Inc. on behalf of the American Society for Bone and Mineral Research. John Wiley and Sons Inc. 2017-11-10 /pmc/articles/PMC6124166/ /pubmed/30283888 http://dx.doi.org/10.1002/jbm4.10021 Text en © 2017 The Authors. JBMR Plus is published by Wiley Periodicals, Inc. on behalf of the American Society for Bone and Mineral Research This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Wein, Marc N
Parathyroid Hormone Signaling in Osteocytes
title Parathyroid Hormone Signaling in Osteocytes
title_full Parathyroid Hormone Signaling in Osteocytes
title_fullStr Parathyroid Hormone Signaling in Osteocytes
title_full_unstemmed Parathyroid Hormone Signaling in Osteocytes
title_short Parathyroid Hormone Signaling in Osteocytes
title_sort parathyroid hormone signaling in osteocytes
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6124166/
https://www.ncbi.nlm.nih.gov/pubmed/30283888
http://dx.doi.org/10.1002/jbm4.10021
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