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      The two faces of serotonin in bone biology

      review-article
      Author(s): 1 , , 2
      Publication date (Print):
      Journal: The Journal of Cell Biology
      Publisher: The Rockefeller University Press

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          Abstract

          The serotonin molecule has some remarkable properties. It is synthesized by two different genes at two different sites, and, surprisingly, plays antagonistic functions on bone mass accrual at these two sites. When produced peripherally, serotonin acts as a hormone to inhibit bone formation. In contrast, when produced in the brain, serotonin acts as a neurotransmitter to exert a positive and dominant effect on bone mass accrual by enhancing bone formation and limiting bone resorption. The effect of serotonin on bone biology could be harnessed pharmacologically to treat diseases such as osteoporosis.

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          Wnt/beta-catenin signaling in mesenchymal progenitors controls osteoblast and chondrocyte differentiation during vertebrate skeletogenesis.

          Timothy F Day, Xizhi Guo, Lisa Garrett-Beal … (2005)
          Chondrocytes and osteoblasts are two primary cell types in the skeletal system that are differentiated from common mesenchymal progenitors. It is believed that osteoblast differentiation is controlled by distinct mechanisms in intramembranous and endochondral ossification. We have found that ectopic canonical Wnt signaling leads to enhanced ossification and suppression of chondrocyte formation. Conversely, genetic inactivation of beta-catenin, an essential component transducing the canonical Wnt signaling, causes ectopic formation of chondrocytes at the expense of osteoblast differentiation during both intramembranous and endochondral ossification. Moreover, inactivation of beta-catenin in mesenchymal progenitor cells in vitro causes chondrocyte differentiation under conditions allowing only osteoblasts to form. Our results demonstrate that beta-catenin is essential in determining whether mesenchymal progenitors will become osteoblasts or chondrocytes regardless of regional locations or ossification mechanisms. Controlling Wnt/beta-catenin signaling is a common molecular mechanism underlying chondrocyte and osteoblast differentiation and specification of intramembranous and endochondral ossification.
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            LDL receptor-related protein 5 (LRP5) affects bone accrual and eye development.

            Yaoqin Gong, Roger B Slee, Naomi Fukai … (2001)
            In humans, low peak bone mass is a significant risk factor for osteoporosis. We report that LRP5, encoding the low-density lipoprotein receptor-related protein 5, affects bone mass accrual during growth. Mutations in LRP5 cause the autosomal recessive disorder osteoporosis-pseudoglioma syndrome (OPPG). We find that OPPG carriers have reduced bone mass when compared to age- and gender-matched controls. We demonstrate LRP5 expression by osteoblasts in situ and show that LRP5 can transduce Wnt signaling in vitro via the canonical pathway. We further show that a mutant-secreted form of LRP5 can reduce bone thickness in mouse calvarial explant cultures. These data indicate that Wnt-mediated signaling via LRP5 affects bone accrual during growth and is important for the establishment of peak bone mass.
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              Synthesis of serotonin by a second tryptophan hydroxylase isoform.

              Diego J Walther, Jens-Uwe Peter, Saleh Bashammakh … (2003)
              Article 0 comments Cited 336 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Cell Biol
                Journal ID (iso-abbrev): J. Cell Biol
                Journal ID (hwp): jcb
                Title: The Journal of Cell Biology
                Publisher: The Rockefeller University Press
                ISSN (Print): 0021-9525
                ISSN (Electronic): 1540-8140
                Publication date (Print): 4 October 2010
                Volume: 191
                Issue: 1
                Pages: 7-13
                Affiliations
                [1 ]Department of Pathology and Cell Biology and [2 ]Department of Genetics and Development, Columbia University Medical Center, New York, NY 10032
                Author notes
                Correspondence to Patricia Ducy: pd2193@ 123456columbia.edu
                Article
                Publisher ID: 201006123
                DOI: 10.1083/jcb.201006123
                PMC ID: 2953449
                PubMed ID: 20921133
                SO-VID: 07e83044-317e-4228-b359-e11cf19d54ef
                Copyright © © 2010 Ducy and Karsenty
                License:

                This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

                History
                Date received : 21 June 2010
                Date accepted : 14 September 2010
                Categories
                Subject: Reviews
                Subject: Review

                ScienceOpen disciplines: Cell biology
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                ScienceOpen disciplines: Cell biology

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