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      Sclerostin and Its Associations With Bone Metabolism Markers and Sex Hormones in Healthy Community-Dwelling Elderly Individuals and Adolescents

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          Abstract

          Sclerostin is an important regulator of bone mass involving Wnt/β-catenin signaling pathway. We aimed to obtain the profile of serum sclerostin level and explore its associations with bone metabolism markers and sex hormones in healthy community-dwelling Chinese elderly individuals and adolescents. A cross-sectional study was performed in three communities in Shanghai. In all, 861 participants, including 574 healthy elderly individuals, and 287 healthy adolescents, were recruited. The levels of serum sclerostin, procollagen type 1 N-terminal propeptide (P1NP), β-CrossLaps of type I collagen containing cross-linked C-telopeptide (β-CTX), parathyroid hormone (PTH), 25-hydroxyvitamin D [25(OH)D], estradiol (E 2), testosterone (T), and sex hormone-binding globulin (SHBG) were measured in blood samples from all participants. Median sclerostin level was higher in males than in females and in elderly individuals than in adolescents (elderly males: 54.89 pmol/L, elderly females: 39.95 pmol/L, adolescent males: 36.58 pmol/L, adolescent females: 27.06 pmol/L; both P < 0.05). In elderly individuals, serum sclerostin was positively correlated with age (β = 0.176, P < 0.001) and T (β = 0.248, P = 0.001), but negatively associated to P1NP (β = −0.140, P = 0.001). In adolescents, circulating sclerostin was significantly and positively associated with P1NP (β = 0.192, P = 0.003). The directions of the association between sclerostin and P1NP were opposite in Chinese elderly individuals and adolescents, which may reflect that sclerostin plays distinct roles in different functional states of the skeleton. Our findings revealed the rough profile of circulating sclerostin level in general healthy Chinese population and its associations with bone metabolism markers and sex hormones, which may provide a clue to further elucidate the cross action of sclerostin in bone metabolism and sexual development.

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          Regulation of bone mass by Wnt signaling.

          Venkatesh Krishnan, Henry Bryant, Ormond A Macdougald (2006)
          Wnt proteins are a family of secreted proteins that regulate many aspects of cell growth, differentiation, function, and death. Considerable progress has been made in our understanding of the molecular links between Wnt signaling and bone development and remodeling since initial reports that mutations in the Wnt coreceptor low-density lipoprotein receptor-related protein 5 (LRP5) are causally linked to alterations in human bone mass. Of the pathways activated by Wnts, it is signaling through the canonical (i.e., Wnt/beta-catenin) pathway that increases bone mass through a number of mechanisms including renewal of stem cells, stimulation of preosteoblast replication, induction of osteoblastogenesis, and inhibition of osteoblast and osteocyte apoptosis. This pathway is an enticing target for developing drugs to battle skeletal diseases as Wnt/beta-catenin signaling is composed of a series of molecular interactions that offer potential places for pharmacological intervention. In considering opportunities for anabolic drug discovery in this area, one must consider multiple factors, including (a) the roles of Wnt signaling for development, remodeling, and pathology of bone; (b) how pharmacological interventions that target this pathway may specifically treat osteoporosis and other aspects of skeletal health; and (c) whether the targets within this pathway are amenable to drug intervention. In this Review we discuss the current understanding of this pathway in terms of bone biology and assess whether targeting this pathway might yield novel therapeutics to treat typical bone disorders.
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            Romosozumab in postmenopausal women with low bone mineral density.

            Michael McClung, Andreas Grauer, Steven Boonen … (2014)
            Sclerostin is an osteocyte-derived inhibitor of osteoblast activity. The monoclonal antibody romosozumab binds to sclerostin and increases bone formation.
            Article 0 comments Cited 365 times – based on 0 reviews     Review now
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              Sex steroids and the construction and conservation of the adult skeleton.

              Sundeep Khosla, L. Joseph Melton, B Riggs (2002)
              Here we review and extend a new unitary model for the pathophysiology of involutional osteoporosis that identifies estrogen (E) as the key hormone for maintaining bone mass and E deficiency as the major cause of age-related bone loss in both sexes. Also, both E and testosterone (T) are key regulators of skeletal growth and maturation, and E, together with GH and IGF-I, initiate a 3- to 4-yr pubertal growth spurt that doubles skeletal mass. Although E is required for the attainment of maximal peak bone mass in both sexes, the additional action of T on stimulating periosteal apposition accounts for the larger size and thicker cortices of the adult male skeleton. Aging women undergo two phases of bone loss, whereas aging men undergo only one. In women, the menopause initiates an accelerated phase of predominantly cancellous bone loss that declines rapidly over 4-8 yr to become asymptotic with a subsequent slow phase that continues indefinitely. The accelerated phase results from the loss of the direct restraining effects of E on bone turnover, an action mediated by E receptors in both osteoblasts and osteoclasts. In the ensuing slow phase, the rate of cancellous bone loss is reduced, but the rate of cortical bone loss is unchanged or increased. This phase is mediated largely by secondary hyperparathyroidism that results from the loss of E actions on extraskeletal calcium metabolism. The resultant external calcium losses increase the level of dietary calcium intake that is required to maintain bone balance. Impaired osteoblast function due to E deficiency, aging, or both also contributes to the slow phase of bone loss. Although both serum bioavailable (Bio) E and Bio T decline in aging men, Bio E is the major predictor of their bone loss. Thus, both sex steroids are important for developing peak bone mass, but E deficiency is the major determinant of age-related bone loss in both sexes.
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                Author and article information

                Contributors
                Journal
                Journal ID (nlm-ta): Front Cell Dev Biol
                Journal ID (iso-abbrev): Front Cell Dev Biol
                Journal ID (publisher-id): Front. Cell Dev. Biol.
                Title: Frontiers in Cell and Developmental Biology
                Publisher: Frontiers Media S.A.
                ISSN (Electronic): 2296-634X
                Publication date (Electronic): 07 February 2020
                Publication date Collection: 2020
                Volume: 8
                Electronic Location Identifier: 57
                Affiliations
                [1] 1Shanghai Clinical Research Center of Bone Disease, Department of Osteoporosis and Bone Diseases, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital , Shanghai, China
                [2] 2Fenglin Community Health Service Center , Shanghai, China
                [3] 3Longhua Community Health Service Center , Shanghai, China
                [4] 4Qixian Community Health Service Center , Shanghai, China
                Author notes

                Edited by: Chao Liang, Hong Kong Baptist University, Hong Kong

                Reviewed by: Xiaoguang Cheng, Beijing Jishuitan Hospital, China; Qun Cheng, Fudan University, China

                *Correspondence: Hua Yue, yueyinglonghua@ 123456163.com

                This article was submitted to Molecular Medicine, a section of the journal Frontiers in Cell and Developmental Biology

                Article
                DOI: 10.3389/fcell.2020.00057
                PMC ID: 7020200
                PubMed ID: 32117956
                SO-VID: a768becc-2e55-4292-b967-50baf33dac67
                Copyright © Copyright © 2020 Xu, Gao, He, Gu, Yi, Chen, Wang, Tang, Xu, Yue and Zhang.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                Date received : 05 November 2019
                Date accepted : 22 January 2020
                Page count
                Figures: 1, Tables: 3, Equations: 0, References: 37, Pages: 7, Words: 0
                Funding
                Funded by: National Key Research and Development Program of China Stem Cell and Translational Research 10.13039/501100013290
                Funded by: Science and Technology Commission of Shanghai Municipality 10.13039/501100003399
                Funded by: National Natural Science Foundation of China 10.13039/501100001809
                Categories
                Subject: Cell and Developmental Biology
                Subject: Original Research

                Keywords: sclerostin,bone metabolism markers,sex hormones,elderly individuals,adolescents,cross-sectional study
                Data availability:
                Keywords: sclerostin, bone metabolism markers, sex hormones, elderly individuals, adolescents, cross-sectional study

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