4
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      ERα and Wnt/β-catenin signaling pathways are involved in angelicin-dependent promotion of osteogenesis

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Reports of the ameliorative effect of angelicin on sex hormone deficiency-induced osteoporosis have highlighted this compound as a candidate for the treatment of osteoporosis. However, the molecular mechanisms of action of angelicin on osteoblast differentiation have not been thoroughly researched. The aim of the present study was to evaluate the effect of angelicin on the proliferation, differentiation and mineralization of rat calvarial osteoblasts using a Cell Counting Kit-8, alkaline phosphatase activity and the expression of osteogenic genes and proteins. Treatment with angelicin promoted the proliferation, matrix mineralization and upregulation of osteogenic marker genes including collagen type I α 1 and bone γ-carboxyglutamate in fetal rat calvarial osteoblasts. Furthermore, angelicin promoted the expression of β-catenin and runt related transcription factor 2, which serve a vital role in the Wnt/β-catenin signaling pathway. Consistently, the osteogenic effect of angelicin was attenuated by the use of a Wnt inhibitor. Moreover, angelicin increased the expression of estrogen receptor α (ERα), which also serves a key role in osteoblast differentiation. Taken together, these results demonstrated that angelicin may promote osteoblast differentiation through activation of ERα and the Wnt/β-catenin signaling pathway.

          Related collections

          Most cited references30

          • Record: found
          • Abstract: found
          • Article: not found

          Role and regulation of RUNX2 in osteogenesis.

          Runt-related transcription factor 2 (RUNX2) is a transcription factor closely associated with the osteoblast phenotype. While frequently referred to, the complexity of its regulation and its interactions within the osteoblast differentiation pathway are often overlooked. This review aims to summarise the knowledge of its regulation at the transcriptional, translational and post-translational level. In addition, the regulation of RUNX2 by factors commonly used during osteogenic studies will be discussed.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Osteoblast physiology in normal and pathological conditions.

            Osteoblasts are mononucleated cells that are derived from mesenchymal stem cells and that are responsible for the synthesis and mineralization of bone during initial bone formation and later bone remodelling. Osteoblasts also have a role in the regulation of osteoclast activity through the receptor activator of nuclear factor κ-B ligand and osteoprotegerin. Abnormalities in osteoblast differentiation and activity occur in some common human diseases such as osteoporosis and osteoarthritis. Recent studies also suggest that osteoblast functions are compromised at sites of focal bone erosion in rheumatoid arthritis.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              BMP2 signaling in bone development and repair.

              BMPs are best known for their actions as bone formation signals. Recent studies using transgenic mice in which individual osteogenic BMPs have been removed from the limb skeleton have identified BMP2 as a fundamental component of the inherent regenerative capacity of bone. This review summarizes current findings on the specific requirement for BMP2 in bone formation and repair.
                Bookmark

                Author and article information

                Journal
                Mol Med Rep
                Mol Med Rep
                Molecular Medicine Reports
                D.A. Spandidos
                1791-2997
                1791-3004
                May 2019
                01 March 2019
                01 March 2019
                : 19
                : 5
                : 3469-3476
                Affiliations
                [1 ]College of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, Shandong 250355, P.R. China
                [2 ]Key Laboratory for Rare and Uncommon Diseases of Shandong Province, Shandong Medicinal Biotechnology Center, Shandong Academy of Medical Sciences, Jinan, Shandong 250062, P.R. China
                [3 ]School of Medicine and Life Sciences, University of Jinan, Shandong Academy of Medical Sciences, Jinan, Shandong 250062, P.R. China
                Author notes
                Correspondence to: Dr Jinxiang Han, Key Laboratory for Rare and Uncommon Diseases of Shandong Province, Shandong Medicinal Biotechnology Center, Shandong Academy of Medical Sciences, 18877 Jingshi Road, Jinan, Shandong 250062, P.R. China, E-mail: samshjx88@ 123456sina.com
                Article
                mmr-19-05-3469
                10.3892/mmr.2019.9999
                6472132
                30864714
                6efe72d1-51a2-4f9b-b19a-4ce05610d814
                Copyright: © Ge et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                : 04 July 2018
                : 20 February 2019
                Categories
                Articles

                angelicin,fetal rat calvarial osteoblasts,estrogen receptor α,wnt/β-catenin,osteoblast differentiation

                Comments

                Comment on this article