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      JAK-STAT and bone metabolism

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          Abstract

          Emerging evidences suggest Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathway plays an important role in bone development and metabolism. Effects of JAK-STAT pathway on skeletal development are summarized based on skeletal phenotype of individual JAK and STAT gene knockout mouse. Furthermore, STAT3 has more profound effects on bone homeostasis compared with the other STATs. STAT3 mutation causes a disease called Job syndrome, most patients with which have associated craniofacial and skeletal features. Selective inactivation of STAT3 in osteoblasts decreases bone formation and skeletal responsiveness to mechanical loading. Future research includes investigating JAK-STAT signaling in osteoclasts and osteocytes.

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          Most cited references38

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          Essential role of Stat6 in IL-4 signalling.

          K Takeda, T. Tanaka, W Shi … (1996)
          Interleukin-4 (IL-4) is a pleiotropic lymphokine which plays an important role in the immune system. IL-4 activates two distinct signalling pathways through tyrosine phosphorylation of Stat6, a signal transducer and activator of transcription, and of a 170K protein called 4PS. To investigate the functional role of Stat6 in IL-4 signalling, we generated mice deficient in Stat6 by gene targeting. We report here that in the mutant mice, expression of CD23 and major histocompatibility complex (MHC) class II in resting B cells was not enhanced in response to IL-4. IL-4 induced B-cell proliferation costimulated by anti-IgM antibody was abolished. The T-cell proliferative response was also notably reduced. Furthermore, production of Th2 cytokines from T cells as well as IgE and IgG1 responses after nematode infection were profoundly reduced. These findings agreed with those obtained in IL-4 deficient mice or using antibodies to IL-4 and the IL-4 receptor. We conclude that Stat6 plays a central role in exerting IL-4 mediated biological responses.
          Article 0 comments Cited 242 times – based on 0 reviews     Review now
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            Stat6 is required for mediating responses to IL-4 and for development of Th2 cells.

            M Kaplan, U Schindler, S T Smiley … (1996)
            Interleukin-4 (IL-4) stimulation of cells leads to the activation of multiple signaling pathways, one of which involves Stat6. We have generated Stat6-deficient mice by gene targeting in embryonic stem cells to determine the role of this transcription factor in mediating the biologic functions of IL-4. IL-4-induced increases in the cell surface expression of both MHC class II antigens and IL-4 receptor are completely abrogated, and lymphocytes from Stat6-deficient animals fail to proliferate in response to IL-4. Stat6-deficient B cells do not produce IgE following in vivo immunization with anti-IgD. In addition, Stat6-deficient T lymphocytes fail to differentiate into Th2 cells in response to either IL-4 or Il-13. These results demonstrate that, despite the existence of multiple signaling pathways activated by IL-4, Stat6 is essential for mediating responses to IL-4 lymphocytes.
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              Lack of IL-4-induced Th2 response and IgE class switching in mice with disrupted Stat6 gene.

              G Grosveld, J Ihle, T Nosaka … (1996)
              Signal transducers and activators of transcription (Stats) are activated by tyrosine phosphorylation in response to cytokines, and are thought to mediate many of their functional responses. Stat6 is activated in response to interleukin (IL)-4 and may contribute to various functions including mitogenesis, T-helper cell differentiation and immunoglobulin isotype switching. To evaluate the role of Stat6, we generated Stat6-null mice (Stat6 -/-) by gene disruption in embryonic stem cells. The mice were viable, indicating the lack of a non-redundant function in normal development. Although naive lymphoid cell development was normal, Stat6 -/- mice were deficient in IL-4-mediated functions including Th2 helper T-cell differentiation, expression of cell surface markers, and immunoglobulin class switching to IgE. In contrast, IL-4-mediated proliferation was only partly affected.
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                Author and article information

                Journal
                Journal ID (nlm-ta): JAKSTAT
                Journal ID (iso-abbrev): JAKSTAT
                Journal ID (publisher-id): JKST
                Title: JAK-STAT
                Publisher: Landes Bioscience
                ISSN (Print): 2162-3988
                ISSN (Electronic): 2162-3996
                Publication date (Print): 01 July 2013
                Publication date (Electronic): 15 August 2013
                Publication date PMC-release: 15 August 2013
                Volume: 2
                Issue: 3
                Electronic Location Identifier: e23930
                Affiliations
                Department of Biology; Indiana University Purdue University Indianapolis; Indianapolis, IN USA
                Author notes
                Correspondence to: Jiliang Li; Email: jilili@ 123456iupui.edu
                Article
                Publisher ID: 2012JAKS0049R Publisher Item ID: 23930
                DOI: 10.4161/jkst.23930
                PMC ID: 3772100
                PubMed ID: 24069548
                SO-VID: c697eef9-3065-45e8-8a8e-3009a92f3fba
                Copyright © Copyright © 2013 Landes Bioscience
                License:

                This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.

                History
                Date received : 10 November 2012
                Date revision received : 08 February 2013
                Date accepted : 08 February 2013
                Categories
                Subject: Review

                Keywords: janus kinase,signal transducer and activator of transcription,skeletal development,bone homeostasis,osteoblast,mechanotransduction
                Data availability:
                Keywords: janus kinase, signal transducer and activator of transcription, skeletal development, bone homeostasis, osteoblast, mechanotransduction

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