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      Hyaluronan Regulates Cell Behavior: A Potential Niche Matrix for Stem Cells

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          Abstract

          Hyaluronan is a linear glycosaminoglycan that has received special attention in the last few decades due to its extraordinary physiological functions. This highly viscous polysaccharide is not only a lubricator, but also a significant regulator of cellular behaviors during embryogenesis, morphogenesis, migration, proliferation, and drug resistance in many cell types, including stem cells. Most hyaluronan functions require binding to its cellular receptors CD44, LYVE-1, HARE, layilin, and RHAMM. After binding, proteins are recruited and messages are sent to alter cellular activities. When low concentrations of hyaluronan are applied to stem cells, the proliferative activity is enhanced. However, at high concentrations, stem cells acquire a dormant state and induce a multidrug resistance phenotype. Due to the influence of hyaluronan on cells and tissue morphogenesis, with regards to cardiogenesis, chondrogenesis, osteogenesis, and neurogenesis, it is now been utilized as a biomaterial for tissue regeneration. This paper summarizes the most important and recent findings regarding the regulation of hyaluronan in cells.

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          CD44: from adhesion molecules to signalling regulators.

          Helmut Ponta, Larry Sherman, Peter A Herrlich (2003)
          Cell-adhesion molecules, once believed to function primarily in tethering cells to extracellular ligands, are now recognized as having broader functions in cellular signalling cascades. The CD44 transmembrane glycoprotein family adds new aspects to these roles by participating in signal-transduction processes--not only by establishing specific transmembrane complexes, but also by organizing signalling cascades through association with the actin cytoskeleton. CD44 and its associated partner proteins monitor changes in the extracellular matrix that influence cell growth, survival and differentiation.
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            Hyaluronan as an immune regulator in human diseases.

            Dianhua Jiang, Jiurong Liang, Paul Noble (2011)
            Accumulation and turnover of extracellular matrix components are the hallmarks of tissue injury. Fragmented hyaluronan stimulates the expression of inflammatory genes by a variety of immune cells at the injury site. Hyaluronan binds to a number of cell surface proteins on various cell types. Hyaluronan fragments signal through both Toll-like receptor (TLR) 4 and TLR2 as well as CD44 to stimulate inflammatory genes in inflammatory cells. Hyaluronan is also present on the cell surface of epithelial cells and provides protection against tissue damage from the environment by interacting with TLR2 and TLR4. Hyaluronan and hyaluronan-binding proteins regulate inflammation, tissue injury, and repair through regulating inflammatory cell recruitment, release of inflammatory cytokines, and cell migration. This review focuses on the role of hyaluronan as an immune regulator in human diseases.
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              Oligosaccharides of Hyaluronan Activate Dendritic Cells via Toll-like Receptor 4

              Christian Termeer, Frauke Benedix, Jonathon Sleeman … (2002)
              Low molecular weight fragmentation products of the polysaccharide of Hyaluronic acid (sHA) produced during inflammation have been shown to be potent activators of immunocompetent cells such as dendritic cells (DCs) and macrophages. Here we report that sHA induces maturation of DCs via the Toll-like receptor (TLR)-4, a receptor complex associated with innate immunity and host defense against bacterial infection. Bone marrow–derived DCs from C3H/HeJ and C57BL/10ScCr mice carrying mutant TLR-4 alleles were nonresponsive to sHA-induced phenotypic and functional maturation. Conversely, DCs from TLR-2–deficient mice were still susceptible to sHA. In accordance, addition of an anti–TLR-4 mAb to human monocyte–derived DCs blocked sHA-induced tumor necrosis factor α production. Western blot analysis revealed that sHA treatment resulted in distinct phosphorylation of p38/p42/44 MAP-kinases and nuclear translocation of nuclear factor (NF)-κB, all components of the TLR-4 signaling pathway. Blockade of this pathway by specific inhibitors completely abrogated the sHA-induced DC maturation. Finally, intravenous injection of sHA-induced DC emigration from the skin and their phenotypic and functional maturation in the spleen, again depending on the expression of TLR-4. In conclusion, this is the first report that polysaccharide degradation products of the extracellular matrix produced during inflammation might serve as an endogenous ligand for the TLR-4 complex on DCs.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Biochem Res Int
                Journal ID (iso-abbrev): Biochem Res Int
                Journal ID (publisher-id): BCRI
                Title: Biochemistry Research International
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2090-2247
                ISSN (Electronic): 2090-2255
                Publication date (Print): 2012
                Publication date (Electronic): 12 February 2012
                Volume: 2012
                Electronic Location Identifier: 346972
                Affiliations
                1Institute of Biotechnology, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, Taiwan
                2Research Center of Excellence in Regenerative Medicine, National Cheng Kung University, Tainan, Taiwan
                3Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan
                4Advanced Optoelectronic Technology Center, National Cheng Kung University, Tainan, Taiwan
                Author notes

                Academic Editor: Manuela Viola

                Article
                DOI: 10.1155/2012/346972
                PMC ID: 3287012
                PubMed ID: 22400115
                SO-VID: 5ec07dcc-63d6-4dca-b22e-7b6e8612157b
                Copyright © Copyright © 2012 Mairim Alexandra Solis et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 15 July 2011
                Date revision received : 24 September 2011
                Date accepted : 18 November 2011
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Biochemistry
                Data availability:
                ScienceOpen disciplines: Biochemistry

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