Isolation and characterization of chondroitin sulfates from sturgeon (Acipenser sinensis) and their effects on growth of fibroblasts

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  • Im A-Rang
    Natural Products Research Institute, College of Pharmacy, Seoul National University
  • Park Youmie
    Natural Products Research Institute, College of Pharmacy, Seoul National University
  • Kim Yeong Shik
    Natural Products Research Institute, College of Pharmacy, Seoul National University

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  • Isolation and Characterization of Chondroitin Sulfates from Sturgeon (<i>Acipenser sinensis</i>) and Their Effects on Growth of Fibroblasts

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Chondroitin sulfate (CS) is a glycosaminoglycan that composed of hexosamine (D-galactosamine) and hexuronic acid (D-glucuronic acid) unit arranged in an alternating unbranched sequence. CS is an essential component of the extracellular matrix (ECM) of connective tissue. It is mainly covalently attached to core proteins in the form of proteoglycans so that it exhibits specific interactions with proteins for cell growth, differentiation, division and migration. In this study, CSs were purified from the cartilage and backbone of sturgeon (Acipenser sinensis). To characterize their biochemical properties, we performed disaccharide compositional analysis after chondroitinase ABC digestion, high performance size exclusion chromatography (HPSEC) and 1H-NMR spectroscopy. We also investigated the effects of CSs on fibroblast proliferation and adhesion to determine whether wound healing was accelerated in vitro and proliferation of different mitogen-activated protein kinases (MAPK) signaling pathways was facilitated. The CS purified from sturgeon cartilage was primarily composed of 4-sulfated CS (88.8%) and sturgeon backbone CS contains more than 60% 6-sulfated CS. The average molecular weights of CSs obtained from sturgeon cartilage and backbone were found to be 8 and 43 kDa, respectively. Our results showed that both CSs are able to increase cell adhesion, induce proliferation and migration on fibroblasts and may accelerate wound healing by inducing MAPK signaling pathways.

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