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The small leucine-rich repeat proteoglycans in tissue repair and atherosclerosis

Forskningsöversiktsartikel
Författare A. Hultgardh-Nilsson
Jan Borén
S. Chakravarti
Publicerad i Journal of Internal Medicine
Volym 278
Nummer/häfte 5
Sidor 447-461
ISSN 0954-6820
Publiceringsår 2015
Publicerad vid Wallenberglaboratoriet
Institutionen för medicin
Sidor 447-461
Språk en
Länkar dx.doi.org/10.1111/joim.12400
Ämnesord atherosclerosis, biglycan, decorin, fibromodulin, lumican, small leucine-rich repeat proteoglycan, LOW-DENSITY LIPOPROTEINS, GROWTH-FACTOR-BETA, KERATAN SULFATE, PROTEOGLYCAN, EXTRACELLULAR-MATRIX PROTEIN, ABNORMAL COLLAGEN FIBRILS, HUMAN CORONARY-ARTERIES, SMOOTH-MUSCLE-CELLS, HUMAN BIGLYCAN GENE, HEPARAN-SULFATE, CRYSTAL-STRUCTURE, Medicine, General & Internal, ERKENS C, 1995, HUMAN GENETICS, V96, P44
Ämneskategorier Kardiologi

Sammanfattning

Proteoglycans consist of a protein core with one or more covalently attached glycosaminoglycan (GAG) side chains and have multiple roles in the initiation and progression of atherosclerosis. Here we discuss the potential and known functions of a group of small leucine-rich repeat proteoglycans (SLRPs) in atherosclerosis. We focus on five SLRPs, decorin, biglycan, lumican, fibromodulin and PRELP, because these have been detected in atherosclerotic plaques or demonstrated to have a role in animal models of atherosclerosis. Decorin and biglycan are modified post-translationally by substitution with chondroitin/dermatan sulphate GAGs, whereas lumican, fibromodulin and PRELP have keratan sulphate side chains, and the core proteins have leucine-rich repeat (LRR) motifs that are characteristic of the LRR superfamily. The chondroitin/dermatan sulphate GAG side chains have been implicated in lipid retention in atherosclerosis. The core proteins are discussed here in the context of (i) interactions with collagens and their implications in tissue integrity, fibrosis and wound repair and (ii) interactions with growth factors, cytokines, pathogen-associated molecular patterns and cell surface receptors that impact normal physiology and disease processes such as inflammation, innate immune responses and wound healing (i.e. processes that are all important in plaque development and progression). Thus, studies of these SLRPs in the context of wound healing are providing clues about their functions in early stages of atherosclerosis to plaque vulnerability and cardiovascular disease at later stages. Understanding of signal transduction pathways regulated by the core protein interactions is leading to novel roles and therapeutic potential for these proteins in wound repair and atherosclerosis.

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