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10.1016/j.matbio.2014.12.001 http://scihub22266oqcxt.onion/10.1016/j.matbio.2014.12.001 C4524654!4524654 !25549589     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25549589 &cmd=llinks): Failed to open stream: HTTP request failed! 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Hyaluronan Controls the Deposition of Fibronectin and Collagen and Modulates TGF-?1 Induction of Lung Myofibroblasts |pdf=|usr=}}{{25549589 }} gab.com Text Hyaluronan Controls the Deposition of Fibronectin and Collagen and Modulates TGF- 1 Induction of Lung Myofibroblasts JO: Matrix Biol http://www.kidney.de/pget.php?&tw=1&pmid=25549589 #FOAvip The contribution of hyaluronan-dependent pericellular matrix to TGF-?1-driven induction and maintenance of myofibroblasts is not understood. Hyaluronan is an extracellular matrix (ECM) glycosaminoglycan important in cell adhesion, proliferation and migration, and is implicated in myofibroblast formation and maintenance. Reduced turnover of hyaluronan has been linked to differentiation of myofibroblasts and potentiation of lung fibrosis. Fibronectin is a fibril forming adhesive glycoprotein that is also upregulated following induction with TGF-?1. Although they are known to bind each other, the interplay between hyaluronan and fibronectin in the pericellular matrix during myofibroblast induction and matrix assembly is not clear. This study addresses the role of hyaluronan and its interaction with fibrillar matrix components during myofibroblast formation. Hyaluronan and fibronectin were increased and co-localized in the ECM following myofibroblast induction by TGF-?1. Inhibition of hyaluronan synthesis in TGF-?1-induced lung myofibroblasts over a 4day period with 4-methyl umbelliferone (4-MU) further enhanced myofibroblast morphology, caused increased deposition of fibronectin and type I collagen in the ECM, and increased expression of alpha-smooth muscle actin and hyaluronan synthase 2 (HAS2) mRNA. Hyaluronan oligosaccharides or hyaluronidase treatment, which more effectively disrupted the pericellular matrix, had similar effects. CD44 and ?1 integrins co-localized in the cell membrane and along some stress fibers. However, CD44 and hyaluronan were specifically excluded from focal adhesions, and associated primarily with cortical actin. Time-lapse imaging of the immediate effects of hyaluronidase digestion showed that hyaluronan matrix primarily mediates attachment of membrane and cortical actin between focal contacts, suggesting that surface adhesion through hyaluronan and CD44 is distinct from focal adhesion through ?1 integrins and fibronectin. Fluorescein-labeled hyaluronan bound regularly along fibronectin fibers and co-localized more with ?1 integrin and less with CD44. Therefore, the hyaluronan matrix can interfere with the assembly of fibrillar ECM components, and this interplay regulates the degree of myofibroblast formation. These data also suggest that adhesion through hyaluronan matrix impacts cytoskeletal organization, and is potentially part of a clutch mechanism that regulates stick and slip of myofibroblasts by affecting the adhesion to and organization of fibronectin and collagen. Twit Text FOAVip Hyaluronan Controls the Deposition of Fibronectin and Collagen and Modulates TGF- 1 Induction of Lung Myofibroblasts ????Matrix Biol http://www.kidney.de/pget.php?&tw=1&pmid=25549589 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25549589 #FOAvip English Wikipedia <ref>{{Cite pmid|25549589 }}</ref> Hyaluronan Controls the Deposition of Fibronectin and Collagen and Modulates TGF-?1 Induction of Lung Myofibroblasts #MMPMID25549589 Evanko SP ; Potter-Perigo S ; Petty LJ ; Workman GA ; Wight TN Matrix Biol 2015[Mar]; 42 (ä): 74-92 PMID25549589 show ga The contribution of hyaluronan-dependent pericellular matrix to TGF-?1-driven induction and maintenance of myofibroblasts is not understood. Hyaluronan is an extracellular matrix (ECM) glycosaminoglycan important in cell adhesion, proliferation and migration, and is implicated in myofibroblast formation and maintenance. Reduced turnover of hyaluronan has been linked to differentiation of myofibroblasts and potentiation of lung fibrosis. Fibronectin is a fibril forming adhesive glycoprotein that is also upregulated following induction with TGF-?1. Although they are known to bind each other, the interplay between hyaluronan and fibronectin in the pericellular matrix during myofibroblast induction and matrix assembly is not clear. This study addresses the role of hyaluronan and its interaction with fibrillar matrix components during myofibroblast formation. Hyaluronan and fibronectin were increased and co-localized in the ECM following myofibroblast induction by TGF-?1. Inhibition of hyaluronan synthesis in TGF-?1-induced lung myofibroblasts over a 4day period with 4-methyl umbelliferone (4-MU) further enhanced myofibroblast morphology, caused increased deposition of fibronectin and type I collagen in the ECM, and increased expression of alpha-smooth muscle actin and hyaluronan synthase 2 (HAS2) mRNA. Hyaluronan oligosaccharides or hyaluronidase treatment, which more effectively disrupted the pericellular matrix, had similar effects. CD44 and ?1 integrins co-localized in the cell membrane and along some stress fibers. However, CD44 and hyaluronan were specifically excluded from focal adhesions, and associated primarily with cortical actin. Time-lapse imaging of the immediate effects of hyaluronidase digestion showed that hyaluronan matrix primarily mediates attachment of membrane and cortical actin between focal contacts, suggesting that surface adhesion through hyaluronan and CD44 is distinct from focal adhesion through ?1 integrins and fibronectin. Fluorescein-labeled hyaluronan bound regularly along fibronectin fibers and co-localized more with ?1 integrin and less with CD44. Therefore, the hyaluronan matrix can interfere with the assembly of fibrillar ECM components, and this interplay regulates the degree of myofibroblast formation. These data also suggest that adhesion through hyaluronan matrix impacts cytoskeletal organization, and is potentially part of a clutch mechanism that regulates stick and slip of myofibroblasts by affecting the adhesion to and organization of fibronectin and collagen. |Actins/genetics [MESH] |Cell Adhesion [MESH] |Cells, Cultured [MESH] |Collagen/*metabolism [MESH] |Extracellular Matrix/metabolism [MESH] |Fibronectins/*metabolism [MESH] |Humans [MESH] |Hyaluronan Receptors/metabolism [MESH] |Hyaluronic Acid/*metabolism/pharmacology [MESH] |Hymecromone/pharmacology [MESH] |Lung/*cytology [MESH] |Myofibroblasts/*drug effects/physiology [MESH] |Time-Lapse Imaging [MESH]Hyaluronan Controls the Deposition of Fibronectin and Collagen and Mod(epmc).pdf DeepDyve Pubget Overpricing