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Hyaluronic acid influence on platelet-induced airway smooth muscle cell proliferation
Division of Drug Research/Pharmacology, Department of Medical and Health Sciences, Faculty of Health Sciences, Linköping University, Linköping, Sweden; Experimental Pathology, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Department of Biomedicine, Department of Biomedicine, School of Health and Medical Sciences, Örebro University, Örebro, Sweden.
Division of Drug Research/Pharmacology, Department of Medical and Health Sciences, Faculty of Health Sciences, Linköping University, Linköping, Sweden.
Division of Drug Research/Pharmacology, Department of Medical and Health Sciences, Faculty of Health Sciences, Linköping University, Linköping, Sweden.
2012 (English)In: Experimental Cell Research, ISSN 0014-4827, E-ISSN 1090-2422, Vol. 318, no 5, p. 632-640Article in journal (Refereed) Published
Abstract [en]

Hyaluronic acid (HA) is one of the main components of the extracellular matrix (ECM) and is expressed throughout the body including the lung and mostly in areas surrounding proliferating and migrating cells. Furthermore, platelets have been implicated as important players in the airway remodelling process, e.g. due to their ability to induce airway smooth muscle cell (ASMC) proliferation. The aim of the present study was to investigate the role of HA, the HA-binding surface receptor CD44 and focal adhesion kinase (FAK) in platelet-induced ASMC proliferation. Proliferation of ASMC was measured using the MTS-assay, and we found that the CD44 blocking antibody and the HA synthase inhibitor 4-Methylumbelliferone (4-MU) significantly inhibited platelet-induced ASMC proliferation. The interaction between ASMC and platelets was studied by fluorescent staining of F-actin. In addition, the ability of ASMC to synthesise HA was investigated by fluorescent staining using biotinylated HA-binding protein and a streptavidin conjugate. We observed that ASMC produced HA and that a CD44 blocking antibody and 4-MU significantly inhibited platelet binding to the area surrounding the ASMC. Furthermore, the FAK-inhibitor PF 573228 inhibited platelet-induced ASMC proliferation. Co-culture of ASMC and platelets also resulted in increased phosphorylation of FAK as detected by Western blot analysis. In addition, 4-MU significantly inhibited the increased FAK-phosphorylation. In conclusion, our findings demonstrate that ECM has the ability to influence platelet-induced ASMC proliferation. Specifically, we propose that HA produced by ASMC is recognised by platelet CD44. The platelet/HA interaction is followed by FAK activation and increased proliferation of co-cultured ASMC. We also suggest that the mitogenic effect of platelets represents a potential important and novel mechanism that may contribute to airway remodelling. (C) 2011 Elsevier Inc. All rights reserved.

Place, publisher, year, edition, pages
San Diego, USA: Elsevier, 2012. Vol. 318, no 5, p. 632-640
Keywords [en]
Airway smooth muscle, Airway remodelling, Extracellular matrix, Hyaluronic acid, CD44, Focal adhesion kinase, Platelets
National Category
Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)
Research subject
Biomedicine
Identifiers
URN: urn:nbn:se:oru:diva-22248DOI: 10.1016/j.yexcr.2011.12.011ISI: 000300966300021PubMedID: 22227408Scopus ID: 2-s2.0-84857060355OAI: oai:DiVA.org:oru-22248DiVA, id: diva2:512149
Funder
Swedish Heart Lung Foundation
Note

Funding Agencies:

strategic areas Cardiovascular Inflammation Research Centre (CIRC)

County of Östergötlands Län 

STIFUD 

Olle E

Swedish Research Council

Available from: 2012-03-26 Created: 2012-03-26 Last updated: 2018-08-28Bibliographically approved

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Bengtsson, Torbjörn

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