Low molecular weight hyaluronan induces lymphangiogenesis through LYVE-1-mediated signaling pathways
Hyaluronan (HA), a large nonsulfated glycosaminogycan in the extracellular matrix, whose degraded fragments termed as low molecular weight hyaluronan (LMW-HA), has been reported as an important regulator of angiogenesis. However, little is known about the influence of LMW-HA on lymphangiogenesis. In...
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| description | Hyaluronan (HA), a large nonsulfated glycosaminogycan in the extracellular matrix, whose degraded fragments termed as low molecular weight hyaluronan (LMW-HA), has been reported as an important regulator of angiogenesis. However, little is known about the influence of LMW-HA on lymphangiogenesis. In this study, we try to explore the in vitro effects of LMW-HA on lymphangiogenesis and identify the underlying molecular mechanisms. Our results showed that LMW-HA stimulation significantly increased lymphatic endothelial cells (LECs) proliferation, migration and tube formation. Further experiments demonstrated that LMW-HA altered actin cytoskeleton rearrangement and increased the formation of intense stress fibers, lamellipodia and filopodia. Mechanistically, LMW-HA stimulation resulted in rapid tyrosine phosphorylation of protein kinase C α/βII (PKCα/βII) and extracellular-regulated kinase 1/2 (ERK1/2). Lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1), a homologue of CD44, is the main cell surface receptor for HA in LECs. Blocking the binding interaction of LMW-HA with LYVE-1 using neutralizing anti-LYVE-1 antibodies significantly inhibited LECs proliferation, migration, tube formation and signal transduction induced by LMW-HA, suggesting that LMW-HA may play a critical role in the processes required for lymphangiogenesis through interactions with its receptor LYVE-1 and triggering intracellular signal cascades. |
| doi_str_mv | 10.1371/journal.pone.0092857 |
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However, little is known about the influence of LMW-HA on lymphangiogenesis. In this study, we try to explore the in vitro effects of LMW-HA on lymphangiogenesis and identify the underlying molecular mechanisms. Our results showed that LMW-HA stimulation significantly increased lymphatic endothelial cells (LECs) proliferation, migration and tube formation. Further experiments demonstrated that LMW-HA altered actin cytoskeleton rearrangement and increased the formation of intense stress fibers, lamellipodia and filopodia. Mechanistically, LMW-HA stimulation resulted in rapid tyrosine phosphorylation of protein kinase C α/βII (PKCα/βII) and extracellular-regulated kinase 1/2 (ERK1/2). Lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1), a homologue of CD44, is the main cell surface receptor for HA in LECs. Blocking the binding interaction of LMW-HA with LYVE-1 using neutralizing anti-LYVE-1 antibodies significantly inhibited LECs proliferation, migration, tube formation and signal transduction induced by LMW-HA, suggesting that LMW-HA may play a critical role in the processes required for lymphangiogenesis through interactions with its receptor LYVE-1 and triggering intracellular signal cascades.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0092857</identifier><identifier>PMID: 24667755</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Actin ; Adjuvants, Immunologic - pharmacology ; Angiogenesis ; Animals ; Antibodies ; Biology and Life Sciences ; Breast cancer ; Cascades ; CD44 antigen ; Cell adhesion & migration ; Cell Line, Transformed ; Cell migration ; Cell Movement - drug effects ; Cell proliferation ; Cell Proliferation - drug effects ; Cell surface ; Cellular signal transduction ; Cytoskeleton ; Endothelial cells ; Endothelial Cells - cytology ; Endothelial Cells - metabolism ; Endothelium ; Extracellular matrix ; Extracellular signal-regulated kinase ; Fibers ; Filopodia ; Glycoproteins - metabolism ; Homology ; Hyaluronic acid ; Hyaluronic Acid - pharmacology ; Kinases ; Lamellipodia ; Low molecular weights ; Lymphangiogenesis - drug effects ; Lymphatic system ; MAP Kinase Signaling System - drug effects ; Mice ; Molecular biology ; Molecular modelling ; Molecular Weight ; Motility ; Muscle proteins ; Phosphorylation ; Protein kinase C ; Protein Kinases - metabolism ; Signal transduction ; Signaling ; Stimulation ; Studies ; Tumors ; Tyrosine ; Wound healing</subject><ispartof>PloS one, 2014-03, Vol.9 (3), p.e92857</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Wu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Wu et al 2014 Wu et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-b7fa3325568f47877891ec1ce678f9491b34cf92d3c99b03895ff40de405605d3</citedby><cites>FETCH-LOGICAL-c758t-b7fa3325568f47877891ec1ce678f9491b34cf92d3c99b03895ff40de405605d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3965470/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3965470/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,862,883,2098,2917,23853,27911,27912,53778,53780,79355,79356</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24667755$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Addison, Christina Lynn</contributor><creatorcontrib>Wu, Man</creatorcontrib><creatorcontrib>Du, Yan</creatorcontrib><creatorcontrib>Liu, Yiwen</creatorcontrib><creatorcontrib>He, Yiqing</creatorcontrib><creatorcontrib>Yang, Cuixia</creatorcontrib><creatorcontrib>Wang, Wenjuan</creatorcontrib><creatorcontrib>Gao, Feng</creatorcontrib><title>Low molecular weight hyaluronan induces lymphangiogenesis through LYVE-1-mediated signaling pathways</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Hyaluronan (HA), a large nonsulfated glycosaminogycan in the extracellular matrix, whose degraded fragments termed as low molecular weight hyaluronan (LMW-HA), has been reported as an important regulator of angiogenesis. However, little is known about the influence of LMW-HA on lymphangiogenesis. In this study, we try to explore the in vitro effects of LMW-HA on lymphangiogenesis and identify the underlying molecular mechanisms. Our results showed that LMW-HA stimulation significantly increased lymphatic endothelial cells (LECs) proliferation, migration and tube formation. Further experiments demonstrated that LMW-HA altered actin cytoskeleton rearrangement and increased the formation of intense stress fibers, lamellipodia and filopodia. Mechanistically, LMW-HA stimulation resulted in rapid tyrosine phosphorylation of protein kinase C α/βII (PKCα/βII) and extracellular-regulated kinase 1/2 (ERK1/2). Lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1), a homologue of CD44, is the main cell surface receptor for HA in LECs. Blocking the binding interaction of LMW-HA with LYVE-1 using neutralizing anti-LYVE-1 antibodies significantly inhibited LECs proliferation, migration, tube formation and signal transduction induced by LMW-HA, suggesting that LMW-HA may play a critical role in the processes required for lymphangiogenesis through interactions with its receptor LYVE-1 and triggering intracellular signal cascades.</description><subject>Actin</subject><subject>Adjuvants, Immunologic - pharmacology</subject><subject>Angiogenesis</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Biology and Life Sciences</subject><subject>Breast cancer</subject><subject>Cascades</subject><subject>CD44 antigen</subject><subject>Cell adhesion & migration</subject><subject>Cell Line, Transformed</subject><subject>Cell migration</subject><subject>Cell Movement - drug effects</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell surface</subject><subject>Cellular signal transduction</subject><subject>Cytoskeleton</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - cytology</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelium</subject><subject>Extracellular matrix</subject><subject>Extracellular signal-regulated kinase</subject><subject>Fibers</subject><subject>Filopodia</subject><subject>Glycoproteins - metabolism</subject><subject>Homology</subject><subject>Hyaluronic acid</subject><subject>Hyaluronic Acid - pharmacology</subject><subject>Kinases</subject><subject>Lamellipodia</subject><subject>Low molecular weights</subject><subject>Lymphangiogenesis - drug effects</subject><subject>Lymphatic system</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>Mice</subject><subject>Molecular biology</subject><subject>Molecular modelling</subject><subject>Molecular Weight</subject><subject>Motility</subject><subject>Muscle proteins</subject><subject>Phosphorylation</subject><subject>Protein kinase C</subject><subject>Protein Kinases - metabolism</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Stimulation</subject><subject>Studies</subject><subject>Tumors</subject><subject>Tyrosine</subject><subject>Wound healing</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl2L1DAUhoso7rr6D0QLguBFx6T5am-EZVl1YGDBjwWvQpqkbYZOMpukjvPvzTjdZQoKkouE5DnvOXl5s-wlBAuIGHy_dqO3YlhsndULAOqyIuxRdg5rVBa0BOjxyfksexbCGgCCKkqfZmclppQxQs4ztXK7fOMGLcdB-HynTdfHvN-LYfTOCpsbq0apQz7sN9te2M64TlsdTMhj793Y9fnqx-11AYuNVkZErfJgujSXsV2-FbHfiX14nj1pxRD0i2m_yL5_vP529blY3XxaXl2uCslIFYuGtQKhkhBatZhVjFU11BJKTVnV1riGDcKyrUuFZF03AFU1aVsMlMaAUEAUusheH3W3gwt8MihwSCCANYGYJmJ5JJQTa771ZiP8njth-J8L5zsufDRy0Bxq0UiAtYKiTW1lRRAWjSoVVaikTCetD1O3sUmfl9pGL4aZ6PzFmp537idHNSWYgSTwZhLw7m7UIf5j5InqRJrK2NYlMbkxQfLLg0ukLDFL1OIvVFpKb4xMEWlNup8VvJsVJCbqX7ETYwh8-fXL_7M3t3P27QnbazHEPrhhjMbZMAfxEZTeheB1--AcBPyQ8Hs3-CHhfEp4Knt16vpD0X2k0W8vn_fv</recordid><startdate>20140325</startdate><enddate>20140325</enddate><creator>Wu, Man</creator><creator>Du, Yan</creator><creator>Liu, Yiwen</creator><creator>He, Yiqing</creator><creator>Yang, Cuixia</creator><creator>Wang, Wenjuan</creator><creator>Gao, Feng</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140325</creationdate><title>Low molecular weight hyaluronan induces lymphangiogenesis through LYVE-1-mediated signaling pathways</title><author>Wu, Man ; Du, Yan ; Liu, Yiwen ; He, Yiqing ; Yang, Cuixia ; Wang, Wenjuan ; Gao, Feng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-b7fa3325568f47877891ec1ce678f9491b34cf92d3c99b03895ff40de405605d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Actin</topic><topic>Adjuvants, Immunologic - pharmacology</topic><topic>Angiogenesis</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Biology and Life Sciences</topic><topic>Breast cancer</topic><topic>Cascades</topic><topic>CD44 antigen</topic><topic>Cell adhesion & migration</topic><topic>Cell Line, Transformed</topic><topic>Cell migration</topic><topic>Cell Movement - drug effects</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell surface</topic><topic>Cellular signal transduction</topic><topic>Cytoskeleton</topic><topic>Endothelial cells</topic><topic>Endothelial Cells - cytology</topic><topic>Endothelial Cells - metabolism</topic><topic>Endothelium</topic><topic>Extracellular matrix</topic><topic>Extracellular signal-regulated kinase</topic><topic>Fibers</topic><topic>Filopodia</topic><topic>Glycoproteins - metabolism</topic><topic>Homology</topic><topic>Hyaluronic acid</topic><topic>Hyaluronic Acid - pharmacology</topic><topic>Kinases</topic><topic>Lamellipodia</topic><topic>Low molecular weights</topic><topic>Lymphangiogenesis - drug effects</topic><topic>Lymphatic system</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>Mice</topic><topic>Molecular biology</topic><topic>Molecular modelling</topic><topic>Molecular Weight</topic><topic>Motility</topic><topic>Muscle proteins</topic><topic>Phosphorylation</topic><topic>Protein kinase C</topic><topic>Protein Kinases - metabolism</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>Stimulation</topic><topic>Studies</topic><topic>Tumors</topic><topic>Tyrosine</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Man</creatorcontrib><creatorcontrib>Du, Yan</creatorcontrib><creatorcontrib>Liu, Yiwen</creatorcontrib><creatorcontrib>He, Yiqing</creatorcontrib><creatorcontrib>Yang, Cuixia</creatorcontrib><creatorcontrib>Wang, Wenjuan</creatorcontrib><creatorcontrib>Gao, Feng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection (ProQuest)</collection><collection>Natural Science Collection (ProQuest)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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However, little is known about the influence of LMW-HA on lymphangiogenesis. In this study, we try to explore the in vitro effects of LMW-HA on lymphangiogenesis and identify the underlying molecular mechanisms. Our results showed that LMW-HA stimulation significantly increased lymphatic endothelial cells (LECs) proliferation, migration and tube formation. Further experiments demonstrated that LMW-HA altered actin cytoskeleton rearrangement and increased the formation of intense stress fibers, lamellipodia and filopodia. Mechanistically, LMW-HA stimulation resulted in rapid tyrosine phosphorylation of protein kinase C α/βII (PKCα/βII) and extracellular-regulated kinase 1/2 (ERK1/2). Lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1), a homologue of CD44, is the main cell surface receptor for HA in LECs. Blocking the binding interaction of LMW-HA with LYVE-1 using neutralizing anti-LYVE-1 antibodies significantly inhibited LECs proliferation, migration, tube formation and signal transduction induced by LMW-HA, suggesting that LMW-HA may play a critical role in the processes required for lymphangiogenesis through interactions with its receptor LYVE-1 and triggering intracellular signal cascades.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24667755</pmid><doi>10.1371/journal.pone.0092857</doi><tpages>e92857</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | PloS one, 2014-03, Vol.9 (3), p.e92857 |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Actin Adjuvants, Immunologic - pharmacology Angiogenesis Animals Antibodies Biology and Life Sciences Breast cancer Cascades CD44 antigen Cell adhesion & migration Cell Line, Transformed Cell migration Cell Movement - drug effects Cell proliferation Cell Proliferation - drug effects Cell surface Cellular signal transduction Cytoskeleton Endothelial cells Endothelial Cells - cytology Endothelial Cells - metabolism Endothelium Extracellular matrix Extracellular signal-regulated kinase Fibers Filopodia Glycoproteins - metabolism Homology Hyaluronic acid Hyaluronic Acid - pharmacology Kinases Lamellipodia Low molecular weights Lymphangiogenesis - drug effects Lymphatic system MAP Kinase Signaling System - drug effects Mice Molecular biology Molecular modelling Molecular Weight Motility Muscle proteins Phosphorylation Protein kinase C Protein Kinases - metabolism Signal transduction Signaling Stimulation Studies Tumors Tyrosine Wound healing |
| title | Low molecular weight hyaluronan induces lymphangiogenesis through LYVE-1-mediated signaling pathways |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-16T03%3A51%3A03IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Low%20molecular%20weight%20hyaluronan%20induces%20lymphangiogenesis%20through%20LYVE-1-mediated%20signaling%20pathways&rft.jtitle=PloS%20one&rft.au=Wu,%20Man&rft.date=2014-03-25&rft.volume=9&rft.issue=3&rft.spage=e92857&rft.pages=e92857-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0092857&rft_dat=%3Cgale_plos_%3EA478752247%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1510195146&rft_id=info:pmid/24667755&rft_galeid=A478752247&rft_doaj_id=oai_doaj_org_article_1eabc04ed1af4cfc8534abd2d6d3267e&rfr_iscdi=true |