RANTES/CCL5-induced pro-angiogenic effects depend on CCR1, CCR5 and glycosaminoglycans
Atherosclerosis involves angiogenesis and inflammation with the ability of endothelial cells and monocytes to respond to chemokines. We addressed here by in vitro and in vivo approaches, the role of the chemokine Regulated on Activation, Normal T Cell Expressed and Secreted (RANTES)/CCL5 on angiogen...
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| Veröffentlicht in: | Angiogenesis (London) 2012-12, Vol.15 (4), p.727-744 |
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| creator | Suffee, N. Hlawaty, H. Meddahi-Pelle, A. Maillard, L. Louedec, L. Haddad, O. Martin, L. Laguillier, C. Richard, B. Oudar, O. Letourneur, D. Charnaux, N. Sutton, A. |
| description | Atherosclerosis involves angiogenesis and inflammation with the ability of endothelial cells and monocytes to respond to chemokines. We addressed here by in vitro and in vivo approaches, the role of the chemokine Regulated on Activation, Normal T Cell Expressed and Secreted (RANTES)/CCL5 on angiogenesis through its receptors CCR1, CCR5, syndecan-1 (SDC-1), syndecan-4 (SDC-4) and CD-44. Our data demonstrate that RANTES/CCL5 is pro-angiogenic in a rat subcutaneous model. This RANTES/CCL5-activity may be related to the in vitro promotion of endothelial cell migration, spreading and neo-vessel formation. RANTES/CCL5-mediated angiogenesis depends at least partly on Vascular Endothelial Growth Factor (VEGF) secretion by endothelial cells, since this effect is decreased when endothelial cells are incubated with anti-VEGF receptor antibodies. RANTES/CCL5-induced chemotaxis is mediated by matrix metalloproteinase-9. We demonstrate that specific receptors of RANTES/CCL5 such as G protein-coupled receptors CCR1 and CCR5, and heparan sulfate proteoglycans, SDC-1, SDC-4 or CD-44, play a major role in RANTES/CCL5-induced angiogenic effects. By the use of two RANTES/CCL5 mutants, [E66A]-RANTES/CCL5 with impaired ability to oligomerize, and [
44
AANA
47
]-RANTES/CCL5 mutated in the main RANTES/CCL5-glycosaminoglycan (GAG) binding site, we demonstrate that chemokine oligomerization and binding to GAGs are essential in RANTES/CCL5-induced angiogenic effects. According to these results, new therapeutic strategies based on RANTES/CCL5 can be proposed for neo-angiogenesis after vascular injury. Mutants of RANTES/CCL5 may also represent an innovative approach to prevent the angiogenesis associated with the formation of atherosclerotic plaque. |
| doi_str_mv | 10.1007/s10456-012-9285-x |
| format | Article |
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44
AANA
47
]-RANTES/CCL5 mutated in the main RANTES/CCL5-glycosaminoglycan (GAG) binding site, we demonstrate that chemokine oligomerization and binding to GAGs are essential in RANTES/CCL5-induced angiogenic effects. According to these results, new therapeutic strategies based on RANTES/CCL5 can be proposed for neo-angiogenesis after vascular injury. Mutants of RANTES/CCL5 may also represent an innovative approach to prevent the angiogenesis associated with the formation of atherosclerotic plaque.</description><identifier>ISSN: 0969-6970</identifier><identifier>EISSN: 1573-7209</identifier><identifier>DOI: 10.1007/s10456-012-9285-x</identifier><identifier>PMID: 22752444</identifier><identifier>CODEN: AGIOFT</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Animals ; Biochemistry ; Biochemistry, Molecular Biology ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Blood and lymphatic vessels ; Cancer ; Cancer Research ; Cardiology ; Cardiology. Vascular system ; Cardiovascular system ; Cell Biology ; Chemical Sciences ; Chemokine CCL5 - physiology ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Enzyme-Linked Immunosorbent Assay ; Glycosaminoglycans - physiology ; Immunohistochemistry ; Life Sciences ; Male ; Medical sciences ; Medicinal Chemistry ; Neovascularization, Physiologic - physiology ; Oncology ; Ophthalmology ; Original Paper ; Pharmacology. Drug treatments ; Rats ; Rats, Wistar ; Receptors, CCR1 - physiology ; Vasodilator agents. Cerebral vasodilators</subject><ispartof>Angiogenesis (London), 2012-12, Vol.15 (4), p.727-744</ispartof><rights>Springer Science+Business Media B.V. 2012</rights><rights>2015 INIST-CNRS</rights><rights>Springer Science+Business Media Dordrecht 2012</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c535t-ca65a030c07ba5afbc2c38fb23feb417ef6113416f7ebbe2006b021e710aaa093</citedby><cites>FETCH-LOGICAL-c535t-ca65a030c07ba5afbc2c38fb23feb417ef6113416f7ebbe2006b021e710aaa093</cites><orcidid>0000-0002-7940-2955 ; 0000-0003-2197-9468</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10456-012-9285-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10456-012-9285-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26615499$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22752444$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://cea.hal.science/cea-02530559$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Suffee, N.</creatorcontrib><creatorcontrib>Hlawaty, H.</creatorcontrib><creatorcontrib>Meddahi-Pelle, A.</creatorcontrib><creatorcontrib>Maillard, L.</creatorcontrib><creatorcontrib>Louedec, L.</creatorcontrib><creatorcontrib>Haddad, O.</creatorcontrib><creatorcontrib>Martin, L.</creatorcontrib><creatorcontrib>Laguillier, C.</creatorcontrib><creatorcontrib>Richard, B.</creatorcontrib><creatorcontrib>Oudar, O.</creatorcontrib><creatorcontrib>Letourneur, D.</creatorcontrib><creatorcontrib>Charnaux, N.</creatorcontrib><creatorcontrib>Sutton, A.</creatorcontrib><title>RANTES/CCL5-induced pro-angiogenic effects depend on CCR1, CCR5 and glycosaminoglycans</title><title>Angiogenesis (London)</title><addtitle>Angiogenesis</addtitle><addtitle>Angiogenesis</addtitle><description>Atherosclerosis involves angiogenesis and inflammation with the ability of endothelial cells and monocytes to respond to chemokines. We addressed here by in vitro and in vivo approaches, the role of the chemokine Regulated on Activation, Normal T Cell Expressed and Secreted (RANTES)/CCL5 on angiogenesis through its receptors CCR1, CCR5, syndecan-1 (SDC-1), syndecan-4 (SDC-4) and CD-44. Our data demonstrate that RANTES/CCL5 is pro-angiogenic in a rat subcutaneous model. This RANTES/CCL5-activity may be related to the in vitro promotion of endothelial cell migration, spreading and neo-vessel formation. RANTES/CCL5-mediated angiogenesis depends at least partly on Vascular Endothelial Growth Factor (VEGF) secretion by endothelial cells, since this effect is decreased when endothelial cells are incubated with anti-VEGF receptor antibodies. RANTES/CCL5-induced chemotaxis is mediated by matrix metalloproteinase-9. We demonstrate that specific receptors of RANTES/CCL5 such as G protein-coupled receptors CCR1 and CCR5, and heparan sulfate proteoglycans, SDC-1, SDC-4 or CD-44, play a major role in RANTES/CCL5-induced angiogenic effects. By the use of two RANTES/CCL5 mutants, [E66A]-RANTES/CCL5 with impaired ability to oligomerize, and [
44
AANA
47
]-RANTES/CCL5 mutated in the main RANTES/CCL5-glycosaminoglycan (GAG) binding site, we demonstrate that chemokine oligomerization and binding to GAGs are essential in RANTES/CCL5-induced angiogenic effects. According to these results, new therapeutic strategies based on RANTES/CCL5 can be proposed for neo-angiogenesis after vascular injury. Mutants of RANTES/CCL5 may also represent an innovative approach to prevent the angiogenesis associated with the formation of atherosclerotic plaque.</description><subject>Animals</subject><subject>Biochemistry</subject><subject>Biochemistry, Molecular Biology</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blood and lymphatic vessels</subject><subject>Cancer</subject><subject>Cancer Research</subject><subject>Cardiology</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular system</subject><subject>Cell Biology</subject><subject>Chemical Sciences</subject><subject>Chemokine CCL5 - physiology</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Glycosaminoglycans - physiology</subject><subject>Immunohistochemistry</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicinal Chemistry</subject><subject>Neovascularization, Physiologic - physiology</subject><subject>Oncology</subject><subject>Ophthalmology</subject><subject>Original Paper</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors, CCR1 - physiology</subject><subject>Vasodilator agents. 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Vascular system</topic><topic>Cardiovascular system</topic><topic>Cell Biology</topic><topic>Chemical Sciences</topic><topic>Chemokine CCL5 - physiology</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Glycosaminoglycans - physiology</topic><topic>Immunohistochemistry</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Medicinal Chemistry</topic><topic>Neovascularization, Physiologic - physiology</topic><topic>Oncology</topic><topic>Ophthalmology</topic><topic>Original Paper</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptors, CCR1 - physiology</topic><topic>Vasodilator agents. 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We addressed here by in vitro and in vivo approaches, the role of the chemokine Regulated on Activation, Normal T Cell Expressed and Secreted (RANTES)/CCL5 on angiogenesis through its receptors CCR1, CCR5, syndecan-1 (SDC-1), syndecan-4 (SDC-4) and CD-44. Our data demonstrate that RANTES/CCL5 is pro-angiogenic in a rat subcutaneous model. This RANTES/CCL5-activity may be related to the in vitro promotion of endothelial cell migration, spreading and neo-vessel formation. RANTES/CCL5-mediated angiogenesis depends at least partly on Vascular Endothelial Growth Factor (VEGF) secretion by endothelial cells, since this effect is decreased when endothelial cells are incubated with anti-VEGF receptor antibodies. RANTES/CCL5-induced chemotaxis is mediated by matrix metalloproteinase-9. We demonstrate that specific receptors of RANTES/CCL5 such as G protein-coupled receptors CCR1 and CCR5, and heparan sulfate proteoglycans, SDC-1, SDC-4 or CD-44, play a major role in RANTES/CCL5-induced angiogenic effects. By the use of two RANTES/CCL5 mutants, [E66A]-RANTES/CCL5 with impaired ability to oligomerize, and [
44
AANA
47
]-RANTES/CCL5 mutated in the main RANTES/CCL5-glycosaminoglycan (GAG) binding site, we demonstrate that chemokine oligomerization and binding to GAGs are essential in RANTES/CCL5-induced angiogenic effects. According to these results, new therapeutic strategies based on RANTES/CCL5 can be proposed for neo-angiogenesis after vascular injury. Mutants of RANTES/CCL5 may also represent an innovative approach to prevent the angiogenesis associated with the formation of atherosclerotic plaque.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>22752444</pmid><doi>10.1007/s10456-012-9285-x</doi><tpages>18</tpages><orcidid>https://orcid.org/0000-0002-7940-2955</orcidid><orcidid>https://orcid.org/0000-0003-2197-9468</orcidid></addata></record> |
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| ispartof | Angiogenesis (London), 2012-12, Vol.15 (4), p.727-744 |
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| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Animals Biochemistry Biochemistry, Molecular Biology Biological and medical sciences Biomedical and Life Sciences Biomedicine Blood and lymphatic vessels Cancer Cancer Research Cardiology Cardiology. Vascular system Cardiovascular system Cell Biology Chemical Sciences Chemokine CCL5 - physiology Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Enzyme-Linked Immunosorbent Assay Glycosaminoglycans - physiology Immunohistochemistry Life Sciences Male Medical sciences Medicinal Chemistry Neovascularization, Physiologic - physiology Oncology Ophthalmology Original Paper Pharmacology. Drug treatments Rats Rats, Wistar Receptors, CCR1 - physiology Vasodilator agents. Cerebral vasodilators |
| title | RANTES/CCL5-induced pro-angiogenic effects depend on CCR1, CCR5 and glycosaminoglycans |
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