Stromal cell-derived factor 1 promotes angiogenesis via a heme oxygenase 1-dependent mechanism
Stromal cell-derived factor 1 (SDF-1) plays a major role in the migration, recruitment, and retention of endothelial progenitor cells to sites of ischemic injury and contributes to neovascularization. We provide direct evidence demonstrating an important role for heme oxygenase 1 (HO-1) in mediating...
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| Veröffentlicht in: | The Journal of experimental medicine 2007-03, Vol.204 (3), p.605-618 |
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| creator | Deshane, Jessy Chen, Sifeng Caballero, Sergio Grochot-Przeczek, Anna Was, Halina Li Calzi, Sergio Lach, Radoslaw Hock, Thomas D Chen, Bo Hill-Kapturczak, Nathalie Siegal, Gene P Dulak, Jozef Jozkowicz, Alicja Grant, Maria B Agarwal, Anupam |
| description | Stromal cell-derived factor 1 (SDF-1) plays a major role in the migration, recruitment, and retention of endothelial progenitor cells to sites of ischemic injury and contributes to neovascularization. We provide direct evidence demonstrating an important role for heme oxygenase 1 (HO-1) in mediating the proangiogenic effects of SDF-1. Nanomolar concentrations of SDF-1 induced HO-1 in endothelial cells through a protein kinase C zeta-dependent and vascular endothelial growth factor-independent mechanism. SDF-1-induced endothelial tube formation and migration was impaired in HO-1-deficient cells. Aortic rings from HO-1(-/-) mice were unable to form capillary sprouts in response to SDF-1, a defect reversed by CO, a byproduct of the HO-1 reaction. Phosphorylation of vasodilator-stimulated phosphoprotein was impaired in HO-1(-/-) cells, an event that was restored by CO. The functional significance of HO-1 in the proangiogenic effects of SDF-1 was confirmed in Matrigel plug, wound healing, and retinal ischemia models in vivo. The absence of HO-1 was associated with impaired wound healing. Intravitreal adoptive transfer of HO-1-deficient endothelial precursors showed defective homing and reendothelialization of the retinal vasculature compared with HO-1 wild-type cells following ischemia. These findings demonstrate a mechanistic role for HO-1 in SDF-1-mediated angiogenesis and provide new avenues for therapeutic approaches in vascular repair. |
| doi_str_mv | 10.1084/jem.20061609 |
| format | Article |
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We provide direct evidence demonstrating an important role for heme oxygenase 1 (HO-1) in mediating the proangiogenic effects of SDF-1. Nanomolar concentrations of SDF-1 induced HO-1 in endothelial cells through a protein kinase C zeta-dependent and vascular endothelial growth factor-independent mechanism. SDF-1-induced endothelial tube formation and migration was impaired in HO-1-deficient cells. Aortic rings from HO-1(-/-) mice were unable to form capillary sprouts in response to SDF-1, a defect reversed by CO, a byproduct of the HO-1 reaction. Phosphorylation of vasodilator-stimulated phosphoprotein was impaired in HO-1(-/-) cells, an event that was restored by CO. The functional significance of HO-1 in the proangiogenic effects of SDF-1 was confirmed in Matrigel plug, wound healing, and retinal ischemia models in vivo. The absence of HO-1 was associated with impaired wound healing. Intravitreal adoptive transfer of HO-1-deficient endothelial precursors showed defective homing and reendothelialization of the retinal vasculature compared with HO-1 wild-type cells following ischemia. These findings demonstrate a mechanistic role for HO-1 in SDF-1-mediated angiogenesis and provide new avenues for therapeutic approaches in vascular repair.</description><identifier>ISSN: 0022-1007</identifier><identifier>EISSN: 1540-9538</identifier><identifier>EISSN: 1892-1007</identifier><identifier>DOI: 10.1084/jem.20061609</identifier><identifier>PMID: 17339405</identifier><language>eng</language><publisher>United States: The Rockefeller University Press</publisher><subject>Animals ; Cells, Cultured ; Chemokine CXCL12 ; Chemokines, CXC - physiology ; Endothelial Cells - enzymology ; Endothelial Cells - physiology ; Endothelium, Vascular - cytology ; Endothelium, Vascular - enzymology ; Endothelium, Vascular - physiology ; Heme Oxygenase-1 - deficiency ; Heme Oxygenase-1 - genetics ; Heme Oxygenase-1 - physiology ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neovascularization, Physiologic ; Stromal Cells - enzymology ; Wound Healing - genetics ; Wound Healing - physiology</subject><ispartof>The Journal of experimental medicine, 2007-03, Vol.204 (3), p.605-618</ispartof><rights>Copyright © 2007, The Rockefeller University Press</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c479t-e9f6340015bfb4ea0e6db07ea8aceab3b0294cad9043c2d0cd06009f83cc8ca53</citedby><cites>FETCH-LOGICAL-c479t-e9f6340015bfb4ea0e6db07ea8aceab3b0294cad9043c2d0cd06009f83cc8ca53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17339405$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Deshane, Jessy</creatorcontrib><creatorcontrib>Chen, Sifeng</creatorcontrib><creatorcontrib>Caballero, Sergio</creatorcontrib><creatorcontrib>Grochot-Przeczek, Anna</creatorcontrib><creatorcontrib>Was, Halina</creatorcontrib><creatorcontrib>Li Calzi, Sergio</creatorcontrib><creatorcontrib>Lach, Radoslaw</creatorcontrib><creatorcontrib>Hock, Thomas D</creatorcontrib><creatorcontrib>Chen, Bo</creatorcontrib><creatorcontrib>Hill-Kapturczak, Nathalie</creatorcontrib><creatorcontrib>Siegal, Gene P</creatorcontrib><creatorcontrib>Dulak, Jozef</creatorcontrib><creatorcontrib>Jozkowicz, Alicja</creatorcontrib><creatorcontrib>Grant, Maria B</creatorcontrib><creatorcontrib>Agarwal, Anupam</creatorcontrib><title>Stromal cell-derived factor 1 promotes angiogenesis via a heme oxygenase 1-dependent mechanism</title><title>The Journal of experimental medicine</title><addtitle>J Exp Med</addtitle><description>Stromal cell-derived factor 1 (SDF-1) plays a major role in the migration, recruitment, and retention of endothelial progenitor cells to sites of ischemic injury and contributes to neovascularization. We provide direct evidence demonstrating an important role for heme oxygenase 1 (HO-1) in mediating the proangiogenic effects of SDF-1. Nanomolar concentrations of SDF-1 induced HO-1 in endothelial cells through a protein kinase C zeta-dependent and vascular endothelial growth factor-independent mechanism. SDF-1-induced endothelial tube formation and migration was impaired in HO-1-deficient cells. Aortic rings from HO-1(-/-) mice were unable to form capillary sprouts in response to SDF-1, a defect reversed by CO, a byproduct of the HO-1 reaction. Phosphorylation of vasodilator-stimulated phosphoprotein was impaired in HO-1(-/-) cells, an event that was restored by CO. The functional significance of HO-1 in the proangiogenic effects of SDF-1 was confirmed in Matrigel plug, wound healing, and retinal ischemia models in vivo. The absence of HO-1 was associated with impaired wound healing. Intravitreal adoptive transfer of HO-1-deficient endothelial precursors showed defective homing and reendothelialization of the retinal vasculature compared with HO-1 wild-type cells following ischemia. These findings demonstrate a mechanistic role for HO-1 in SDF-1-mediated angiogenesis and provide new avenues for therapeutic approaches in vascular repair.</description><subject>Animals</subject><subject>Cells, Cultured</subject><subject>Chemokine CXCL12</subject><subject>Chemokines, CXC - physiology</subject><subject>Endothelial Cells - enzymology</subject><subject>Endothelial Cells - physiology</subject><subject>Endothelium, Vascular - cytology</subject><subject>Endothelium, Vascular - enzymology</subject><subject>Endothelium, Vascular - physiology</subject><subject>Heme Oxygenase-1 - deficiency</subject><subject>Heme Oxygenase-1 - genetics</subject><subject>Heme Oxygenase-1 - physiology</subject><subject>Humans</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Neovascularization, Physiologic</subject><subject>Stromal Cells - enzymology</subject><subject>Wound Healing - genetics</subject><subject>Wound Healing - physiology</subject><issn>0022-1007</issn><issn>1540-9538</issn><issn>1892-1007</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1PGzEQxa2qCELaG2fkU09dGK-9H74goYjSSpE4AFesWe9sYrS7Tu1NVP57jBL6cepppJnfPL2Zx9iZgAsBtbp8puEiByhFCfoDm4lCQaYLWX9kM4A8zwRAdcJOY3wGEEoV5TE7EZWUWkExY0_3U_AD9txS32ctBbejlndoJx-44Js09BNFjuPK-RWNFF3kO4cc-ZoG4v7XS-piJC7S9obGlsaJD2TXOLo4fGJHHfaRPh_qnD1-u3lYfM-Wd7c_FtfLzKpKTxnprpQq-SuarlGEQGXbQEVYoyVsZAO5VhZbDUravAXbQgmgu1paW1ss5Jxd7XU322ag1iYTAXuzCW7A8GI8OvPvZHRrs_I7I-qiULJKAl8OAsH_3FKczODi209wJL-NpkoO0vf0f0GhS1CqFgn8ugdt8DEG6n67EWDekjMpOfOeXMLP_77gD3yISr4C0pKW2A</recordid><startdate>20070319</startdate><enddate>20070319</enddate><creator>Deshane, Jessy</creator><creator>Chen, Sifeng</creator><creator>Caballero, Sergio</creator><creator>Grochot-Przeczek, Anna</creator><creator>Was, Halina</creator><creator>Li Calzi, Sergio</creator><creator>Lach, Radoslaw</creator><creator>Hock, Thomas D</creator><creator>Chen, Bo</creator><creator>Hill-Kapturczak, Nathalie</creator><creator>Siegal, Gene P</creator><creator>Dulak, Jozef</creator><creator>Jozkowicz, Alicja</creator><creator>Grant, Maria B</creator><creator>Agarwal, Anupam</creator><general>The Rockefeller University Press</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>7T5</scope><scope>H94</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20070319</creationdate><title>Stromal cell-derived factor 1 promotes angiogenesis via a heme oxygenase 1-dependent mechanism</title><author>Deshane, Jessy ; Chen, Sifeng ; Caballero, Sergio ; Grochot-Przeczek, Anna ; Was, Halina ; Li Calzi, Sergio ; Lach, Radoslaw ; Hock, Thomas D ; Chen, Bo ; Hill-Kapturczak, Nathalie ; Siegal, Gene P ; Dulak, Jozef ; Jozkowicz, Alicja ; Grant, Maria B ; Agarwal, Anupam</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c479t-e9f6340015bfb4ea0e6db07ea8aceab3b0294cad9043c2d0cd06009f83cc8ca53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Cells, Cultured</topic><topic>Chemokine CXCL12</topic><topic>Chemokines, CXC - physiology</topic><topic>Endothelial Cells - enzymology</topic><topic>Endothelial Cells - physiology</topic><topic>Endothelium, Vascular - cytology</topic><topic>Endothelium, Vascular - enzymology</topic><topic>Endothelium, Vascular - physiology</topic><topic>Heme Oxygenase-1 - deficiency</topic><topic>Heme Oxygenase-1 - genetics</topic><topic>Heme Oxygenase-1 - physiology</topic><topic>Humans</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Neovascularization, Physiologic</topic><topic>Stromal Cells - enzymology</topic><topic>Wound Healing - genetics</topic><topic>Wound Healing - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Deshane, Jessy</creatorcontrib><creatorcontrib>Chen, Sifeng</creatorcontrib><creatorcontrib>Caballero, Sergio</creatorcontrib><creatorcontrib>Grochot-Przeczek, Anna</creatorcontrib><creatorcontrib>Was, Halina</creatorcontrib><creatorcontrib>Li Calzi, Sergio</creatorcontrib><creatorcontrib>Lach, Radoslaw</creatorcontrib><creatorcontrib>Hock, Thomas D</creatorcontrib><creatorcontrib>Chen, Bo</creatorcontrib><creatorcontrib>Hill-Kapturczak, Nathalie</creatorcontrib><creatorcontrib>Siegal, Gene P</creatorcontrib><creatorcontrib>Dulak, Jozef</creatorcontrib><creatorcontrib>Jozkowicz, Alicja</creatorcontrib><creatorcontrib>Grant, Maria B</creatorcontrib><creatorcontrib>Agarwal, Anupam</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of experimental medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Deshane, Jessy</au><au>Chen, Sifeng</au><au>Caballero, Sergio</au><au>Grochot-Przeczek, Anna</au><au>Was, Halina</au><au>Li Calzi, Sergio</au><au>Lach, Radoslaw</au><au>Hock, Thomas D</au><au>Chen, Bo</au><au>Hill-Kapturczak, Nathalie</au><au>Siegal, Gene P</au><au>Dulak, Jozef</au><au>Jozkowicz, Alicja</au><au>Grant, Maria B</au><au>Agarwal, Anupam</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Stromal cell-derived factor 1 promotes angiogenesis via a heme oxygenase 1-dependent mechanism</atitle><jtitle>The Journal of experimental medicine</jtitle><addtitle>J Exp Med</addtitle><date>2007-03-19</date><risdate>2007</risdate><volume>204</volume><issue>3</issue><spage>605</spage><epage>618</epage><pages>605-618</pages><issn>0022-1007</issn><eissn>1540-9538</eissn><eissn>1892-1007</eissn><abstract>Stromal cell-derived factor 1 (SDF-1) plays a major role in the migration, recruitment, and retention of endothelial progenitor cells to sites of ischemic injury and contributes to neovascularization. We provide direct evidence demonstrating an important role for heme oxygenase 1 (HO-1) in mediating the proangiogenic effects of SDF-1. Nanomolar concentrations of SDF-1 induced HO-1 in endothelial cells through a protein kinase C zeta-dependent and vascular endothelial growth factor-independent mechanism. SDF-1-induced endothelial tube formation and migration was impaired in HO-1-deficient cells. Aortic rings from HO-1(-/-) mice were unable to form capillary sprouts in response to SDF-1, a defect reversed by CO, a byproduct of the HO-1 reaction. Phosphorylation of vasodilator-stimulated phosphoprotein was impaired in HO-1(-/-) cells, an event that was restored by CO. The functional significance of HO-1 in the proangiogenic effects of SDF-1 was confirmed in Matrigel plug, wound healing, and retinal ischemia models in vivo. The absence of HO-1 was associated with impaired wound healing. Intravitreal adoptive transfer of HO-1-deficient endothelial precursors showed defective homing and reendothelialization of the retinal vasculature compared with HO-1 wild-type cells following ischemia. These findings demonstrate a mechanistic role for HO-1 in SDF-1-mediated angiogenesis and provide new avenues for therapeutic approaches in vascular repair.</abstract><cop>United States</cop><pub>The Rockefeller University Press</pub><pmid>17339405</pmid><doi>10.1084/jem.20061609</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Cells, Cultured Chemokine CXCL12 Chemokines, CXC - physiology Endothelial Cells - enzymology Endothelial Cells - physiology Endothelium, Vascular - cytology Endothelium, Vascular - enzymology Endothelium, Vascular - physiology Heme Oxygenase-1 - deficiency Heme Oxygenase-1 - genetics Heme Oxygenase-1 - physiology Humans Mice Mice, Inbred C57BL Mice, Knockout Neovascularization, Physiologic Stromal Cells - enzymology Wound Healing - genetics Wound Healing - physiology |
| title | Stromal cell-derived factor 1 promotes angiogenesis via a heme oxygenase 1-dependent mechanism |
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