Differential Macrophage Polarization Promotes Tissue Remodeling and Repair in a Model of Ischemic Retinopathy
Diabetic retinopathy is the leading cause of visual loss in individuals under the age of 55. Umbilical cord blood (UCB)–derived myeloid progenitor cells have been shown to decrease neuronal damage associated with ischemia in the central nervous system. In this study we show that UCB-derived CD14 + p...
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description | Diabetic retinopathy is the leading cause of visual loss in individuals under the age of 55. Umbilical cord blood (UCB)–derived myeloid progenitor cells have been shown to decrease neuronal damage associated with ischemia in the central nervous system. In this study we show that UCB-derived CD14
+
progenitor cells provide rescue effects in a mouse model of ischemic retinopathy by promoting physiological angiogenesis and reducing associated inflammation. We use confocal microscopy to trace the fate of injected human UCB-derived CD14
+
cells and PCR with species-specific probes to investigate their gene expression profile before and after injection. Metabolomic analysis measures changes induced by CD14
+
cells. Our results demonstrate that human cells differentiate
in vivo
into M2 macrophages and induce the polarization of resident M2 macrophages. This leads to stabilization of the ischemia-injured retinal vasculature by modulating the inflammatory response, reducing oxidative stress and apoptosis and promoting tissue repair. |
doi_str_mv | 10.1038/srep00076 |
format | Article |
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+
progenitor cells provide rescue effects in a mouse model of ischemic retinopathy by promoting physiological angiogenesis and reducing associated inflammation. We use confocal microscopy to trace the fate of injected human UCB-derived CD14
+
cells and PCR with species-specific probes to investigate their gene expression profile before and after injection. Metabolomic analysis measures changes induced by CD14
+
cells. Our results demonstrate that human cells differentiate
in vivo
into M2 macrophages and induce the polarization of resident M2 macrophages. This leads to stabilization of the ischemia-injured retinal vasculature by modulating the inflammatory response, reducing oxidative stress and apoptosis and promoting tissue repair.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep00076</identifier><identifier>PMID: 22355595</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/136/16 ; 631/443/592 ; 631/45/320 ; 631/532 ; Angiogenesis ; Animals ; Apoptosis ; CD14 antigen ; Cells, Cultured ; Central nervous system ; Confocal microscopy ; Cord blood ; Diabetes mellitus ; Diabetic retinopathy ; Disease Models, Animal ; Gene expression ; Hemopoiesis ; Humanities and Social Sciences ; Humans ; Inflammation ; Ischemia ; Ischemia - pathology ; Lipopolysaccharide Receptors - immunology ; Macrophages ; Macrophages - immunology ; Macrophages - physiology ; Metabolomics ; Mice ; Microscopy, Confocal ; multidisciplinary ; Neural stem cells ; Oxidative stress ; Polarization ; Polymerase Chain Reaction ; Probes ; Retina ; Retinal Diseases - pathology ; Retinal Vessels - pathology ; Retinopathy ; Rodents ; Science ; Umbilical cord</subject><ispartof>Scientific reports, 2011-08, Vol.1 (1), p.76-76, Article 76</ispartof><rights>The Author(s) 2011</rights><rights>Copyright Nature Publishing Group Aug 2011</rights><rights>Copyright © 2011, Macmillan Publishers Limited. All rights reserved 2011 Macmillan Publishers Limited. All rights reserved</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-daeb3d5af343fd86bac03fc1b828428cf3bca252bd94ad42936445f698043aeb3</citedby><cites>FETCH-LOGICAL-c503t-daeb3d5af343fd86bac03fc1b828428cf3bca252bd94ad42936445f698043aeb3</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/PMC3216563/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3216563/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22355595$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Marchetti, Valentina</creatorcontrib><creatorcontrib>Yanes, Oscar</creatorcontrib><creatorcontrib>Aguilar, Edith</creatorcontrib><creatorcontrib>Wang, Matthew</creatorcontrib><creatorcontrib>Friedlander, David</creatorcontrib><creatorcontrib>Moreno, Stacey</creatorcontrib><creatorcontrib>Storm, Kathleen</creatorcontrib><creatorcontrib>Zhan, Min</creatorcontrib><creatorcontrib>Naccache, Samia</creatorcontrib><creatorcontrib>Nemerow, Glen</creatorcontrib><creatorcontrib>Siuzdak, Gary</creatorcontrib><creatorcontrib>Friedlander, Martin</creatorcontrib><title>Differential Macrophage Polarization Promotes Tissue Remodeling and Repair in a Model of Ischemic Retinopathy</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Diabetic retinopathy is the leading cause of visual loss in individuals under the age of 55. Umbilical cord blood (UCB)–derived myeloid progenitor cells have been shown to decrease neuronal damage associated with ischemia in the central nervous system. In this study we show that UCB-derived CD14
+
progenitor cells provide rescue effects in a mouse model of ischemic retinopathy by promoting physiological angiogenesis and reducing associated inflammation. We use confocal microscopy to trace the fate of injected human UCB-derived CD14
+
cells and PCR with species-specific probes to investigate their gene expression profile before and after injection. Metabolomic analysis measures changes induced by CD14
+
cells. Our results demonstrate that human cells differentiate
in vivo
into M2 macrophages and induce the polarization of resident M2 macrophages. This leads to stabilization of the ischemia-injured retinal vasculature by modulating the inflammatory response, reducing oxidative stress and apoptosis and promoting tissue repair.</description><subject>631/136/16</subject><subject>631/443/592</subject><subject>631/45/320</subject><subject>631/532</subject><subject>Angiogenesis</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>CD14 antigen</subject><subject>Cells, Cultured</subject><subject>Central nervous system</subject><subject>Confocal microscopy</subject><subject>Cord blood</subject><subject>Diabetes mellitus</subject><subject>Diabetic retinopathy</subject><subject>Disease Models, Animal</subject><subject>Gene expression</subject><subject>Hemopoiesis</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Ischemia</subject><subject>Ischemia - pathology</subject><subject>Lipopolysaccharide Receptors - immunology</subject><subject>Macrophages</subject><subject>Macrophages - immunology</subject><subject>Macrophages - physiology</subject><subject>Metabolomics</subject><subject>Mice</subject><subject>Microscopy, Confocal</subject><subject>multidisciplinary</subject><subject>Neural stem cells</subject><subject>Oxidative stress</subject><subject>Polarization</subject><subject>Polymerase Chain Reaction</subject><subject>Probes</subject><subject>Retina</subject><subject>Retinal Diseases - pathology</subject><subject>Retinal Vessels - pathology</subject><subject>Retinopathy</subject><subject>Rodents</subject><subject>Science</subject><subject>Umbilical cord</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNplkV9LHDEUxYNYVKwPfgEJ9EEsbJvJn5nJS0HUqqAoos_hTibZjcwk02RG0E9vltVl2z6EJJxfzr03B6HDgvwoCKt_pmgGQkhVbqE9SriYUUbp9sZ5Fx2k9JwRIqjkhdxBu5QyIYQUe6g_d9aaaPzooMO3oGMYFjA3-D50EN0bjC54fB9DH0aT8KNLaTL4wfShNZ3zcwy-zdcBXMTOY8C3SwEHi6-TXpje6ayOzocBxsXrV_TFQpfMwce-j55-XzyeXc1u7i6vz05vZloQNs5aMA1rBVjGmW3rsgFNmNVFU9Oa01pb1miggjat5NByKlnJubClrAlny7f76NfKd5ia3rQ6jxehU0N0PcRXFcCpvxXvFmoeXhSjRSlKlg2OPwxi-DOZNKreJW26DrwJU1KSsiKvSmTy2z_kc5iiz9OpopYVk7SuqkydrKj8vyknZte9FEQtY1TrGDN7tNn8mvwMLQPfV0DKkp-buFHyP7d3vNao1Q</recordid><startdate>20110830</startdate><enddate>20110830</enddate><creator>Marchetti, Valentina</creator><creator>Yanes, Oscar</creator><creator>Aguilar, Edith</creator><creator>Wang, Matthew</creator><creator>Friedlander, David</creator><creator>Moreno, Stacey</creator><creator>Storm, Kathleen</creator><creator>Zhan, Min</creator><creator>Naccache, Samia</creator><creator>Nemerow, Glen</creator><creator>Siuzdak, Gary</creator><creator>Friedlander, Martin</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20110830</creationdate><title>Differential Macrophage Polarization Promotes Tissue Remodeling and Repair in a Model of Ischemic Retinopathy</title><author>Marchetti, Valentina ; Yanes, Oscar ; Aguilar, Edith ; Wang, Matthew ; Friedlander, David ; Moreno, Stacey ; Storm, Kathleen ; Zhan, Min ; Naccache, Samia ; Nemerow, Glen ; Siuzdak, Gary ; Friedlander, Martin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-daeb3d5af343fd86bac03fc1b828428cf3bca252bd94ad42936445f698043aeb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>631/136/16</topic><topic>631/443/592</topic><topic>631/45/320</topic><topic>631/532</topic><topic>Angiogenesis</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>CD14 antigen</topic><topic>Cells, Cultured</topic><topic>Central nervous system</topic><topic>Confocal microscopy</topic><topic>Cord blood</topic><topic>Diabetes mellitus</topic><topic>Diabetic retinopathy</topic><topic>Disease Models, Animal</topic><topic>Gene expression</topic><topic>Hemopoiesis</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Ischemia</topic><topic>Ischemia - pathology</topic><topic>Lipopolysaccharide Receptors - immunology</topic><topic>Macrophages</topic><topic>Macrophages - immunology</topic><topic>Macrophages - physiology</topic><topic>Metabolomics</topic><topic>Mice</topic><topic>Microscopy, Confocal</topic><topic>multidisciplinary</topic><topic>Neural stem cells</topic><topic>Oxidative stress</topic><topic>Polarization</topic><topic>Polymerase Chain Reaction</topic><topic>Probes</topic><topic>Retina</topic><topic>Retinal Diseases - pathology</topic><topic>Retinal Vessels - pathology</topic><topic>Retinopathy</topic><topic>Rodents</topic><topic>Science</topic><topic>Umbilical cord</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Marchetti, Valentina</creatorcontrib><creatorcontrib>Yanes, Oscar</creatorcontrib><creatorcontrib>Aguilar, Edith</creatorcontrib><creatorcontrib>Wang, Matthew</creatorcontrib><creatorcontrib>Friedlander, David</creatorcontrib><creatorcontrib>Moreno, Stacey</creatorcontrib><creatorcontrib>Storm, Kathleen</creatorcontrib><creatorcontrib>Zhan, Min</creatorcontrib><creatorcontrib>Naccache, Samia</creatorcontrib><creatorcontrib>Nemerow, Glen</creatorcontrib><creatorcontrib>Siuzdak, Gary</creatorcontrib><creatorcontrib>Friedlander, Martin</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech 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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>Proquest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Marchetti, Valentina</au><au>Yanes, Oscar</au><au>Aguilar, Edith</au><au>Wang, Matthew</au><au>Friedlander, David</au><au>Moreno, Stacey</au><au>Storm, Kathleen</au><au>Zhan, Min</au><au>Naccache, Samia</au><au>Nemerow, Glen</au><au>Siuzdak, Gary</au><au>Friedlander, Martin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential Macrophage Polarization Promotes Tissue Remodeling and Repair in a Model of Ischemic Retinopathy</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2011-08-30</date><risdate>2011</risdate><volume>1</volume><issue>1</issue><spage>76</spage><epage>76</epage><pages>76-76</pages><artnum>76</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Diabetic retinopathy is the leading cause of visual loss in individuals under the age of 55. Umbilical cord blood (UCB)–derived myeloid progenitor cells have been shown to decrease neuronal damage associated with ischemia in the central nervous system. In this study we show that UCB-derived CD14
+
progenitor cells provide rescue effects in a mouse model of ischemic retinopathy by promoting physiological angiogenesis and reducing associated inflammation. We use confocal microscopy to trace the fate of injected human UCB-derived CD14
+
cells and PCR with species-specific probes to investigate their gene expression profile before and after injection. Metabolomic analysis measures changes induced by CD14
+
cells. Our results demonstrate that human cells differentiate
in vivo
into M2 macrophages and induce the polarization of resident M2 macrophages. This leads to stabilization of the ischemia-injured retinal vasculature by modulating the inflammatory response, reducing oxidative stress and apoptosis and promoting tissue repair.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>22355595</pmid><doi>10.1038/srep00076</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 631/136/16 631/443/592 631/45/320 631/532 Angiogenesis Animals Apoptosis CD14 antigen Cells, Cultured Central nervous system Confocal microscopy Cord blood Diabetes mellitus Diabetic retinopathy Disease Models, Animal Gene expression Hemopoiesis Humanities and Social Sciences Humans Inflammation Ischemia Ischemia - pathology Lipopolysaccharide Receptors - immunology Macrophages Macrophages - immunology Macrophages - physiology Metabolomics Mice Microscopy, Confocal multidisciplinary Neural stem cells Oxidative stress Polarization Polymerase Chain Reaction Probes Retina Retinal Diseases - pathology Retinal Vessels - pathology Retinopathy Rodents Science Umbilical cord |
title | Differential Macrophage Polarization Promotes Tissue Remodeling and Repair in a Model of Ischemic Retinopathy |
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