Autologous Transplantation of Peripheral Blood-derived Circulating Endothelial Progenitor Cells Attenuates Endotoxin-induced Acute Lung Injury in Rabbits by Direct Endothelial Repair and Indirect Immunomodulation
Studies have demonstrated the role of circulating endothelial progenitor cells (EPCs) in maintaining normal endothelial function and in endothelial repairing. This study was aimed to observe the protective effects of autologous transplantation of circulating EPCs against endotoxin-induced acute lung...
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Veröffentlicht in: | Anesthesiology (Philadelphia) 2012-06, Vol.116 (6), p.1278-1287 |
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description | Studies have demonstrated the role of circulating endothelial progenitor cells (EPCs) in maintaining normal endothelial function and in endothelial repairing. This study was aimed to observe the protective effects of autologous transplantation of circulating EPCs against endotoxin-induced acute lung injury in rabbits and to investigate the underlying mechanisms.
One-hundred-and-fifty rabbits were enrolled. After acute lung injury was induced by endotoxin, autologous circulating EPCs, endothelial cell, or normal saline were transfused intravenously, respectively. Pao(2)/FiO(2) ratios, concentrations of plasma nitric oxide, malonyldialdehyde, and activity of superoxide dismutase were examined. The lung wet-to-dry weight ratios were counted; polymorphonuclear cell ratios and areas of hyaline membrane formation and hemorrhage were measured. The levels of interleukin-1β, E-selectin, intercellular adhesion molecule-1, interleukin-10, vascular endothelial growth factor protein, and inducible nitric oxide synthase protein were analyzed.
Pao(2)/FiO(2) ratios were significantly increased with EPC transfusion. Infiltration of polymorphonuclear cells, lung wet-to-dry weight ratios, and area of hyaline membrane and hemorrhage in lung tissue were significantly decreased after EPC transplantation. Plasma level of nitric oxide and malondialdehyde were significantly inhibited, and the activity of superoxide dismutase was enhanced in the EPC-treated animals. EPC transplantation significantly increased level of interleukin-10 and vascular endothelial growth factor protein and reduced levels of interleukin-1β, E-selectin, intercellular adhesion molecule-1, and inducible nitric oxide synthase in injury lung tissues.
Autologous transplantation of circulating EPCs can partly restore the pulmonary endothelial function and effectively attenuate endotoxin-induced acute lung injury by direct endothelial repair and indirect immunomodulation of antioxidation and antiinflammation. |
doi_str_mv | 10.1097/aln.0b013e3182567f84 |
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One-hundred-and-fifty rabbits were enrolled. After acute lung injury was induced by endotoxin, autologous circulating EPCs, endothelial cell, or normal saline were transfused intravenously, respectively. Pao(2)/FiO(2) ratios, concentrations of plasma nitric oxide, malonyldialdehyde, and activity of superoxide dismutase were examined. The lung wet-to-dry weight ratios were counted; polymorphonuclear cell ratios and areas of hyaline membrane formation and hemorrhage were measured. The levels of interleukin-1β, E-selectin, intercellular adhesion molecule-1, interleukin-10, vascular endothelial growth factor protein, and inducible nitric oxide synthase protein were analyzed.
Pao(2)/FiO(2) ratios were significantly increased with EPC transfusion. Infiltration of polymorphonuclear cells, lung wet-to-dry weight ratios, and area of hyaline membrane and hemorrhage in lung tissue were significantly decreased after EPC transplantation. Plasma level of nitric oxide and malondialdehyde were significantly inhibited, and the activity of superoxide dismutase was enhanced in the EPC-treated animals. EPC transplantation significantly increased level of interleukin-10 and vascular endothelial growth factor protein and reduced levels of interleukin-1β, E-selectin, intercellular adhesion molecule-1, and inducible nitric oxide synthase in injury lung tissues.
Autologous transplantation of circulating EPCs can partly restore the pulmonary endothelial function and effectively attenuate endotoxin-induced acute lung injury by direct endothelial repair and indirect immunomodulation of antioxidation and antiinflammation.</description><identifier>ISSN: 0003-3022</identifier><identifier>EISSN: 1528-1175</identifier><identifier>DOI: 10.1097/aln.0b013e3182567f84</identifier><identifier>PMID: 22546965</identifier><identifier>CODEN: ANESAV</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Acute Lung Injury - chemically induced ; Acute Lung Injury - therapy ; Allografts ; Anesthesia ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Autografts ; Biological and medical sciences ; Blood ; Blood Gas Analysis ; Cells, Cultured ; E-selectin ; E-Selectin - biosynthesis ; Endothelial cells ; Endothelial Cells - transplantation ; Endothelium, Vascular - pathology ; Endotoxins ; Endotoxins - toxicity ; Green Fluorescent Proteins - metabolism ; Hematopoietic Stem Cell Transplantation - methods ; Hemorrhage ; Immunomodulation ; Immunomodulation - drug effects ; Injuries ; intercellular adhesion molecule 1 ; Intercellular Adhesion Molecule-1 - biosynthesis ; Interleukin 1 ; Interleukin 10 ; Interleukin-10 - biosynthesis ; Interleukin-1beta - biosynthesis ; Lentivirus - genetics ; Leukocytes (polymorphonuclear) ; Lung ; Malondialdehyde ; Malondialdehyde - blood ; Medical sciences ; Neutrophil Infiltration - physiology ; Nitric oxide ; Nitric Oxide - blood ; Nitric Oxide Synthase Type II - biosynthesis ; Nitric-oxide synthase ; Plasma levels ; Rabbits ; Stem cells ; Superoxide dismutase ; Superoxide Dismutase - blood ; Transfusion ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - biosynthesis</subject><ispartof>Anesthesiology (Philadelphia), 2012-06, Vol.116 (6), p.1278-1287</ispartof><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c533t-ef56027063a77a349e2b2336ee1829d4ee3f31e22c3bec1319361cce997ba9f93</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27926,27927</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25923548$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22546965$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>CAO, Jian-Ping</creatorcontrib><creatorcontrib>HE, Xing-Ying</creatorcontrib><creatorcontrib>XU, Hai-Tao</creatorcontrib><creatorcontrib>ZUI ZOU</creatorcontrib><creatorcontrib>SHI, Xue-Yin</creatorcontrib><title>Autologous Transplantation of Peripheral Blood-derived Circulating Endothelial Progenitor Cells Attenuates Endotoxin-induced Acute Lung Injury in Rabbits by Direct Endothelial Repair and Indirect Immunomodulation</title><title>Anesthesiology (Philadelphia)</title><addtitle>Anesthesiology</addtitle><description>Studies have demonstrated the role of circulating endothelial progenitor cells (EPCs) in maintaining normal endothelial function and in endothelial repairing. This study was aimed to observe the protective effects of autologous transplantation of circulating EPCs against endotoxin-induced acute lung injury in rabbits and to investigate the underlying mechanisms.
One-hundred-and-fifty rabbits were enrolled. After acute lung injury was induced by endotoxin, autologous circulating EPCs, endothelial cell, or normal saline were transfused intravenously, respectively. Pao(2)/FiO(2) ratios, concentrations of plasma nitric oxide, malonyldialdehyde, and activity of superoxide dismutase were examined. The lung wet-to-dry weight ratios were counted; polymorphonuclear cell ratios and areas of hyaline membrane formation and hemorrhage were measured. The levels of interleukin-1β, E-selectin, intercellular adhesion molecule-1, interleukin-10, vascular endothelial growth factor protein, and inducible nitric oxide synthase protein were analyzed.
Pao(2)/FiO(2) ratios were significantly increased with EPC transfusion. Infiltration of polymorphonuclear cells, lung wet-to-dry weight ratios, and area of hyaline membrane and hemorrhage in lung tissue were significantly decreased after EPC transplantation. Plasma level of nitric oxide and malondialdehyde were significantly inhibited, and the activity of superoxide dismutase was enhanced in the EPC-treated animals. EPC transplantation significantly increased level of interleukin-10 and vascular endothelial growth factor protein and reduced levels of interleukin-1β, E-selectin, intercellular adhesion molecule-1, and inducible nitric oxide synthase in injury lung tissues.
Autologous transplantation of circulating EPCs can partly restore the pulmonary endothelial function and effectively attenuate endotoxin-induced acute lung injury by direct endothelial repair and indirect immunomodulation of antioxidation and antiinflammation.</description><subject>Acute Lung Injury - chemically induced</subject><subject>Acute Lung Injury - therapy</subject><subject>Allografts</subject><subject>Anesthesia</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Autografts</subject><subject>Biological and medical sciences</subject><subject>Blood</subject><subject>Blood Gas Analysis</subject><subject>Cells, Cultured</subject><subject>E-selectin</subject><subject>E-Selectin - biosynthesis</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - transplantation</subject><subject>Endothelium, Vascular - pathology</subject><subject>Endotoxins</subject><subject>Endotoxins - toxicity</subject><subject>Green Fluorescent Proteins - metabolism</subject><subject>Hematopoietic Stem Cell Transplantation - methods</subject><subject>Hemorrhage</subject><subject>Immunomodulation</subject><subject>Immunomodulation - drug effects</subject><subject>Injuries</subject><subject>intercellular adhesion molecule 1</subject><subject>Intercellular Adhesion Molecule-1 - biosynthesis</subject><subject>Interleukin 1</subject><subject>Interleukin 10</subject><subject>Interleukin-10 - biosynthesis</subject><subject>Interleukin-1beta - biosynthesis</subject><subject>Lentivirus - genetics</subject><subject>Leukocytes (polymorphonuclear)</subject><subject>Lung</subject><subject>Malondialdehyde</subject><subject>Malondialdehyde - blood</subject><subject>Medical sciences</subject><subject>Neutrophil Infiltration - physiology</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - blood</subject><subject>Nitric Oxide Synthase Type II - biosynthesis</subject><subject>Nitric-oxide synthase</subject><subject>Plasma levels</subject><subject>Rabbits</subject><subject>Stem cells</subject><subject>Superoxide dismutase</subject><subject>Superoxide Dismutase - blood</subject><subject>Transfusion</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - biosynthesis</subject><issn>0003-3022</issn><issn>1528-1175</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1u1DAUhSMEokPhDRDyBolNin_iOF4OQ4GRRlBVZR05zs3UlWMH_1TMe_JAGGYAwYaVZfs759j3VNVzgi8IluK1su4CD5gwYKSjvBVT1zyoVoTTriZE8IfVCmPMaoYpPauexHhXtoKz7nF1RilvWtnyVfVtnZO3fu9zRDdBubhY5ZJKxjvkJ3QFwSy3EJRFb6z3Yz2Wg3sY0cYEnW3h3B5dutGnW7CmUFfB78GZ5APagLURrVMCl1WCeOT8V-Nq48asi8ta5wRol4vJ1t3lcEDGoWs1DCZFNBzQWxNAp78CrmFRJiDlxiIZj_fbec7Oz378-SLvnlaPJmUjPDut59Xnd5c3mw_17tP77Wa9qzVnLNUw8RZTgVumhFCskUAHylgLUAYqxwaATYwApZoNoAkjkrVEa5BSDEpOkp1Xr46-S_BfMsTUzybq8m3loAy0L5KulYIS-n8Uk7YVJZwVtDmiOvgYA0z9EsyswqFA_Y_q-_XuY_9v9UX24pSQhxnG36JfXRfg5QlQUSs7lba1iX84LinjTce-A0s1vTk</recordid><startdate>20120601</startdate><enddate>20120601</enddate><creator>CAO, Jian-Ping</creator><creator>HE, Xing-Ying</creator><creator>XU, Hai-Tao</creator><creator>ZUI ZOU</creator><creator>SHI, Xue-Yin</creator><general>Lippincott Williams & Wilkins</general><scope>IQODW</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>7X8</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>20120601</creationdate><title>Autologous Transplantation of Peripheral Blood-derived Circulating Endothelial Progenitor Cells Attenuates Endotoxin-induced Acute Lung Injury in Rabbits by Direct Endothelial Repair and Indirect Immunomodulation</title><author>CAO, Jian-Ping ; HE, Xing-Ying ; XU, Hai-Tao ; ZUI ZOU ; SHI, Xue-Yin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c533t-ef56027063a77a349e2b2336ee1829d4ee3f31e22c3bec1319361cce997ba9f93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Acute Lung Injury - chemically induced</topic><topic>Acute Lung Injury - therapy</topic><topic>Allografts</topic><topic>Anesthesia</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Autografts</topic><topic>Biological and medical sciences</topic><topic>Blood</topic><topic>Blood Gas Analysis</topic><topic>Cells, Cultured</topic><topic>E-selectin</topic><topic>E-Selectin - biosynthesis</topic><topic>Endothelial cells</topic><topic>Endothelial Cells - transplantation</topic><topic>Endothelium, Vascular - pathology</topic><topic>Endotoxins</topic><topic>Endotoxins - toxicity</topic><topic>Green Fluorescent Proteins - metabolism</topic><topic>Hematopoietic Stem Cell Transplantation - methods</topic><topic>Hemorrhage</topic><topic>Immunomodulation</topic><topic>Immunomodulation - drug effects</topic><topic>Injuries</topic><topic>intercellular adhesion molecule 1</topic><topic>Intercellular Adhesion Molecule-1 - biosynthesis</topic><topic>Interleukin 1</topic><topic>Interleukin 10</topic><topic>Interleukin-10 - biosynthesis</topic><topic>Interleukin-1beta - biosynthesis</topic><topic>Lentivirus - genetics</topic><topic>Leukocytes (polymorphonuclear)</topic><topic>Lung</topic><topic>Malondialdehyde</topic><topic>Malondialdehyde - blood</topic><topic>Medical sciences</topic><topic>Neutrophil Infiltration - physiology</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - blood</topic><topic>Nitric Oxide Synthase Type II - biosynthesis</topic><topic>Nitric-oxide synthase</topic><topic>Plasma levels</topic><topic>Rabbits</topic><topic>Stem cells</topic><topic>Superoxide dismutase</topic><topic>Superoxide Dismutase - blood</topic><topic>Transfusion</topic><topic>Vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor A - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>CAO, Jian-Ping</creatorcontrib><creatorcontrib>HE, Xing-Ying</creatorcontrib><creatorcontrib>XU, Hai-Tao</creatorcontrib><creatorcontrib>ZUI ZOU</creatorcontrib><creatorcontrib>SHI, Xue-Yin</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Anesthesiology (Philadelphia)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>CAO, Jian-Ping</au><au>HE, Xing-Ying</au><au>XU, Hai-Tao</au><au>ZUI ZOU</au><au>SHI, Xue-Yin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Autologous Transplantation of Peripheral Blood-derived Circulating Endothelial Progenitor Cells Attenuates Endotoxin-induced Acute Lung Injury in Rabbits by Direct Endothelial Repair and Indirect Immunomodulation</atitle><jtitle>Anesthesiology (Philadelphia)</jtitle><addtitle>Anesthesiology</addtitle><date>2012-06-01</date><risdate>2012</risdate><volume>116</volume><issue>6</issue><spage>1278</spage><epage>1287</epage><pages>1278-1287</pages><issn>0003-3022</issn><eissn>1528-1175</eissn><coden>ANESAV</coden><abstract>Studies have demonstrated the role of circulating endothelial progenitor cells (EPCs) in maintaining normal endothelial function and in endothelial repairing. This study was aimed to observe the protective effects of autologous transplantation of circulating EPCs against endotoxin-induced acute lung injury in rabbits and to investigate the underlying mechanisms.
One-hundred-and-fifty rabbits were enrolled. After acute lung injury was induced by endotoxin, autologous circulating EPCs, endothelial cell, or normal saline were transfused intravenously, respectively. Pao(2)/FiO(2) ratios, concentrations of plasma nitric oxide, malonyldialdehyde, and activity of superoxide dismutase were examined. The lung wet-to-dry weight ratios were counted; polymorphonuclear cell ratios and areas of hyaline membrane formation and hemorrhage were measured. The levels of interleukin-1β, E-selectin, intercellular adhesion molecule-1, interleukin-10, vascular endothelial growth factor protein, and inducible nitric oxide synthase protein were analyzed.
Pao(2)/FiO(2) ratios were significantly increased with EPC transfusion. Infiltration of polymorphonuclear cells, lung wet-to-dry weight ratios, and area of hyaline membrane and hemorrhage in lung tissue were significantly decreased after EPC transplantation. Plasma level of nitric oxide and malondialdehyde were significantly inhibited, and the activity of superoxide dismutase was enhanced in the EPC-treated animals. EPC transplantation significantly increased level of interleukin-10 and vascular endothelial growth factor protein and reduced levels of interleukin-1β, E-selectin, intercellular adhesion molecule-1, and inducible nitric oxide synthase in injury lung tissues.
Autologous transplantation of circulating EPCs can partly restore the pulmonary endothelial function and effectively attenuate endotoxin-induced acute lung injury by direct endothelial repair and indirect immunomodulation of antioxidation and antiinflammation.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>22546965</pmid><doi>10.1097/aln.0b013e3182567f84</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Acute Lung Injury - chemically induced Acute Lung Injury - therapy Allografts Anesthesia Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Autografts Biological and medical sciences Blood Blood Gas Analysis Cells, Cultured E-selectin E-Selectin - biosynthesis Endothelial cells Endothelial Cells - transplantation Endothelium, Vascular - pathology Endotoxins Endotoxins - toxicity Green Fluorescent Proteins - metabolism Hematopoietic Stem Cell Transplantation - methods Hemorrhage Immunomodulation Immunomodulation - drug effects Injuries intercellular adhesion molecule 1 Intercellular Adhesion Molecule-1 - biosynthesis Interleukin 1 Interleukin 10 Interleukin-10 - biosynthesis Interleukin-1beta - biosynthesis Lentivirus - genetics Leukocytes (polymorphonuclear) Lung Malondialdehyde Malondialdehyde - blood Medical sciences Neutrophil Infiltration - physiology Nitric oxide Nitric Oxide - blood Nitric Oxide Synthase Type II - biosynthesis Nitric-oxide synthase Plasma levels Rabbits Stem cells Superoxide dismutase Superoxide Dismutase - blood Transfusion Vascular endothelial growth factor Vascular Endothelial Growth Factor A - biosynthesis |
title | Autologous Transplantation of Peripheral Blood-derived Circulating Endothelial Progenitor Cells Attenuates Endotoxin-induced Acute Lung Injury in Rabbits by Direct Endothelial Repair and Indirect Immunomodulation |
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