Recombinant human erythropoietin ameliorated endothelial dysfunction and macrophage infiltration by increasing nitric oxide in hypertensive 5/6 nephrectomized rat aorta
Recombinant human erythropoietin (rHuEPO), used clinically for renal anemia, reportedly exhibits pleiotropic properties in various tissues. To test whether it ameliorates vascular injury, rHuEPO (75U/kg) was administered subcutaneously every 3days for 10days to 5/6 nephrectomized hypertensive rats (...
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| Veröffentlicht in: | European journal of pharmacology 2011-04, Vol.656 (1-3), p.81-87 |
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| creator | Toba, Hiroe Morishita, Masayuki Tojo, Chisato Nakano, Arisa Oshima, Yuko Kojima, Yushi Yoshida, Mamiko Nakashima, Kohei Wang, Jiahong Kobara, Miyuki Nakata, Tetsuo |
| description | Recombinant human erythropoietin (rHuEPO), used clinically for renal anemia, reportedly exhibits pleiotropic properties in various tissues. To test whether it ameliorates vascular injury, rHuEPO (75U/kg) was administered subcutaneously every 3days for 10days to 5/6 nephrectomized hypertensive rats (5/6Nx) treated with 1% NaCl. rHuEPO had no effect on increased systolic blood pressure or decreased hematocrit values, but normalized levels of proteinuria and creatinine clearance. Vasodilation in response to acetylcholine in the aortic ring was impaired in the 5/6Nx, and improved by treatment with rHuEPO. Immunohistochemical analysis revealed that the infiltration of adventitial areas by macrophages and expression of osteopontin were enhanced in the 5/6Nx aorta and the overexpression was suppressed by rHuEPO. rHuEPO also attenuated medial hyperplasia. Akt signaling was activated by the increased expression of phosphorylated Akt and GSK-3β in aorta from rHuEPO-treated 5/6Nx. rHuEPO restored plasma NOx (NO2−+NO3−) levels and endothelial nitric oxide synthase (eNOS) content in the 5/6Nx aorta. Treatment with an eNOS substrate, l-arginine, which caused a similar increase in plasma NOx levels as the rHuEPO treatment, resulted in a normalization of endothelial dysfunction and vascular inflammation. These results suggest that a low dose of rHuEPO exerted vasoprotective effects in rats with hypertensive renal failure. |
| doi_str_mv | 10.1016/j.ejphar.2011.01.043 |
| format | Article |
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To test whether it ameliorates vascular injury, rHuEPO (75U/kg) was administered subcutaneously every 3days for 10days to 5/6 nephrectomized hypertensive rats (5/6Nx) treated with 1% NaCl. rHuEPO had no effect on increased systolic blood pressure or decreased hematocrit values, but normalized levels of proteinuria and creatinine clearance. Vasodilation in response to acetylcholine in the aortic ring was impaired in the 5/6Nx, and improved by treatment with rHuEPO. Immunohistochemical analysis revealed that the infiltration of adventitial areas by macrophages and expression of osteopontin were enhanced in the 5/6Nx aorta and the overexpression was suppressed by rHuEPO. rHuEPO also attenuated medial hyperplasia. Akt signaling was activated by the increased expression of phosphorylated Akt and GSK-3β in aorta from rHuEPO-treated 5/6Nx. rHuEPO restored plasma NOx (NO2−+NO3−) levels and endothelial nitric oxide synthase (eNOS) content in the 5/6Nx aorta. Treatment with an eNOS substrate, l-arginine, which caused a similar increase in plasma NOx levels as the rHuEPO treatment, resulted in a normalization of endothelial dysfunction and vascular inflammation. These results suggest that a low dose of rHuEPO exerted vasoprotective effects in rats with hypertensive renal failure.</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/j.ejphar.2011.01.043</identifier><identifier>PMID: 21296066</identifier><identifier>CODEN: EJPHAZ</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Acetylcholine ; Acetylcholine - pharmacology ; AKT protein ; Anemia ; Animals ; Aorta ; Aorta - drug effects ; Aorta - injuries ; Aorta - metabolism ; Aorta - physiopathology ; Aorta, Thoracic - drug effects ; Aorta, Thoracic - pathology ; Arginine ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood pressure ; Blood Pressure - drug effects ; Body Weight - drug effects ; Cardiology. Vascular system ; Connective Tissue - drug effects ; Connective Tissue - immunology ; Creatinine ; Dose-Response Relationship, Drug ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - metabolism ; Erythropoietin ; Erythropoietin - pharmacology ; Gene Expression Regulation, Enzymologic - drug effects ; Hematocrit ; Hematopoiesis - drug effects ; Humans ; Hyperplasia ; Hypertension ; Hypertension - blood ; Hypertension - immunology ; Hypertension - metabolism ; Hypertension - physiopathology ; Inflammation ; Injuries ; Kidney ; Macrophages ; Macrophages - drug effects ; Macrophages - immunology ; Male ; Medical sciences ; Nephrectomy ; Nitric oxide ; Nitric Oxide - metabolism ; Nitric Oxide Synthase Type III - metabolism ; Nitric-oxide synthase ; Nitrogen Dioxide - blood ; Nitrogen Oxides - blood ; Nitroprusside - pharmacology ; Osteopontin ; Osteopontin - metabolism ; Pharmacology. Drug treatments ; Phosphoproteins - metabolism ; Rats ; Rats, Wistar ; Recombinant Proteins - pharmacology ; Renal failure ; Sodium chloride ; Vasodilation</subject><ispartof>European journal of pharmacology, 2011-04, Vol.656 (1-3), p.81-87</ispartof><rights>2011 Elsevier B.V.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2011 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c490t-ac77d59451b98aff3f657cdfed50a58597b8bc78c963aae229d2dc6fa52fc04f3</citedby><cites>FETCH-LOGICAL-c490t-ac77d59451b98aff3f657cdfed50a58597b8bc78c963aae229d2dc6fa52fc04f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0014299911001014$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23952458$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21296066$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Toba, Hiroe</creatorcontrib><creatorcontrib>Morishita, Masayuki</creatorcontrib><creatorcontrib>Tojo, Chisato</creatorcontrib><creatorcontrib>Nakano, Arisa</creatorcontrib><creatorcontrib>Oshima, Yuko</creatorcontrib><creatorcontrib>Kojima, Yushi</creatorcontrib><creatorcontrib>Yoshida, Mamiko</creatorcontrib><creatorcontrib>Nakashima, Kohei</creatorcontrib><creatorcontrib>Wang, Jiahong</creatorcontrib><creatorcontrib>Kobara, Miyuki</creatorcontrib><creatorcontrib>Nakata, Tetsuo</creatorcontrib><title>Recombinant human erythropoietin ameliorated endothelial dysfunction and macrophage infiltration by increasing nitric oxide in hypertensive 5/6 nephrectomized rat aorta</title><title>European journal of pharmacology</title><addtitle>Eur J Pharmacol</addtitle><description>Recombinant human erythropoietin (rHuEPO), used clinically for renal anemia, reportedly exhibits pleiotropic properties in various tissues. To test whether it ameliorates vascular injury, rHuEPO (75U/kg) was administered subcutaneously every 3days for 10days to 5/6 nephrectomized hypertensive rats (5/6Nx) treated with 1% NaCl. rHuEPO had no effect on increased systolic blood pressure or decreased hematocrit values, but normalized levels of proteinuria and creatinine clearance. Vasodilation in response to acetylcholine in the aortic ring was impaired in the 5/6Nx, and improved by treatment with rHuEPO. Immunohistochemical analysis revealed that the infiltration of adventitial areas by macrophages and expression of osteopontin were enhanced in the 5/6Nx aorta and the overexpression was suppressed by rHuEPO. rHuEPO also attenuated medial hyperplasia. Akt signaling was activated by the increased expression of phosphorylated Akt and GSK-3β in aorta from rHuEPO-treated 5/6Nx. rHuEPO restored plasma NOx (NO2−+NO3−) levels and endothelial nitric oxide synthase (eNOS) content in the 5/6Nx aorta. Treatment with an eNOS substrate, l-arginine, which caused a similar increase in plasma NOx levels as the rHuEPO treatment, resulted in a normalization of endothelial dysfunction and vascular inflammation. These results suggest that a low dose of rHuEPO exerted vasoprotective effects in rats with hypertensive renal failure.</description><subject>Acetylcholine</subject><subject>Acetylcholine - pharmacology</subject><subject>AKT protein</subject><subject>Anemia</subject><subject>Animals</subject><subject>Aorta</subject><subject>Aorta - drug effects</subject><subject>Aorta - injuries</subject><subject>Aorta - metabolism</subject><subject>Aorta - physiopathology</subject><subject>Aorta, Thoracic - drug effects</subject><subject>Aorta, Thoracic - pathology</subject><subject>Arginine</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood pressure</subject><subject>Blood Pressure - drug effects</subject><subject>Body Weight - drug effects</subject><subject>Cardiology. Vascular system</subject><subject>Connective Tissue - drug effects</subject><subject>Connective Tissue - immunology</subject><subject>Creatinine</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Erythropoietin</subject><subject>Erythropoietin - pharmacology</subject><subject>Gene Expression Regulation, Enzymologic - drug effects</subject><subject>Hematocrit</subject><subject>Hematopoiesis - drug effects</subject><subject>Humans</subject><subject>Hyperplasia</subject><subject>Hypertension</subject><subject>Hypertension - blood</subject><subject>Hypertension - immunology</subject><subject>Hypertension - metabolism</subject><subject>Hypertension - physiopathology</subject><subject>Inflammation</subject><subject>Injuries</subject><subject>Kidney</subject><subject>Macrophages</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - immunology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nephrectomy</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase Type III - metabolism</subject><subject>Nitric-oxide synthase</subject><subject>Nitrogen Dioxide - blood</subject><subject>Nitrogen Oxides - blood</subject><subject>Nitroprusside - pharmacology</subject><subject>Osteopontin</subject><subject>Osteopontin - metabolism</subject><subject>Pharmacology. Drug treatments</subject><subject>Phosphoproteins - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Recombinant Proteins - pharmacology</subject><subject>Renal failure</subject><subject>Sodium chloride</subject><subject>Vasodilation</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kd-K1TAQxoso7nH1DURyI3pzziZp0zY3wrL4DxYE0esyTSbbHNqkJulifSIf05Rz1LuFgTDk980M31cULxk9MMrqq-MBj_MA4cApYweaqyofFTvWNnJPG8YfFztKWbXnUsqL4lmMR0qpkFw8LS4447Kmdb0rfn9F5afeOnCJDMsEjmBY0xD87C0m6whMOFofIKEm6LRPQ-5hJHqNZnEqWZ8Zp8kEKosGuENinbFjypLtr19zrwJCtO6OOJuCVcT_tHrjyLDOGBK6aO-RiKuaOJyHgCr5yf7KG_MQAj4keF48MTBGfHF-L4vvH95_u_m0v_3y8fPN9e1eVZKmPaim0UJWgvWyBWNKU4tGaYNaUBCtkE3f9qpplaxLAORcaq5VbUBwo2hlysvizWnuHPyPBWPqJhsVjiM49EvsWiGy4W3LMvn2QTKn1EhRN6LMaHVCs0UxBjTdHOwEYc3QxtXdsTul2W1pdjRXtclenTcs_YT6n-hvfBl4fQYgKhhNAKds_M-VUvBKtJl7d-IwO3dvMXRRWXQKtd287rS3D1_yB1coxSs</recordid><startdate>20110410</startdate><enddate>20110410</enddate><creator>Toba, Hiroe</creator><creator>Morishita, Masayuki</creator><creator>Tojo, Chisato</creator><creator>Nakano, Arisa</creator><creator>Oshima, Yuko</creator><creator>Kojima, Yushi</creator><creator>Yoshida, Mamiko</creator><creator>Nakashima, Kohei</creator><creator>Wang, Jiahong</creator><creator>Kobara, Miyuki</creator><creator>Nakata, Tetsuo</creator><general>Elsevier B.V</general><general>Elsevier</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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20110410</creationdate><title>Recombinant human erythropoietin ameliorated endothelial dysfunction and macrophage infiltration by increasing nitric oxide in hypertensive 5/6 nephrectomized rat aorta</title><author>Toba, Hiroe ; Morishita, Masayuki ; Tojo, Chisato ; Nakano, Arisa ; Oshima, Yuko ; Kojima, Yushi ; Yoshida, Mamiko ; Nakashima, Kohei ; Wang, Jiahong ; Kobara, Miyuki ; Nakata, Tetsuo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c490t-ac77d59451b98aff3f657cdfed50a58597b8bc78c963aae229d2dc6fa52fc04f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Acetylcholine</topic><topic>Acetylcholine - pharmacology</topic><topic>AKT protein</topic><topic>Anemia</topic><topic>Animals</topic><topic>Aorta</topic><topic>Aorta - drug effects</topic><topic>Aorta - injuries</topic><topic>Aorta - metabolism</topic><topic>Aorta - physiopathology</topic><topic>Aorta, Thoracic - drug effects</topic><topic>Aorta, Thoracic - pathology</topic><topic>Arginine</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood pressure</topic><topic>Blood Pressure - drug effects</topic><topic>Body Weight - drug effects</topic><topic>Cardiology. Vascular system</topic><topic>Connective Tissue - drug effects</topic><topic>Connective Tissue - immunology</topic><topic>Creatinine</topic><topic>Dose-Response Relationship, Drug</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Erythropoietin</topic><topic>Erythropoietin - pharmacology</topic><topic>Gene Expression Regulation, Enzymologic - drug effects</topic><topic>Hematocrit</topic><topic>Hematopoiesis - drug effects</topic><topic>Humans</topic><topic>Hyperplasia</topic><topic>Hypertension</topic><topic>Hypertension - blood</topic><topic>Hypertension - immunology</topic><topic>Hypertension - metabolism</topic><topic>Hypertension - physiopathology</topic><topic>Inflammation</topic><topic>Injuries</topic><topic>Kidney</topic><topic>Macrophages</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - immunology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nephrectomy</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase Type III - metabolism</topic><topic>Nitric-oxide synthase</topic><topic>Nitrogen Dioxide - blood</topic><topic>Nitrogen Oxides - blood</topic><topic>Nitroprusside - pharmacology</topic><topic>Osteopontin</topic><topic>Osteopontin - metabolism</topic><topic>Pharmacology. Drug treatments</topic><topic>Phosphoproteins - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Recombinant Proteins - pharmacology</topic><topic>Renal failure</topic><topic>Sodium chloride</topic><topic>Vasodilation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Toba, Hiroe</creatorcontrib><creatorcontrib>Morishita, Masayuki</creatorcontrib><creatorcontrib>Tojo, Chisato</creatorcontrib><creatorcontrib>Nakano, Arisa</creatorcontrib><creatorcontrib>Oshima, Yuko</creatorcontrib><creatorcontrib>Kojima, Yushi</creatorcontrib><creatorcontrib>Yoshida, Mamiko</creatorcontrib><creatorcontrib>Nakashima, Kohei</creatorcontrib><creatorcontrib>Wang, Jiahong</creatorcontrib><creatorcontrib>Kobara, Miyuki</creatorcontrib><creatorcontrib>Nakata, Tetsuo</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>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Toba, Hiroe</au><au>Morishita, Masayuki</au><au>Tojo, Chisato</au><au>Nakano, Arisa</au><au>Oshima, Yuko</au><au>Kojima, Yushi</au><au>Yoshida, Mamiko</au><au>Nakashima, Kohei</au><au>Wang, Jiahong</au><au>Kobara, Miyuki</au><au>Nakata, Tetsuo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Recombinant human erythropoietin ameliorated endothelial dysfunction and macrophage infiltration by increasing nitric oxide in hypertensive 5/6 nephrectomized rat aorta</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>2011-04-10</date><risdate>2011</risdate><volume>656</volume><issue>1-3</issue><spage>81</spage><epage>87</epage><pages>81-87</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><coden>EJPHAZ</coden><abstract>Recombinant human erythropoietin (rHuEPO), used clinically for renal anemia, reportedly exhibits pleiotropic properties in various tissues. To test whether it ameliorates vascular injury, rHuEPO (75U/kg) was administered subcutaneously every 3days for 10days to 5/6 nephrectomized hypertensive rats (5/6Nx) treated with 1% NaCl. rHuEPO had no effect on increased systolic blood pressure or decreased hematocrit values, but normalized levels of proteinuria and creatinine clearance. Vasodilation in response to acetylcholine in the aortic ring was impaired in the 5/6Nx, and improved by treatment with rHuEPO. Immunohistochemical analysis revealed that the infiltration of adventitial areas by macrophages and expression of osteopontin were enhanced in the 5/6Nx aorta and the overexpression was suppressed by rHuEPO. rHuEPO also attenuated medial hyperplasia. Akt signaling was activated by the increased expression of phosphorylated Akt and GSK-3β in aorta from rHuEPO-treated 5/6Nx. rHuEPO restored plasma NOx (NO2−+NO3−) levels and endothelial nitric oxide synthase (eNOS) content in the 5/6Nx aorta. Treatment with an eNOS substrate, l-arginine, which caused a similar increase in plasma NOx levels as the rHuEPO treatment, resulted in a normalization of endothelial dysfunction and vascular inflammation. These results suggest that a low dose of rHuEPO exerted vasoprotective effects in rats with hypertensive renal failure.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>21296066</pmid><doi>10.1016/j.ejphar.2011.01.043</doi><tpages>7</tpages></addata></record> |
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| ispartof | European journal of pharmacology, 2011-04, Vol.656 (1-3), p.81-87 |
| issn | 0014-2999 1879-0712 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Acetylcholine Acetylcholine - pharmacology AKT protein Anemia Animals Aorta Aorta - drug effects Aorta - injuries Aorta - metabolism Aorta - physiopathology Aorta, Thoracic - drug effects Aorta, Thoracic - pathology Arginine Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Blood pressure Blood Pressure - drug effects Body Weight - drug effects Cardiology. Vascular system Connective Tissue - drug effects Connective Tissue - immunology Creatinine Dose-Response Relationship, Drug Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Erythropoietin Erythropoietin - pharmacology Gene Expression Regulation, Enzymologic - drug effects Hematocrit Hematopoiesis - drug effects Humans Hyperplasia Hypertension Hypertension - blood Hypertension - immunology Hypertension - metabolism Hypertension - physiopathology Inflammation Injuries Kidney Macrophages Macrophages - drug effects Macrophages - immunology Male Medical sciences Nephrectomy Nitric oxide Nitric Oxide - metabolism Nitric Oxide Synthase Type III - metabolism Nitric-oxide synthase Nitrogen Dioxide - blood Nitrogen Oxides - blood Nitroprusside - pharmacology Osteopontin Osteopontin - metabolism Pharmacology. Drug treatments Phosphoproteins - metabolism Rats Rats, Wistar Recombinant Proteins - pharmacology Renal failure Sodium chloride Vasodilation |
| title | Recombinant human erythropoietin ameliorated endothelial dysfunction and macrophage infiltration by increasing nitric oxide in hypertensive 5/6 nephrectomized rat aorta |
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