Catalase activity prevents exercise‐induced up‐regulation of vasoprotective proteins in venous tissue
Physical activity induces favourable changes of arterial gene expression and protein activity, although little is known about its effect in venous tissue. Although our understanding of the initiating molecular signals is still incomplete, increased expression of endothelial nitric oxide synthase (eN...
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description | Physical activity induces favourable changes of arterial gene expression and protein activity, although little is known about its effect in venous tissue. Although our understanding of the initiating molecular signals is still incomplete, increased expression of endothelial nitric oxide synthase (eNOS) is considered a key event. This study sought to investigate the effects of two different training protocols on the expression of eNOS and extracellular superoxide dismutase (ecSOD) in venous and lung tissue and to evaluate the underlying molecular mechanisms. C57Bl/6 mice underwent voluntary exercise or forced physical activity. Changes of vascular mRNA and protein levels and activity of eNOS, ecSOD and catalase were determined in aorta, heart, lung and vena cava. Both training protocols similarly increased relative heart weight and resulted in up‐regulation of aortic and myocardial eNOS. In striking contrast, eNOS expression in vena cava and lung remained unchanged. Likewise, exercise up‐regulated ecSOD in the aorta and in left ventricular tissue but remained unchanged in lung tissue. Catalase expression in lung tissue and vena cava of exercised mice exceeded that in aorta by 6.9‐ and 10‐fold, respectively, suggesting a lack of stimulatory effects of hydrogen peroxide. In accordance, treatment of mice with the catalase inhibitor aminotriazole for 6 weeks resulted in significant up‐regulation of eNOS and ecSOD in vena cava. These data suggest that physiological venous catalase activity prevents exercise‐induced up‐regulation of eNOS and ecSOD. Furthermore, therapeutic inhibition of vascular catalase might improve pulmonary rehabilitation. |
doi_str_mv | 10.1111/j.1582-4934.2010.01227.x |
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Although our understanding of the initiating molecular signals is still incomplete, increased expression of endothelial nitric oxide synthase (eNOS) is considered a key event. This study sought to investigate the effects of two different training protocols on the expression of eNOS and extracellular superoxide dismutase (ecSOD) in venous and lung tissue and to evaluate the underlying molecular mechanisms. C57Bl/6 mice underwent voluntary exercise or forced physical activity. Changes of vascular mRNA and protein levels and activity of eNOS, ecSOD and catalase were determined in aorta, heart, lung and vena cava. Both training protocols similarly increased relative heart weight and resulted in up‐regulation of aortic and myocardial eNOS. In striking contrast, eNOS expression in vena cava and lung remained unchanged. Likewise, exercise up‐regulated ecSOD in the aorta and in left ventricular tissue but remained unchanged in lung tissue. Catalase expression in lung tissue and vena cava of exercised mice exceeded that in aorta by 6.9‐ and 10‐fold, respectively, suggesting a lack of stimulatory effects of hydrogen peroxide. In accordance, treatment of mice with the catalase inhibitor aminotriazole for 6 weeks resulted in significant up‐regulation of eNOS and ecSOD in vena cava. These data suggest that physiological venous catalase activity prevents exercise‐induced up‐regulation of eNOS and ecSOD. Furthermore, therapeutic inhibition of vascular catalase might improve pulmonary rehabilitation.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/j.1582-4934.2010.01227.x</identifier><identifier>PMID: 21129156</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Amitrole - pharmacology ; Animals ; Aorta ; Aorta - metabolism ; Catalase ; Catalase - antagonists & inhibitors ; Catalase - metabolism ; endothelial nitric oxide synthase ; Endothelium, Vascular - metabolism ; Exercise ; Fitness training programs ; Gene expression ; Heart ; Hydrogen peroxide ; Lung - metabolism ; Lungs ; Male ; Mice ; Mice, Inbred C57BL ; Molecular modelling ; Motor Activity ; Myocardium - metabolism ; Nitric oxide ; Nitric Oxide Synthase Type III - biosynthesis ; Nitric Oxide Synthase Type III - genetics ; Nitric Oxide Synthase Type III - metabolism ; Nitric-oxide synthase ; Original ; Physical activity ; Physical Conditioning, Animal ; Physical fitness ; Polyclonal antibodies ; pulmonary rehabilitation ; RNA, Messenger - biosynthesis ; RNA, Messenger - genetics ; Shear stress ; Superoxide Dismutase - biosynthesis ; Up-regulation ; Venae Cavae - metabolism</subject><ispartof>Journal of cellular and molecular medicine, 2011-11, Vol.15 (11), p.2326-2334</ispartof><rights>2011 The Authors Journal of Cellular and Molecular Medicine © 2011 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd</rights><rights>2011 The Authors Journal of Cellular and Molecular Medicine © 2011 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.</rights><rights>2011. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2011 The Authors Journal of Cellular and Molecular Medicine © 2011 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5687-1be59757aa8bcc9420e2a98f7252604f26014f235b3551268bbca9da79e2c043</citedby><cites>FETCH-LOGICAL-c5687-1be59757aa8bcc9420e2a98f7252604f26014f235b3551268bbca9da79e2c043</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/PMC3822944/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3822944/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><linktorsrc>$$Uhttps://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1582-4934.2010.01227.x$$EView_record_in_Wiley-Blackwell$$FView_record_in_$$GWiley-Blackwell</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21129156$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dao, Vu Thao‐Vi</creatorcontrib><creatorcontrib>Floeren, Melanie</creatorcontrib><creatorcontrib>Kumpf, Stephanie</creatorcontrib><creatorcontrib>Both, Charlotte</creatorcontrib><creatorcontrib>Peter, Bärbel</creatorcontrib><creatorcontrib>Balz, Vera</creatorcontrib><creatorcontrib>Suvorava, Tatsiana</creatorcontrib><creatorcontrib>Kojda, Georg</creatorcontrib><title>Catalase activity prevents exercise‐induced up‐regulation of vasoprotective proteins in venous tissue</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Physical activity induces favourable changes of arterial gene expression and protein activity, although little is known about its effect in venous tissue. Although our understanding of the initiating molecular signals is still incomplete, increased expression of endothelial nitric oxide synthase (eNOS) is considered a key event. This study sought to investigate the effects of two different training protocols on the expression of eNOS and extracellular superoxide dismutase (ecSOD) in venous and lung tissue and to evaluate the underlying molecular mechanisms. C57Bl/6 mice underwent voluntary exercise or forced physical activity. Changes of vascular mRNA and protein levels and activity of eNOS, ecSOD and catalase were determined in aorta, heart, lung and vena cava. Both training protocols similarly increased relative heart weight and resulted in up‐regulation of aortic and myocardial eNOS. In striking contrast, eNOS expression in vena cava and lung remained unchanged. Likewise, exercise up‐regulated ecSOD in the aorta and in left ventricular tissue but remained unchanged in lung tissue. Catalase expression in lung tissue and vena cava of exercised mice exceeded that in aorta by 6.9‐ and 10‐fold, respectively, suggesting a lack of stimulatory effects of hydrogen peroxide. In accordance, treatment of mice with the catalase inhibitor aminotriazole for 6 weeks resulted in significant up‐regulation of eNOS and ecSOD in vena cava. These data suggest that physiological venous catalase activity prevents exercise‐induced up‐regulation of eNOS and ecSOD. Furthermore, therapeutic inhibition of vascular catalase might improve pulmonary rehabilitation.</description><subject>Amitrole - pharmacology</subject><subject>Animals</subject><subject>Aorta</subject><subject>Aorta - metabolism</subject><subject>Catalase</subject><subject>Catalase - antagonists & inhibitors</subject><subject>Catalase - metabolism</subject><subject>endothelial nitric oxide synthase</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Exercise</subject><subject>Fitness training programs</subject><subject>Gene expression</subject><subject>Heart</subject><subject>Hydrogen peroxide</subject><subject>Lung - metabolism</subject><subject>Lungs</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Molecular modelling</subject><subject>Motor Activity</subject><subject>Myocardium - metabolism</subject><subject>Nitric oxide</subject><subject>Nitric Oxide Synthase Type III - biosynthesis</subject><subject>Nitric Oxide Synthase Type III - genetics</subject><subject>Nitric Oxide Synthase Type III - metabolism</subject><subject>Nitric-oxide synthase</subject><subject>Original</subject><subject>Physical activity</subject><subject>Physical Conditioning, Animal</subject><subject>Physical fitness</subject><subject>Polyclonal antibodies</subject><subject>pulmonary rehabilitation</subject><subject>RNA, Messenger - biosynthesis</subject><subject>RNA, Messenger - genetics</subject><subject>Shear stress</subject><subject>Superoxide Dismutase - biosynthesis</subject><subject>Up-regulation</subject><subject>Venae Cavae - metabolism</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><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>eNqNUctOGzEUtSpQQ2l_AVnqglVSP8Yz9gapiqAPEbFhb3mcO-BoMh7smZDs-AS-sV9STxIC7Qovrq99zzm6RwchTMmEpvNtMaFCsnGmeDZhJP0SylgxWX9AJ4fB0b6nkssR-hTjghCeU64-ohGjlCkq8hPkpqYztYmAje3cynUb3AZYQdNFDGsI1kX48_TsmnlvYY77Nj0C3PW16ZxvsK_wykTfBt_BwAe8bV0TsWtwkvF9xJ2LsYfP6LgydYQv-_sU3V5d3k5_jq9vfvyafr8eW5HLYkxLEKoQhTGytFZljAAzSlYFEywnWZUKTZWLkgtBWS7L0ho1N4UCZknGT9HFTrbtyyXMbXISTK3b4JYmbLQ3Tv87ady9vvMrzSVjKhsEzvcCwT_0EDu9dNFCXZsGkhutCMkzTnKRkF__Qy58H5pkTnNSCCUkVyqh5A5lg48xQHXYhRI9pKkXeghKD6HpIU29TVOvE_XsrZcD8SW-V7OProbNu4X17-lsNrT8L0UVsts</recordid><startdate>201111</startdate><enddate>201111</enddate><creator>Dao, Vu Thao‐Vi</creator><creator>Floeren, Melanie</creator><creator>Kumpf, Stephanie</creator><creator>Both, Charlotte</creator><creator>Peter, Bärbel</creator><creator>Balz, Vera</creator><creator>Suvorava, Tatsiana</creator><creator>Kojda, Georg</creator><general>Blackwell Publishing Ltd</general><general>John Wiley & Sons, Inc</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>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</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>FR3</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>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201111</creationdate><title>Catalase activity prevents exercise‐induced up‐regulation of vasoprotective proteins in venous tissue</title><author>Dao, Vu Thao‐Vi ; Floeren, Melanie ; Kumpf, Stephanie ; Both, Charlotte ; Peter, Bärbel ; Balz, Vera ; Suvorava, Tatsiana ; Kojda, Georg</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5687-1be59757aa8bcc9420e2a98f7252604f26014f235b3551268bbca9da79e2c043</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Amitrole - pharmacology</topic><topic>Animals</topic><topic>Aorta</topic><topic>Aorta - metabolism</topic><topic>Catalase</topic><topic>Catalase - antagonists & inhibitors</topic><topic>Catalase - metabolism</topic><topic>endothelial nitric oxide synthase</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Exercise</topic><topic>Fitness training programs</topic><topic>Gene expression</topic><topic>Heart</topic><topic>Hydrogen peroxide</topic><topic>Lung - metabolism</topic><topic>Lungs</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Molecular modelling</topic><topic>Motor Activity</topic><topic>Myocardium - metabolism</topic><topic>Nitric oxide</topic><topic>Nitric Oxide Synthase Type III - biosynthesis</topic><topic>Nitric Oxide Synthase Type III - genetics</topic><topic>Nitric Oxide Synthase Type III - metabolism</topic><topic>Nitric-oxide synthase</topic><topic>Original</topic><topic>Physical activity</topic><topic>Physical Conditioning, Animal</topic><topic>Physical fitness</topic><topic>Polyclonal antibodies</topic><topic>pulmonary rehabilitation</topic><topic>RNA, Messenger - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Dao, Vu Thao‐Vi</au><au>Floeren, Melanie</au><au>Kumpf, Stephanie</au><au>Both, Charlotte</au><au>Peter, Bärbel</au><au>Balz, Vera</au><au>Suvorava, Tatsiana</au><au>Kojda, Georg</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Catalase activity prevents exercise‐induced up‐regulation of vasoprotective proteins in venous tissue</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2011-11</date><risdate>2011</risdate><volume>15</volume><issue>11</issue><spage>2326</spage><epage>2334</epage><pages>2326-2334</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Physical activity induces favourable changes of arterial gene expression and protein activity, although little is known about its effect in venous tissue. Although our understanding of the initiating molecular signals is still incomplete, increased expression of endothelial nitric oxide synthase (eNOS) is considered a key event. This study sought to investigate the effects of two different training protocols on the expression of eNOS and extracellular superoxide dismutase (ecSOD) in venous and lung tissue and to evaluate the underlying molecular mechanisms. C57Bl/6 mice underwent voluntary exercise or forced physical activity. Changes of vascular mRNA and protein levels and activity of eNOS, ecSOD and catalase were determined in aorta, heart, lung and vena cava. Both training protocols similarly increased relative heart weight and resulted in up‐regulation of aortic and myocardial eNOS. In striking contrast, eNOS expression in vena cava and lung remained unchanged. Likewise, exercise up‐regulated ecSOD in the aorta and in left ventricular tissue but remained unchanged in lung tissue. Catalase expression in lung tissue and vena cava of exercised mice exceeded that in aorta by 6.9‐ and 10‐fold, respectively, suggesting a lack of stimulatory effects of hydrogen peroxide. In accordance, treatment of mice with the catalase inhibitor aminotriazole for 6 weeks resulted in significant up‐regulation of eNOS and ecSOD in vena cava. These data suggest that physiological venous catalase activity prevents exercise‐induced up‐regulation of eNOS and ecSOD. Furthermore, therapeutic inhibition of vascular catalase might improve pulmonary rehabilitation.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>21129156</pmid><doi>10.1111/j.1582-4934.2010.01227.x</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Amitrole - pharmacology Animals Aorta Aorta - metabolism Catalase Catalase - antagonists & inhibitors Catalase - metabolism endothelial nitric oxide synthase Endothelium, Vascular - metabolism Exercise Fitness training programs Gene expression Heart Hydrogen peroxide Lung - metabolism Lungs Male Mice Mice, Inbred C57BL Molecular modelling Motor Activity Myocardium - metabolism Nitric oxide Nitric Oxide Synthase Type III - biosynthesis Nitric Oxide Synthase Type III - genetics Nitric Oxide Synthase Type III - metabolism Nitric-oxide synthase Original Physical activity Physical Conditioning, Animal Physical fitness Polyclonal antibodies pulmonary rehabilitation RNA, Messenger - biosynthesis RNA, Messenger - genetics Shear stress Superoxide Dismutase - biosynthesis Up-regulation Venae Cavae - metabolism |
title | Catalase activity prevents exercise‐induced up‐regulation of vasoprotective proteins in venous tissue |
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