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Lactate-upregulation of lactate oxidation complex-related genes is blunted in left ventricle of myocardial infarcted rats
Lactate modulates the expression of lactate oxidation complex (LOC)-related genes and cardiac blood flow under physiological conditions, but its modulatory role remains to be elucidated regarding pathological cardiac stress. The present study evaluated the effect of lactate on LOC-related genes expr...
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Published in: | Brazilian journal of medical and biological research 2018-01, Vol.51 (11), p.e7660-e7660 |
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description | Lactate modulates the expression of lactate oxidation complex (LOC)-related genes and cardiac blood flow under physiological conditions, but its modulatory role remains to be elucidated regarding pathological cardiac stress. The present study evaluated the effect of lactate on LOC-related genes expression and hemodynamics of hearts submitted to myocardial infarction (MI). Four weeks after MI or sham operation, isolated hearts of male Wistar rats were perfused for 60 min with Na+-lactate (20 mM). As expected, MI reduced cardiac contractility and relaxation with no changes in perfusion. The impaired cardiac hemodynamics were associated with increased reactive oxygen species (ROS) levels (Sham: 19.3±0.5 vs MI: 23.8±0.3 µM), NADPH oxidase (NOX) activity (Sham: 42.2±1.3 vs MI: 60.5±1.5 nmol·h-1·mg-1) and monocarboxylate transporter 1 (mct1) mRNA levels (Sham: 1.0±0.06 vs MI: 1.7±0.2 a.u.), but no changes in superoxide dismutase (SOD), catalase, NADH oxidase (NADox), and xanthine oxidase activities. Lactate perfusion in MI hearts had no additional effect on ROS levels, NADox, and NOX activity, however, it partially reduced mct1 mRNA expression (MI-Lactate 1.3±0.08 a.u.). Interestingly, lactate significantly decreased SOD (MI-Lactate: 54.5±4.2 µmol·mg-1·min-1) and catalase (MI: 1.1±0.1 nmol·mg-1·min-1) activities in MI. Collectively, our data suggest that under pathological stress, lactate lacks its ability to modulate the expression of cardiac LOC-related genes and the perfused pressure in hearts submitted to chronic MI. Together, these data contribute to elucidate the mechanisms involved in the pathogenesis of heart failure induced by MI. |
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The present study evaluated the effect of lactate on LOC-related genes expression and hemodynamics of hearts submitted to myocardial infarction (MI). Four weeks after MI or sham operation, isolated hearts of male Wistar rats were perfused for 60 min with Na+-lactate (20 mM). As expected, MI reduced cardiac contractility and relaxation with no changes in perfusion. The impaired cardiac hemodynamics were associated with increased reactive oxygen species (ROS) levels (Sham: 19.3±0.5 vs MI: 23.8±0.3 µM), NADPH oxidase (NOX) activity (Sham: 42.2±1.3 vs MI: 60.5±1.5 nmol·h-1·mg-1) and monocarboxylate transporter 1 (mct1) mRNA levels (Sham: 1.0±0.06 vs MI: 1.7±0.2 a.u.), but no changes in superoxide dismutase (SOD), catalase, NADH oxidase (NADox), and xanthine oxidase activities. Lactate perfusion in MI hearts had no additional effect on ROS levels, NADox, and NOX activity, however, it partially reduced mct1 mRNA expression (MI-Lactate 1.3±0.08 a.u.). Interestingly, lactate significantly decreased SOD (MI-Lactate: 54.5±4.2 µmol·mg-1·min-1) and catalase (MI: 1.1±0.1 nmol·mg-1·min-1) activities in MI. Collectively, our data suggest that under pathological stress, lactate lacks its ability to modulate the expression of cardiac LOC-related genes and the perfused pressure in hearts submitted to chronic MI. Together, these data contribute to elucidate the mechanisms involved in the pathogenesis of heart failure induced by MI.</description><identifier>ISSN: 0100-879X</identifier><identifier>ISSN: 1414-431X</identifier><identifier>EISSN: 1414-431X</identifier><identifier>EISSN: 1678-4510</identifier><identifier>DOI: 10.1590/1414-431X20187660</identifier><identifier>PMID: 30304133</identifier><language>eng</language><publisher>Brazil: Revista Brasileira de Pesquisas Medicas</publisher><subject>BIOLOGY ; Blood flow ; Catalase ; Gene expression ; Heart diseases ; Hemodynamics ; Lactate ; Lactate oxidation complex ; Lactic acid ; MEDICINE, RESEARCH & EXPERIMENTAL ; Muscle contraction ; Myocardial infarction ; NAD(P)H oxidase ; NADH ; NADH oxidase ; Oxidation ; Oxidative stress ; Perfusion ; Perfusion pressure ; Reactive oxygen species ; Rodents ; Superoxide dismutase ; Ventricle ; Xanthine oxidase</subject><ispartof>Brazilian journal of medical and biological research, 2018-01, Vol.51 (11), p.e7660-e7660</ispartof><rights>Copyright Revista Brasileira de Pesquisas Medicas 2018</rights><rights>This work is licensed under a Creative Commons Attribution 4.0 International License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c532t-6f740f50fca686ae49fd359e5e5de0016e07cc65705a76197f45a880d86d61a23</citedby><cites>FETCH-LOGICAL-c532t-6f740f50fca686ae49fd359e5e5de0016e07cc65705a76197f45a880d86d61a23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,24150,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30304133$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gabriel-Costa, D</creatorcontrib><creatorcontrib>Cunha, T F</creatorcontrib><creatorcontrib>Paixão, N A</creatorcontrib><creatorcontrib>Fortunato, R S</creatorcontrib><creatorcontrib>Rego-Monteiro, I C C</creatorcontrib><creatorcontrib>Barreto-Chaves, M L M</creatorcontrib><creatorcontrib>Brum, P C</creatorcontrib><title>Lactate-upregulation of lactate oxidation complex-related genes is blunted in left ventricle of myocardial infarcted rats</title><title>Brazilian journal of medical and biological research</title><addtitle>Braz J Med Biol Res</addtitle><description>Lactate modulates the expression of lactate oxidation complex (LOC)-related genes and cardiac blood flow under physiological conditions, but its modulatory role remains to be elucidated regarding pathological cardiac stress. The present study evaluated the effect of lactate on LOC-related genes expression and hemodynamics of hearts submitted to myocardial infarction (MI). Four weeks after MI or sham operation, isolated hearts of male Wistar rats were perfused for 60 min with Na+-lactate (20 mM). As expected, MI reduced cardiac contractility and relaxation with no changes in perfusion. The impaired cardiac hemodynamics were associated with increased reactive oxygen species (ROS) levels (Sham: 19.3±0.5 vs MI: 23.8±0.3 µM), NADPH oxidase (NOX) activity (Sham: 42.2±1.3 vs MI: 60.5±1.5 nmol·h-1·mg-1) and monocarboxylate transporter 1 (mct1) mRNA levels (Sham: 1.0±0.06 vs MI: 1.7±0.2 a.u.), but no changes in superoxide dismutase (SOD), catalase, NADH oxidase (NADox), and xanthine oxidase activities. Lactate perfusion in MI hearts had no additional effect on ROS levels, NADox, and NOX activity, however, it partially reduced mct1 mRNA expression (MI-Lactate 1.3±0.08 a.u.). Interestingly, lactate significantly decreased SOD (MI-Lactate: 54.5±4.2 µmol·mg-1·min-1) and catalase (MI: 1.1±0.1 nmol·mg-1·min-1) activities in MI. Collectively, our data suggest that under pathological stress, lactate lacks its ability to modulate the expression of cardiac LOC-related genes and the perfused pressure in hearts submitted to chronic MI. Together, these data contribute to elucidate the mechanisms involved in the pathogenesis of heart failure induced by MI.</description><subject>BIOLOGY</subject><subject>Blood flow</subject><subject>Catalase</subject><subject>Gene expression</subject><subject>Heart diseases</subject><subject>Hemodynamics</subject><subject>Lactate</subject><subject>Lactate oxidation complex</subject><subject>Lactic acid</subject><subject>MEDICINE, RESEARCH & EXPERIMENTAL</subject><subject>Muscle contraction</subject><subject>Myocardial infarction</subject><subject>NAD(P)H oxidase</subject><subject>NADH</subject><subject>NADH oxidase</subject><subject>Oxidation</subject><subject>Oxidative stress</subject><subject>Perfusion</subject><subject>Perfusion pressure</subject><subject>Reactive oxygen species</subject><subject>Rodents</subject><subject>Superoxide dismutase</subject><subject>Ventricle</subject><subject>Xanthine oxidase</subject><issn>0100-879X</issn><issn>1414-431X</issn><issn>1414-431X</issn><issn>1678-4510</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNpdUk2P0zAUjBCILQs_gAuKxIVLFn87uSChFR8rVeIASHuzXp3n4sqNi52s2n-PQ3YrlpPt8cxo_DxV9ZqSKyo78p4KKhrB6S0jtNVKkSfV6ow9rVaEEtK0uru9qF7kvCOESSLo8-qCE142nK-q0xrsCCM20yHhdgow-jjU0dVhwet49P0C2rg_BDw2CQsL-3qLA-ba53oTpmEG_FAHdGN9h8OYvA04--xP0ULqPYRy7yDZmZlgzC-rZw5Cxlf362X18_OnH9dfm_W3LzfXH9eNlZyNjXJaECeJs6BaBSg613PZoUTZIyFUIdHWKqmJBK1op52Q0Lakb1WvKDB-Wd0svn2EnTkkv4d0MhG8-QvEtDWQxjmu2TB0oJijQvUCgIO2GpRS1NqW001bvK4Wr2w9hmh2cUpDCW--z6M286jnryixylERWQQfFsFh2uyxt_NkIDxK8fhm8L_MNt4ZRTXrWFcM3t0bpPh7wjyavc8WQ4AB45QNo7REI0KIQn37H_Ucj1HWSdoxqguLLiybYs4J3TkMJWZulZkbZEqDjg-tKpo3_77irHioEf8D8wDHYg</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Gabriel-Costa, D</creator><creator>Cunha, T F</creator><creator>Paixão, N A</creator><creator>Fortunato, R S</creator><creator>Rego-Monteiro, I C C</creator><creator>Barreto-Chaves, M L M</creator><creator>Brum, P C</creator><general>Revista Brasileira de Pesquisas Medicas</general><general>Associação Brasileira de Divulgação Científica</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope><scope>GPN</scope><scope>DOA</scope></search><sort><creationdate>20180101</creationdate><title>Lactate-upregulation of lactate oxidation complex-related genes is blunted in left ventricle of myocardial infarcted rats</title><author>Gabriel-Costa, D ; Cunha, T F ; Paixão, N A ; Fortunato, R S ; Rego-Monteiro, I C C ; Barreto-Chaves, M L M ; Brum, P C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c532t-6f740f50fca686ae49fd359e5e5de0016e07cc65705a76197f45a880d86d61a23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>BIOLOGY</topic><topic>Blood flow</topic><topic>Catalase</topic><topic>Gene expression</topic><topic>Heart diseases</topic><topic>Hemodynamics</topic><topic>Lactate</topic><topic>Lactate oxidation complex</topic><topic>Lactic acid</topic><topic>MEDICINE, RESEARCH & EXPERIMENTAL</topic><topic>Muscle contraction</topic><topic>Myocardial infarction</topic><topic>NAD(P)H oxidase</topic><topic>NADH</topic><topic>NADH oxidase</topic><topic>Oxidation</topic><topic>Oxidative stress</topic><topic>Perfusion</topic><topic>Perfusion pressure</topic><topic>Reactive oxygen species</topic><topic>Rodents</topic><topic>Superoxide dismutase</topic><topic>Ventricle</topic><topic>Xanthine oxidase</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gabriel-Costa, D</creatorcontrib><creatorcontrib>Cunha, T F</creatorcontrib><creatorcontrib>Paixão, N A</creatorcontrib><creatorcontrib>Fortunato, R S</creatorcontrib><creatorcontrib>Rego-Monteiro, I C C</creatorcontrib><creatorcontrib>Barreto-Chaves, M L M</creatorcontrib><creatorcontrib>Brum, P C</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>SciELO</collection><collection>Directory of Open Access Journals</collection><jtitle>Brazilian journal of medical and biological research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gabriel-Costa, D</au><au>Cunha, T F</au><au>Paixão, N A</au><au>Fortunato, R S</au><au>Rego-Monteiro, I C C</au><au>Barreto-Chaves, M L M</au><au>Brum, P C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lactate-upregulation of lactate oxidation complex-related genes is blunted in left ventricle of myocardial infarcted rats</atitle><jtitle>Brazilian journal of medical and biological research</jtitle><addtitle>Braz J Med Biol Res</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>51</volume><issue>11</issue><spage>e7660</spage><epage>e7660</epage><pages>e7660-e7660</pages><issn>0100-879X</issn><issn>1414-431X</issn><eissn>1414-431X</eissn><eissn>1678-4510</eissn><abstract>Lactate modulates the expression of lactate oxidation complex (LOC)-related genes and cardiac blood flow under physiological conditions, but its modulatory role remains to be elucidated regarding pathological cardiac stress. The present study evaluated the effect of lactate on LOC-related genes expression and hemodynamics of hearts submitted to myocardial infarction (MI). Four weeks after MI or sham operation, isolated hearts of male Wistar rats were perfused for 60 min with Na+-lactate (20 mM). As expected, MI reduced cardiac contractility and relaxation with no changes in perfusion. The impaired cardiac hemodynamics were associated with increased reactive oxygen species (ROS) levels (Sham: 19.3±0.5 vs MI: 23.8±0.3 µM), NADPH oxidase (NOX) activity (Sham: 42.2±1.3 vs MI: 60.5±1.5 nmol·h-1·mg-1) and monocarboxylate transporter 1 (mct1) mRNA levels (Sham: 1.0±0.06 vs MI: 1.7±0.2 a.u.), but no changes in superoxide dismutase (SOD), catalase, NADH oxidase (NADox), and xanthine oxidase activities. Lactate perfusion in MI hearts had no additional effect on ROS levels, NADox, and NOX activity, however, it partially reduced mct1 mRNA expression (MI-Lactate 1.3±0.08 a.u.). Interestingly, lactate significantly decreased SOD (MI-Lactate: 54.5±4.2 µmol·mg-1·min-1) and catalase (MI: 1.1±0.1 nmol·mg-1·min-1) activities in MI. Collectively, our data suggest that under pathological stress, lactate lacks its ability to modulate the expression of cardiac LOC-related genes and the perfused pressure in hearts submitted to chronic MI. Together, these data contribute to elucidate the mechanisms involved in the pathogenesis of heart failure induced by MI.</abstract><cop>Brazil</cop><pub>Revista Brasileira de Pesquisas Medicas</pub><pmid>30304133</pmid><doi>10.1590/1414-431X20187660</doi><oa>free_for_read</oa></addata></record> |
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subjects | BIOLOGY Blood flow Catalase Gene expression Heart diseases Hemodynamics Lactate Lactate oxidation complex Lactic acid MEDICINE, RESEARCH & EXPERIMENTAL Muscle contraction Myocardial infarction NAD(P)H oxidase NADH NADH oxidase Oxidation Oxidative stress Perfusion Perfusion pressure Reactive oxygen species Rodents Superoxide dismutase Ventricle Xanthine oxidase |
title | Lactate-upregulation of lactate oxidation complex-related genes is blunted in left ventricle of myocardial infarcted rats |
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