Tumor Necrosis Factor - Alpha Is Essential for Angiotensin II-Induced Ventricular Remodeling: Role for Oxidative Stress
The functional crosstalk between angiotensin II (Ang II) and tumor necrosis factor (TNF)-α has been shown to cause adverse left ventricular remodeling and hypertrophy in hypertension. Previous studies from our lab showed that mice lacking TNF-α (TNF-α-/-) have attenuated hypertensive response to Ang...
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| description | The functional crosstalk between angiotensin II (Ang II) and tumor necrosis factor (TNF)-α has been shown to cause adverse left ventricular remodeling and hypertrophy in hypertension. Previous studies from our lab showed that mice lacking TNF-α (TNF-α-/-) have attenuated hypertensive response to Ang II; however, the signaling mechanisms involved are not known. In this study, we investigated the signaling pathways involved in the Ang II and TNF-α interaction. Chronic Ang II infusion (1 μg/kg/min, 14 days) significantly increased cardiac collagen I, collagen III, CTGF and TGF-β mRNA and protein expression in wild-type (WT) mice, whereas these changes were decreased in TNF-α-/- mice. TNF-α-/- mice with Ang II infusion showed reduced myocardial perivascular and interstitial fibrosis compared to WT mice with Ang II infusion. In WT mice, Ang II infusion increased reactive oxygen species formation and the expression of NADPH oxidase subunits, indicating increased oxidative stress, but not in TNF-α-/- mice. In addition, treatment with etanercept (8 mg/kg, every 3 days) for two weeks blunted the Ang II-induced hypertension (133 ± 4 vs 154 ± 3 mmHg, p |
| doi_str_mv | 10.1371/journal.pone.0138372 |
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Previous studies from our lab showed that mice lacking TNF-α (TNF-α-/-) have attenuated hypertensive response to Ang II; however, the signaling mechanisms involved are not known. In this study, we investigated the signaling pathways involved in the Ang II and TNF-α interaction. Chronic Ang II infusion (1 μg/kg/min, 14 days) significantly increased cardiac collagen I, collagen III, CTGF and TGF-β mRNA and protein expression in wild-type (WT) mice, whereas these changes were decreased in TNF-α-/- mice. TNF-α-/- mice with Ang II infusion showed reduced myocardial perivascular and interstitial fibrosis compared to WT mice with Ang II infusion. In WT mice, Ang II infusion increased reactive oxygen species formation and the expression of NADPH oxidase subunits, indicating increased oxidative stress, but not in TNF-α-/- mice. In addition, treatment with etanercept (8 mg/kg, every 3 days) for two weeks blunted the Ang II-induced hypertension (133 ± 4 vs 154 ± 3 mmHg, p<0.05) and cardiac hypertrophy (heart weight to body weight ratio, 4.8 ± 0.2 vs 5.6 ± 0.3, p<0.05) in WT mice. Furthermore, Ang II-induced activation of NF-κB, p38 MAPK, and JNK were reduced in both TNF-α-/- mice and mice treated with etanercept. Together, these findings indicate that TNF-α contributes to Ang II-induced hypertension and adverse cardiac remodeling, and that these effects are associated with changes in the oxidative stress dependent MAPK/TGF-β/NF-κB pathway. These results may provide new insight into the mechanisms of Ang II and TNF-α interaction.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0138372</identifier><identifier>PMID: 26378790</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Angiotensin ; Angiotensin II ; Angiotensin II - pharmacology ; Angiotensins ; Animals ; Blood pressure ; Blood Pressure - drug effects ; Blood Pressure - physiology ; Body weight ; Bone morphogenetic proteins ; Cardiomegaly - metabolism ; Collagen ; Collagen (type I) ; Collagen (type III) ; Collagen Type I - metabolism ; Collagen Type III - metabolism ; Collagens ; Connective tissue growth factor ; Connective Tissue Growth Factor - metabolism ; Crosstalk ; Etanercept ; Fibrosis ; Fibrosis - metabolism ; Fibrosis - pathology ; Gene expression ; Heart ; Heart - drug effects ; Heart - physiopathology ; Heart diseases ; Heart hypertrophy ; Hypertension ; Hypertension - metabolism ; Hypertension - physiopathology ; Hypertrophy ; Infusion ; JNK protein ; Kinases ; Male ; MAP kinase ; MAP Kinase Signaling System - drug effects ; MAP Kinase Signaling System - physiology ; Mice ; mRNA ; Myocardium - metabolism ; NAD(P)H oxidase ; NADPH Oxidases - metabolism ; Necrosis ; NF-kappa B - metabolism ; NF-κB protein ; Nitric oxide ; Oxidases ; Oxidative stress ; Oxidative Stress - drug effects ; Oxidative Stress - physiology ; Oxygen ; p38 Mitogen-Activated Protein Kinases - metabolism ; Reactive oxygen species ; Receptor, Angiotensin, Type 1 - metabolism ; RNA ; RNA, Messenger - metabolism ; Signal transduction ; Signal Transduction - drug effects ; Signal Transduction - physiology ; Signaling ; Transforming Growth Factor beta - metabolism ; Transforming growth factors ; Tumor necrosis factor ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Tumors ; Ventricle ; Ventricular Remodeling - drug effects ; Ventricular Remodeling - physiology ; Veterinary colleges</subject><ispartof>PloS one, 2015-09, Vol.10 (9), p.e0138372-e0138372</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Sriramula, Francis. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Sriramula, Francis 2015 Sriramula, Francis</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-6b6cb372244dbb79d1a48534b02618b7b9f5ff7fe17293b44be76aac0dd911f13</citedby><cites>FETCH-LOGICAL-c758t-6b6cb372244dbb79d1a48534b02618b7b9f5ff7fe17293b44be76aac0dd911f13</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/PMC4574701/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4574701/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79569,79570</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26378790$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sriramula, Srinivas</creatorcontrib><creatorcontrib>Francis, Joseph</creatorcontrib><title>Tumor Necrosis Factor - Alpha Is Essential for Angiotensin II-Induced Ventricular Remodeling: Role for Oxidative Stress</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The functional crosstalk between angiotensin II (Ang II) and tumor necrosis factor (TNF)-α has been shown to cause adverse left ventricular remodeling and hypertrophy in hypertension. Previous studies from our lab showed that mice lacking TNF-α (TNF-α-/-) have attenuated hypertensive response to Ang II; however, the signaling mechanisms involved are not known. In this study, we investigated the signaling pathways involved in the Ang II and TNF-α interaction. Chronic Ang II infusion (1 μg/kg/min, 14 days) significantly increased cardiac collagen I, collagen III, CTGF and TGF-β mRNA and protein expression in wild-type (WT) mice, whereas these changes were decreased in TNF-α-/- mice. TNF-α-/- mice with Ang II infusion showed reduced myocardial perivascular and interstitial fibrosis compared to WT mice with Ang II infusion. In WT mice, Ang II infusion increased reactive oxygen species formation and the expression of NADPH oxidase subunits, indicating increased oxidative stress, but not in TNF-α-/- mice. In addition, treatment with etanercept (8 mg/kg, every 3 days) for two weeks blunted the Ang II-induced hypertension (133 ± 4 vs 154 ± 3 mmHg, p<0.05) and cardiac hypertrophy (heart weight to body weight ratio, 4.8 ± 0.2 vs 5.6 ± 0.3, p<0.05) in WT mice. Furthermore, Ang II-induced activation of NF-κB, p38 MAPK, and JNK were reduced in both TNF-α-/- mice and mice treated with etanercept. Together, these findings indicate that TNF-α contributes to Ang II-induced hypertension and adverse cardiac remodeling, and that these effects are associated with changes in the oxidative stress dependent MAPK/TGF-β/NF-κB pathway. These results may provide new insight into the mechanisms of Ang II and TNF-α interaction.</description><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Angiotensin II - pharmacology</subject><subject>Angiotensins</subject><subject>Animals</subject><subject>Blood pressure</subject><subject>Blood Pressure - drug effects</subject><subject>Blood Pressure - physiology</subject><subject>Body weight</subject><subject>Bone morphogenetic proteins</subject><subject>Cardiomegaly - metabolism</subject><subject>Collagen</subject><subject>Collagen (type I)</subject><subject>Collagen (type III)</subject><subject>Collagen Type I - metabolism</subject><subject>Collagen Type III - metabolism</subject><subject>Collagens</subject><subject>Connective tissue growth factor</subject><subject>Connective Tissue Growth Factor - metabolism</subject><subject>Crosstalk</subject><subject>Etanercept</subject><subject>Fibrosis</subject><subject>Fibrosis - metabolism</subject><subject>Fibrosis - pathology</subject><subject>Gene expression</subject><subject>Heart</subject><subject>Heart - drug effects</subject><subject>Heart - physiopathology</subject><subject>Heart diseases</subject><subject>Heart hypertrophy</subject><subject>Hypertension</subject><subject>Hypertension - metabolism</subject><subject>Hypertension - physiopathology</subject><subject>Hypertrophy</subject><subject>Infusion</subject><subject>JNK protein</subject><subject>Kinases</subject><subject>Male</subject><subject>MAP kinase</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>MAP Kinase Signaling System - physiology</subject><subject>Mice</subject><subject>mRNA</subject><subject>Myocardium - metabolism</subject><subject>NAD(P)H oxidase</subject><subject>NADPH Oxidases - metabolism</subject><subject>Necrosis</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Nitric oxide</subject><subject>Oxidases</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxidative Stress - physiology</subject><subject>Oxygen</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Reactive oxygen species</subject><subject>Receptor, Angiotensin, Type 1 - metabolism</subject><subject>RNA</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - physiology</subject><subject>Signaling</subject><subject>Transforming Growth Factor beta - metabolism</subject><subject>Transforming growth factors</subject><subject>Tumor necrosis factor</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>Tumors</subject><subject>Ventricle</subject><subject>Ventricular Remodeling - drug effects</subject><subject>Ventricular Remodeling - physiology</subject><subject>Veterinary colleges</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk1Fv1SAUxxujcXP6DYw2MTH60GtpKVAfTG6WTZss3uRu7pVQoL0sFO6gnfPbS-_tlluzB9MHCvz-_8M5cKLoLUgXIMfgy40dnGF6sbVGLlKQkxxnz6JjUOZZgrI0f37wfxS98v4mTYucIPQyOspQjgku0-Po99XQWRf_lNxZr3x8zngf5km81NsNiysfn3kvTa-YjpuwsTStsr00Xpm4qpLKiIFLEV8HxCk-aObiteyskFqZ9mu8tlrudKt7JViv7mR82Tvp_evoRcO0l2-m8ST6dX52dfojuVh9r06XFwnHBekTVCNeh8QyCEVd41IABkmRwzrNECA1rsumaBrcSICzMq8hrCVGjPFUiBKABuQn0fu971ZbT6eaeQowKDMSfLNAVHtCWHZDt051zP2hlim6W7Cupcz1imtJBRCE1xiVCDVQSEEAgiUPoUrBCoFQ8Po2RRvqTgo-VoXpmel8x6gNbe0dhQWGOB2P-2kycPZ2kL6nnfJcas2MtMPu3HkJIQFpQD_8gz6d3US1LCSgTGNDXD6a0iXMSFlgQsawiyeo8AnZKR4eWKPC-kzweSYITC_v-5YN3tPqcv3_7Op6zn48YDeS6X7jrR56ZY2fg3APju_WO9k8FhmkdOyPh2rQsT_o1B9B9u7wgh5FDw2R_wVieAtK</recordid><startdate>20150917</startdate><enddate>20150917</enddate><creator>Sriramula, Srinivas</creator><creator>Francis, Joseph</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20150917</creationdate><title>Tumor Necrosis Factor - Alpha Is Essential for Angiotensin II-Induced Ventricular Remodeling: Role for Oxidative Stress</title><author>Sriramula, Srinivas ; Francis, Joseph</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-6b6cb372244dbb79d1a48534b02618b7b9f5ff7fe17293b44be76aac0dd911f13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Angiotensin</topic><topic>Angiotensin II</topic><topic>Angiotensin II - pharmacology</topic><topic>Angiotensins</topic><topic>Animals</topic><topic>Blood pressure</topic><topic>Blood Pressure - drug effects</topic><topic>Blood Pressure - physiology</topic><topic>Body weight</topic><topic>Bone morphogenetic proteins</topic><topic>Cardiomegaly - metabolism</topic><topic>Collagen</topic><topic>Collagen (type I)</topic><topic>Collagen (type III)</topic><topic>Collagen Type I - metabolism</topic><topic>Collagen Type III - metabolism</topic><topic>Collagens</topic><topic>Connective tissue growth factor</topic><topic>Connective Tissue Growth Factor - metabolism</topic><topic>Crosstalk</topic><topic>Etanercept</topic><topic>Fibrosis</topic><topic>Fibrosis - metabolism</topic><topic>Fibrosis - pathology</topic><topic>Gene expression</topic><topic>Heart</topic><topic>Heart - drug effects</topic><topic>Heart - physiopathology</topic><topic>Heart diseases</topic><topic>Heart hypertrophy</topic><topic>Hypertension</topic><topic>Hypertension - metabolism</topic><topic>Hypertension - physiopathology</topic><topic>Hypertrophy</topic><topic>Infusion</topic><topic>JNK protein</topic><topic>Kinases</topic><topic>Male</topic><topic>MAP kinase</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>MAP Kinase Signaling System - physiology</topic><topic>Mice</topic><topic>mRNA</topic><topic>Myocardium - metabolism</topic><topic>NAD(P)H oxidase</topic><topic>NADPH Oxidases - metabolism</topic><topic>Necrosis</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>Nitric oxide</topic><topic>Oxidases</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Oxidative Stress - physiology</topic><topic>Oxygen</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Reactive oxygen species</topic><topic>Receptor, Angiotensin, Type 1 - metabolism</topic><topic>RNA</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - physiology</topic><topic>Signaling</topic><topic>Transforming Growth Factor beta - metabolism</topic><topic>Transforming growth factors</topic><topic>Tumor necrosis factor</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><topic>Tumors</topic><topic>Ventricle</topic><topic>Ventricular Remodeling - drug effects</topic><topic>Ventricular Remodeling - physiology</topic><topic>Veterinary colleges</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sriramula, Srinivas</creatorcontrib><creatorcontrib>Francis, Joseph</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale in Context : Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>ProQuest Nursing and Allied Health Journals</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection (ProQuest)</collection><collection>Natural Science Collection (ProQuest)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sriramula, Srinivas</au><au>Francis, Joseph</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tumor Necrosis Factor - Alpha Is Essential for Angiotensin II-Induced Ventricular Remodeling: Role for Oxidative Stress</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-09-17</date><risdate>2015</risdate><volume>10</volume><issue>9</issue><spage>e0138372</spage><epage>e0138372</epage><pages>e0138372-e0138372</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The functional crosstalk between angiotensin II (Ang II) and tumor necrosis factor (TNF)-α has been shown to cause adverse left ventricular remodeling and hypertrophy in hypertension. Previous studies from our lab showed that mice lacking TNF-α (TNF-α-/-) have attenuated hypertensive response to Ang II; however, the signaling mechanisms involved are not known. In this study, we investigated the signaling pathways involved in the Ang II and TNF-α interaction. Chronic Ang II infusion (1 μg/kg/min, 14 days) significantly increased cardiac collagen I, collagen III, CTGF and TGF-β mRNA and protein expression in wild-type (WT) mice, whereas these changes were decreased in TNF-α-/- mice. TNF-α-/- mice with Ang II infusion showed reduced myocardial perivascular and interstitial fibrosis compared to WT mice with Ang II infusion. In WT mice, Ang II infusion increased reactive oxygen species formation and the expression of NADPH oxidase subunits, indicating increased oxidative stress, but not in TNF-α-/- mice. In addition, treatment with etanercept (8 mg/kg, every 3 days) for two weeks blunted the Ang II-induced hypertension (133 ± 4 vs 154 ± 3 mmHg, p<0.05) and cardiac hypertrophy (heart weight to body weight ratio, 4.8 ± 0.2 vs 5.6 ± 0.3, p<0.05) in WT mice. Furthermore, Ang II-induced activation of NF-κB, p38 MAPK, and JNK were reduced in both TNF-α-/- mice and mice treated with etanercept. Together, these findings indicate that TNF-α contributes to Ang II-induced hypertension and adverse cardiac remodeling, and that these effects are associated with changes in the oxidative stress dependent MAPK/TGF-β/NF-κB pathway. These results may provide new insight into the mechanisms of Ang II and TNF-α interaction.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26378790</pmid><doi>10.1371/journal.pone.0138372</doi><tpages>e0138372</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1719287222 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Angiotensin Angiotensin II Angiotensin II - pharmacology Angiotensins Animals Blood pressure Blood Pressure - drug effects Blood Pressure - physiology Body weight Bone morphogenetic proteins Cardiomegaly - metabolism Collagen Collagen (type I) Collagen (type III) Collagen Type I - metabolism Collagen Type III - metabolism Collagens Connective tissue growth factor Connective Tissue Growth Factor - metabolism Crosstalk Etanercept Fibrosis Fibrosis - metabolism Fibrosis - pathology Gene expression Heart Heart - drug effects Heart - physiopathology Heart diseases Heart hypertrophy Hypertension Hypertension - metabolism Hypertension - physiopathology Hypertrophy Infusion JNK protein Kinases Male MAP kinase MAP Kinase Signaling System - drug effects MAP Kinase Signaling System - physiology Mice mRNA Myocardium - metabolism NAD(P)H oxidase NADPH Oxidases - metabolism Necrosis NF-kappa B - metabolism NF-κB protein Nitric oxide Oxidases Oxidative stress Oxidative Stress - drug effects Oxidative Stress - physiology Oxygen p38 Mitogen-Activated Protein Kinases - metabolism Reactive oxygen species Receptor, Angiotensin, Type 1 - metabolism RNA RNA, Messenger - metabolism Signal transduction Signal Transduction - drug effects Signal Transduction - physiology Signaling Transforming Growth Factor beta - metabolism Transforming growth factors Tumor necrosis factor Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-TNF Tumor necrosis factor-α Tumors Ventricle Ventricular Remodeling - drug effects Ventricular Remodeling - physiology Veterinary colleges |
| title | Tumor Necrosis Factor - Alpha Is Essential for Angiotensin II-Induced Ventricular Remodeling: Role for Oxidative Stress |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-18T22%3A42%3A14IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Tumor%20Necrosis%20Factor%20-%20Alpha%20Is%20Essential%20for%20Angiotensin%20II-Induced%20Ventricular%20Remodeling:%20Role%20for%20Oxidative%20Stress&rft.jtitle=PloS%20one&rft.au=Sriramula,%20Srinivas&rft.date=2015-09-17&rft.volume=10&rft.issue=9&rft.spage=e0138372&rft.epage=e0138372&rft.pages=e0138372-e0138372&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0138372&rft_dat=%3Cgale_plos_%3EA428957881%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1719287222&rft_id=info:pmid/26378790&rft_galeid=A428957881&rft_doaj_id=oai_doaj_org_article_d1d8cb76966f4ded81649cdd99da5d66&rfr_iscdi=true |