AMPK attenuates ventricular remodeling and dysfunction following aortic banding in mice via the Sirt3/Oxidative stress pathway
Although recent findings have suggested that AMP-activated protein kinase (AMPK) exerts inhibitory effects on cardiac remodeling secondary to hypertension, the mechanism and optimal duration of treatment remain unknown. Mice with descending aortic banding (AB) or subjected to sham operation received...
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Veröffentlicht in: | European journal of pharmacology 2017-11, Vol.814, p.335-342 |
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description | Although recent findings have suggested that AMP-activated protein kinase (AMPK) exerts inhibitory effects on cardiac remodeling secondary to hypertension, the mechanism and optimal duration of treatment remain unknown. Mice with descending aortic banding (AB) or subjected to sham operation received subcutaneous injection of either AICAR (0.5mgg-1day-1) or vehicle over 4 week periods. At the end of 4 week treatment, left ventricular (LV) remodeling and function were evaluated with histological analysis and echocardiography. Collagen deposition within the LV myocardium was detected with Masson's trichrome staining. Collagen I, Collagen III, Smad 2, Smad 3, NOX2, NOX4 and Sirt3 (an important antioxidant factor) within the LV tissue were also evaluated. Compared with the sham group, the vehicle-treated AB group exhibited significant elevations in cardiac remodeling and heart failure, characterized by an increase in LV weight relative to body weight, an increase in the area of collagen deposition, an increase in LV end-diastolic diameter, an increase in mitral E inflow velocity to mitral A inflow velocity and increases in the gene expressions of the fibrosis markers Collagen I, III and Smad 2, 3 mRNA and decreases in EF and fractional shortening. AMPK attenuate the cardiac remodeling parameters and improve cardiac function. Moreover, the expressions of NOX2, NOX4 were significantly elevated in vehicle-treated AB group. AMPK was able to significantly inhibit NOX2, NOX4 expression, while activate Sirt3 expression. AMPK significantly attenuated hypertension-induced Ventricular remodeling and dysfunction, which may be mediated by the Sirt3/Oxidative stress signaling pathway. |
doi_str_mv | 10.1016/j.ejphar.2017.08.042 |
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Mice with descending aortic banding (AB) or subjected to sham operation received subcutaneous injection of either AICAR (0.5mgg-1day-1) or vehicle over 4 week periods. At the end of 4 week treatment, left ventricular (LV) remodeling and function were evaluated with histological analysis and echocardiography. Collagen deposition within the LV myocardium was detected with Masson's trichrome staining. Collagen I, Collagen III, Smad 2, Smad 3, NOX2, NOX4 and Sirt3 (an important antioxidant factor) within the LV tissue were also evaluated. Compared with the sham group, the vehicle-treated AB group exhibited significant elevations in cardiac remodeling and heart failure, characterized by an increase in LV weight relative to body weight, an increase in the area of collagen deposition, an increase in LV end-diastolic diameter, an increase in mitral E inflow velocity to mitral A inflow velocity and increases in the gene expressions of the fibrosis markers Collagen I, III and Smad 2, 3 mRNA and decreases in EF and fractional shortening. AMPK attenuate the cardiac remodeling parameters and improve cardiac function. Moreover, the expressions of NOX2, NOX4 were significantly elevated in vehicle-treated AB group. AMPK was able to significantly inhibit NOX2, NOX4 expression, while activate Sirt3 expression. AMPK significantly attenuated hypertension-induced Ventricular remodeling and dysfunction, which may be mediated by the Sirt3/Oxidative stress signaling pathway.</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/j.ejphar.2017.08.042</identifier><identifier>PMID: 28867609</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>AMP-activated protein kinase (AMPK) ; AMP-Activated Protein Kinases - metabolism ; Animals ; Aorta - pathology ; Collagen Type I - genetics ; Collagen Type III - genetics ; Gene Expression Regulation ; Heart failure ; Male ; Mice ; Mice, Inbred C57BL ; NADPH Oxidase 2 - metabolism ; NADPH Oxidase 4 - metabolism ; Oxidative Stress ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Signal Transduction ; Silent information regulator (Sirt) ; Sirtuin 3 - metabolism ; Smad2 Protein - genetics ; Smad3 Protein - genetics ; Ventricular Remodeling</subject><ispartof>European journal of pharmacology, 2017-11, Vol.814, p.335-342</ispartof><rights>2017</rights><rights>Copyright © 2017. Published by Elsevier B.V.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c408t-e886d2249e45d1a850f64040bf90b282c5e787edb241576ea6a31aa125f6a4633</citedby><cites>FETCH-LOGICAL-c408t-e886d2249e45d1a850f64040bf90b282c5e787edb241576ea6a31aa125f6a4633</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.ejphar.2017.08.042$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27926,27927,45997</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28867609$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Yili</creatorcontrib><creatorcontrib>Chen, Cong</creatorcontrib><creatorcontrib>Dong, Bin</creatorcontrib><creatorcontrib>Xing, Fuwei</creatorcontrib><creatorcontrib>Huang, Huiling</creatorcontrib><creatorcontrib>Yao, Fengjuan</creatorcontrib><creatorcontrib>Ma, Yuedong</creatorcontrib><creatorcontrib>He, Jiangui</creatorcontrib><creatorcontrib>Dong, Yugang</creatorcontrib><title>AMPK attenuates ventricular remodeling and dysfunction following aortic banding in mice via the Sirt3/Oxidative stress pathway</title><title>European journal of pharmacology</title><addtitle>Eur J Pharmacol</addtitle><description>Although recent findings have suggested that AMP-activated protein kinase (AMPK) exerts inhibitory effects on cardiac remodeling secondary to hypertension, the mechanism and optimal duration of treatment remain unknown. Mice with descending aortic banding (AB) or subjected to sham operation received subcutaneous injection of either AICAR (0.5mgg-1day-1) or vehicle over 4 week periods. At the end of 4 week treatment, left ventricular (LV) remodeling and function were evaluated with histological analysis and echocardiography. Collagen deposition within the LV myocardium was detected with Masson's trichrome staining. Collagen I, Collagen III, Smad 2, Smad 3, NOX2, NOX4 and Sirt3 (an important antioxidant factor) within the LV tissue were also evaluated. Compared with the sham group, the vehicle-treated AB group exhibited significant elevations in cardiac remodeling and heart failure, characterized by an increase in LV weight relative to body weight, an increase in the area of collagen deposition, an increase in LV end-diastolic diameter, an increase in mitral E inflow velocity to mitral A inflow velocity and increases in the gene expressions of the fibrosis markers Collagen I, III and Smad 2, 3 mRNA and decreases in EF and fractional shortening. AMPK attenuate the cardiac remodeling parameters and improve cardiac function. Moreover, the expressions of NOX2, NOX4 were significantly elevated in vehicle-treated AB group. AMPK was able to significantly inhibit NOX2, NOX4 expression, while activate Sirt3 expression. AMPK significantly attenuated hypertension-induced Ventricular remodeling and dysfunction, which may be mediated by the Sirt3/Oxidative stress signaling pathway.</description><subject>AMP-activated protein kinase (AMPK)</subject><subject>AMP-Activated Protein Kinases - metabolism</subject><subject>Animals</subject><subject>Aorta - pathology</subject><subject>Collagen Type I - genetics</subject><subject>Collagen Type III - genetics</subject><subject>Gene Expression Regulation</subject><subject>Heart failure</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>NADPH Oxidase 2 - metabolism</subject><subject>NADPH Oxidase 4 - metabolism</subject><subject>Oxidative Stress</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal Transduction</subject><subject>Silent information regulator (Sirt)</subject><subject>Sirtuin 3 - metabolism</subject><subject>Smad2 Protein - genetics</subject><subject>Smad3 Protein - genetics</subject><subject>Ventricular Remodeling</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1v1DAQQC0EotvCP0DIRy5Jx46T2BekqipQUVSklrPl2BPWq8RZbGfLXvrbybKlR06j0bz5eoS8Y1AyYM35psTNdm1iyYG1JcgSBH9BVky2qoCW8ZdkBcBEwZVSJ-Q0pQ0A1IrXr8kJl7JpG1Ar8njx7ftXanLGMJuMie4w5OjtPJhII46Tw8GHn9QER90-9XOw2U-B9tMwTA9_K1PM3tJuIQ6pD3T0FunOG5rXSO98zNX57W_vTPY7pClHTIluTV4_mP0b8qo3Q8K3T_GM_Ph0dX_5pbi5_Xx9eXFTWAEyF7jc6zgXCkXtmJE19I0AAV2voOOS2xpb2aLruGB126BpTMWMYbzuGyOaqjojH45zt3H6NWPKevTJ4jCYgNOcNFNVXamFVwsqjqiNU0oRe72NfjRxrxnog3m90Ufz-mBeg9SL-aXt_dOGuRvRPTf9U70AH48ALn_uPEadrMdg0fmINms3-f9v-AN1uZhp</recordid><startdate>20171105</startdate><enddate>20171105</enddate><creator>Chen, Yili</creator><creator>Chen, Cong</creator><creator>Dong, Bin</creator><creator>Xing, Fuwei</creator><creator>Huang, Huiling</creator><creator>Yao, Fengjuan</creator><creator>Ma, Yuedong</creator><creator>He, Jiangui</creator><creator>Dong, Yugang</creator><general>Elsevier B.V</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>7X8</scope></search><sort><creationdate>20171105</creationdate><title>AMPK attenuates ventricular remodeling and dysfunction following aortic banding in mice via the Sirt3/Oxidative stress pathway</title><author>Chen, Yili ; Chen, Cong ; Dong, Bin ; Xing, Fuwei ; Huang, Huiling ; Yao, Fengjuan ; Ma, Yuedong ; He, Jiangui ; Dong, Yugang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c408t-e886d2249e45d1a850f64040bf90b282c5e787edb241576ea6a31aa125f6a4633</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>AMP-activated protein kinase (AMPK)</topic><topic>AMP-Activated Protein Kinases - metabolism</topic><topic>Animals</topic><topic>Aorta - pathology</topic><topic>Collagen Type I - genetics</topic><topic>Collagen Type III - genetics</topic><topic>Gene Expression Regulation</topic><topic>Heart failure</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>NADPH Oxidase 2 - metabolism</topic><topic>NADPH Oxidase 4 - metabolism</topic><topic>Oxidative Stress</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal Transduction</topic><topic>Silent information regulator (Sirt)</topic><topic>Sirtuin 3 - metabolism</topic><topic>Smad2 Protein - genetics</topic><topic>Smad3 Protein - genetics</topic><topic>Ventricular Remodeling</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Yili</creatorcontrib><creatorcontrib>Chen, Cong</creatorcontrib><creatorcontrib>Dong, Bin</creatorcontrib><creatorcontrib>Xing, Fuwei</creatorcontrib><creatorcontrib>Huang, Huiling</creatorcontrib><creatorcontrib>Yao, Fengjuan</creatorcontrib><creatorcontrib>Ma, Yuedong</creatorcontrib><creatorcontrib>He, Jiangui</creatorcontrib><creatorcontrib>Dong, Yugang</creatorcontrib><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><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Yili</au><au>Chen, Cong</au><au>Dong, Bin</au><au>Xing, Fuwei</au><au>Huang, Huiling</au><au>Yao, Fengjuan</au><au>Ma, Yuedong</au><au>He, Jiangui</au><au>Dong, Yugang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>AMPK attenuates ventricular remodeling and dysfunction following aortic banding in mice via the Sirt3/Oxidative stress pathway</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>2017-11-05</date><risdate>2017</risdate><volume>814</volume><spage>335</spage><epage>342</epage><pages>335-342</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><abstract>Although recent findings have suggested that AMP-activated protein kinase (AMPK) exerts inhibitory effects on cardiac remodeling secondary to hypertension, the mechanism and optimal duration of treatment remain unknown. Mice with descending aortic banding (AB) or subjected to sham operation received subcutaneous injection of either AICAR (0.5mgg-1day-1) or vehicle over 4 week periods. At the end of 4 week treatment, left ventricular (LV) remodeling and function were evaluated with histological analysis and echocardiography. Collagen deposition within the LV myocardium was detected with Masson's trichrome staining. Collagen I, Collagen III, Smad 2, Smad 3, NOX2, NOX4 and Sirt3 (an important antioxidant factor) within the LV tissue were also evaluated. Compared with the sham group, the vehicle-treated AB group exhibited significant elevations in cardiac remodeling and heart failure, characterized by an increase in LV weight relative to body weight, an increase in the area of collagen deposition, an increase in LV end-diastolic diameter, an increase in mitral E inflow velocity to mitral A inflow velocity and increases in the gene expressions of the fibrosis markers Collagen I, III and Smad 2, 3 mRNA and decreases in EF and fractional shortening. AMPK attenuate the cardiac remodeling parameters and improve cardiac function. Moreover, the expressions of NOX2, NOX4 were significantly elevated in vehicle-treated AB group. AMPK was able to significantly inhibit NOX2, NOX4 expression, while activate Sirt3 expression. AMPK significantly attenuated hypertension-induced Ventricular remodeling and dysfunction, which may be mediated by the Sirt3/Oxidative stress signaling pathway.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>28867609</pmid><doi>10.1016/j.ejphar.2017.08.042</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | AMP-activated protein kinase (AMPK) AMP-Activated Protein Kinases - metabolism Animals Aorta - pathology Collagen Type I - genetics Collagen Type III - genetics Gene Expression Regulation Heart failure Male Mice Mice, Inbred C57BL NADPH Oxidase 2 - metabolism NADPH Oxidase 4 - metabolism Oxidative Stress RNA, Messenger - genetics RNA, Messenger - metabolism Signal Transduction Silent information regulator (Sirt) Sirtuin 3 - metabolism Smad2 Protein - genetics Smad3 Protein - genetics Ventricular Remodeling |
title | AMPK attenuates ventricular remodeling and dysfunction following aortic banding in mice via the Sirt3/Oxidative stress pathway |
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