DPP-4 inhibitor anagliptin protects against hypoxia-induced cytotoxicity in cardiac H9C2 cells
Cardiovascular complications are the leading cause of mortality and morbidity in type 2 diabetes patients. Diabetes greatly increases the risk of heart disease; therefore, the management of diabetes often involves the prevention of heart disease. DPP-4 inhibitors have been proven to be the effective...
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| creator | Ma, Yunxiang Wang, Junkai Wang, Changhua Zhang, Qiong Xu, Yannan Liu, Huajin Xiang, Xia Ma, Jiangwei |
| description | Cardiovascular complications are the leading cause of mortality and morbidity in type 2 diabetes patients. Diabetes greatly increases the risk of heart disease; therefore, the management of diabetes often involves the prevention of heart disease. DPP-4 inhibitors have been proven to be the effective therapeutic agents of glycaemic control. Recent studies have shown that certain types of DPP-4 inhibitors could also have cardiovascular benefits. In this study, we examined the protective role of the newly developed DPP-4 inhibitor anagliptin in cultured cardiac myocytic cell line H9C2 cells. Our data show that exposure of H9C2 cells to hypoxic conditions induced higher expression of DPP-4, indicating that DPP-4 is a hypoxia-inducible factor. The inhibition of DPP-4 by anagliptin ameliorates hypoxia-induced cytotoxicity and induction of the pro-inflammatory cytokines IL-6 and MCP-1. Anagliptin also suppresses hypoxia-induced oxidative stress as revealed by the detected levels of cellular ROS and reduced GSH. Moreover, anagliptin protects myocytes from hypoxia-associated reduced mitochondrial membrane potential. Mechanistically, we show that anagliptin promotes hypoxia-induced NFR2/HO1 induction but suppresses HMGB1 and MyD88 generation. Collectively, our data indicate that anagliptin-mediated DPP-4 inhibition is a protective mechanism in cardiomyocytes and imply that the DDP-4 inhibitor anagliptin plays dual roles by lowering glucose and protecting cardiomyocytes. |
| doi_str_mv | 10.1080/21691401.2019.1652624 |
| format | Article |
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Diabetes greatly increases the risk of heart disease; therefore, the management of diabetes often involves the prevention of heart disease. DPP-4 inhibitors have been proven to be the effective therapeutic agents of glycaemic control. Recent studies have shown that certain types of DPP-4 inhibitors could also have cardiovascular benefits. In this study, we examined the protective role of the newly developed DPP-4 inhibitor anagliptin in cultured cardiac myocytic cell line H9C2 cells. Our data show that exposure of H9C2 cells to hypoxic conditions induced higher expression of DPP-4, indicating that DPP-4 is a hypoxia-inducible factor. The inhibition of DPP-4 by anagliptin ameliorates hypoxia-induced cytotoxicity and induction of the pro-inflammatory cytokines IL-6 and MCP-1. Anagliptin also suppresses hypoxia-induced oxidative stress as revealed by the detected levels of cellular ROS and reduced GSH. Moreover, anagliptin protects myocytes from hypoxia-associated reduced mitochondrial membrane potential. Mechanistically, we show that anagliptin promotes hypoxia-induced NFR2/HO1 induction but suppresses HMGB1 and MyD88 generation. Collectively, our data indicate that anagliptin-mediated DPP-4 inhibition is a protective mechanism in cardiomyocytes and imply that the DDP-4 inhibitor anagliptin plays dual roles by lowering glucose and protecting cardiomyocytes.</description><identifier>ISSN: 2169-1401</identifier><identifier>EISSN: 2169-141X</identifier><identifier>DOI: 10.1080/21691401.2019.1652624</identifier><identifier>PMID: 31556325</identifier><language>eng</language><publisher>England: Taylor & Francis</publisher><subject>anagliptin ; Animals ; Apoptosis - drug effects ; cardiomyocyte protection ; Cardiomyocytes ; Cardiovascular disease ; Cell Hypoxia - drug effects ; Cell Line ; Cell Survival - drug effects ; Chemical compounds ; Chemokine CCL2 - biosynthesis ; Coronary artery disease ; Cytokines ; Cytoprotection - drug effects ; Cytotoxicity ; Diabetes ; Diabetes mellitus (non-insulin dependent) ; Dipeptidyl Peptidase 4 - genetics ; Dipeptidyl Peptidase 4 - metabolism ; Dipeptidyl-Peptidase IV Inhibitors - pharmacology ; Disease control ; DPP-4 ; Gene Expression Regulation, Enzymologic - drug effects ; H9C2 cells ; Heart diseases ; Heme Oxygenase (Decyclizing) - genetics ; HMGB1 protein ; HMGB1 Protein - genetics ; Hypoxia ; Hypoxia-inducible factors ; Inflammation ; Inhibitors ; Interleukin 6 ; Interleukin-6 - biosynthesis ; Membrane potential ; Membrane Potential, Mitochondrial - drug effects ; Mitochondria ; Monocyte chemoattractant protein 1 ; Morbidity ; MyD88 protein ; Myocytes ; Myocytes, Cardiac - cytology ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; Oxidative stress ; Oxidative Stress - drug effects ; Pharmacology ; Pyrimidines - pharmacology ; Rats ; Toxicity</subject><ispartof>Artificial cells, nanomedicine, and biotechnology, 2019-12, Vol.47 (1), p.3823-3831</ispartof><rights>2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group 2019</rights><rights>2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. This work is licensed under the Creative Commons Attribution License http://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><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c507t-c3f6d0e9df595207a602e0c5f93d0fa99ae9fc46e4d14771d6eb45c2cacbc33a3</citedby><cites>FETCH-LOGICAL-c507t-c3f6d0e9df595207a602e0c5f93d0fa99ae9fc46e4d14771d6eb45c2cacbc33a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,860,2096,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31556325$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ma, Yunxiang</creatorcontrib><creatorcontrib>Wang, Junkai</creatorcontrib><creatorcontrib>Wang, Changhua</creatorcontrib><creatorcontrib>Zhang, Qiong</creatorcontrib><creatorcontrib>Xu, Yannan</creatorcontrib><creatorcontrib>Liu, Huajin</creatorcontrib><creatorcontrib>Xiang, Xia</creatorcontrib><creatorcontrib>Ma, Jiangwei</creatorcontrib><title>DPP-4 inhibitor anagliptin protects against hypoxia-induced cytotoxicity in cardiac H9C2 cells</title><title>Artificial cells, nanomedicine, and biotechnology</title><addtitle>Artif Cells Nanomed Biotechnol</addtitle><description>Cardiovascular complications are the leading cause of mortality and morbidity in type 2 diabetes patients. Diabetes greatly increases the risk of heart disease; therefore, the management of diabetes often involves the prevention of heart disease. DPP-4 inhibitors have been proven to be the effective therapeutic agents of glycaemic control. Recent studies have shown that certain types of DPP-4 inhibitors could also have cardiovascular benefits. In this study, we examined the protective role of the newly developed DPP-4 inhibitor anagliptin in cultured cardiac myocytic cell line H9C2 cells. Our data show that exposure of H9C2 cells to hypoxic conditions induced higher expression of DPP-4, indicating that DPP-4 is a hypoxia-inducible factor. The inhibition of DPP-4 by anagliptin ameliorates hypoxia-induced cytotoxicity and induction of the pro-inflammatory cytokines IL-6 and MCP-1. Anagliptin also suppresses hypoxia-induced oxidative stress as revealed by the detected levels of cellular ROS and reduced GSH. Moreover, anagliptin protects myocytes from hypoxia-associated reduced mitochondrial membrane potential. Mechanistically, we show that anagliptin promotes hypoxia-induced NFR2/HO1 induction but suppresses HMGB1 and MyD88 generation. Collectively, our data indicate that anagliptin-mediated DPP-4 inhibition is a protective mechanism in cardiomyocytes and imply that the DDP-4 inhibitor anagliptin plays dual roles by lowering glucose and protecting cardiomyocytes.</description><subject>anagliptin</subject><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>cardiomyocyte protection</subject><subject>Cardiomyocytes</subject><subject>Cardiovascular disease</subject><subject>Cell Hypoxia - drug effects</subject><subject>Cell Line</subject><subject>Cell Survival - drug effects</subject><subject>Chemical compounds</subject><subject>Chemokine CCL2 - biosynthesis</subject><subject>Coronary artery disease</subject><subject>Cytokines</subject><subject>Cytoprotection - drug effects</subject><subject>Cytotoxicity</subject><subject>Diabetes</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Dipeptidyl Peptidase 4 - genetics</subject><subject>Dipeptidyl Peptidase 4 - metabolism</subject><subject>Dipeptidyl-Peptidase IV Inhibitors - pharmacology</subject><subject>Disease control</subject><subject>DPP-4</subject><subject>Gene Expression Regulation, Enzymologic - drug effects</subject><subject>H9C2 cells</subject><subject>Heart diseases</subject><subject>Heme Oxygenase (Decyclizing) - genetics</subject><subject>HMGB1 protein</subject><subject>HMGB1 Protein - genetics</subject><subject>Hypoxia</subject><subject>Hypoxia-inducible factors</subject><subject>Inflammation</subject><subject>Inhibitors</subject><subject>Interleukin 6</subject><subject>Interleukin-6 - biosynthesis</subject><subject>Membrane potential</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Mitochondria</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Morbidity</subject><subject>MyD88 protein</subject><subject>Myocytes</subject><subject>Myocytes, Cardiac - cytology</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Pharmacology</subject><subject>Pyrimidines - pharmacology</subject><subject>Rats</subject><subject>Toxicity</subject><issn>2169-1401</issn><issn>2169-141X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>0YH</sourceid><sourceid>EIF</sourceid><sourceid>DOA</sourceid><recordid>eNp9kUtvEzEUhUcIRKvSnwAaiQ2bCdfPiXeg8GilSnQBEius68ekjibjYHsE-fc4JM2CBd7YOvru8T06TfOSwILAEt5SIhXhQBYUiFoQKaik_ElzedA7wsn3p-c3kIvmOucN1LMkshf8eXPBiBCSUXHZ_Phwf9_xNkwPwYQSU4sTrsewK2FqdykWb0tucY1hyqV92O_i74BdmNxsvWvtvsRSFRvKvlq0FpMLaNsbtaKt9eOYXzTPBhyzvz7dV823Tx-_rm66uy-fb1fv7zoroC-dZYN04JUbhBIUepRAPVgxKOZgQKXQq8Fy6bkjvO-Jk95wYalFayxjyK6a26Ovi7jRuxS2mPY6YtB_hZjWGlMJdvQaBBjJnbSGGN4zY0Q1kYQZid6ggOr15uhV8_-cfS56G_IhDU4-zllTqpZ1C8F4RV__g27inKaaVFMmKFMASlZKHCmbYs7JD-cFCehDn_qxT33oU5_6rHOvTu6z2Xp3nnpsrwLvjkCYhpi2-Cum0emC-zGmIeFkQ67wf__4Az-Aro0</recordid><startdate>20191204</startdate><enddate>20191204</enddate><creator>Ma, Yunxiang</creator><creator>Wang, Junkai</creator><creator>Wang, Changhua</creator><creator>Zhang, Qiong</creator><creator>Xu, Yannan</creator><creator>Liu, Huajin</creator><creator>Xiang, Xia</creator><creator>Ma, Jiangwei</creator><general>Taylor & Francis</general><general>Taylor & Francis Ltd</general><general>Taylor & Francis Group</general><scope>0YH</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>7X8</scope><scope>DOA</scope></search><sort><creationdate>20191204</creationdate><title>DPP-4 inhibitor anagliptin protects against hypoxia-induced cytotoxicity in cardiac H9C2 cells</title><author>Ma, Yunxiang ; Wang, Junkai ; Wang, Changhua ; Zhang, Qiong ; Xu, Yannan ; Liu, Huajin ; Xiang, Xia ; Ma, Jiangwei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c507t-c3f6d0e9df595207a602e0c5f93d0fa99ae9fc46e4d14771d6eb45c2cacbc33a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>anagliptin</topic><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>cardiomyocyte protection</topic><topic>Cardiomyocytes</topic><topic>Cardiovascular disease</topic><topic>Cell Hypoxia - drug effects</topic><topic>Cell Line</topic><topic>Cell Survival - drug effects</topic><topic>Chemical compounds</topic><topic>Chemokine CCL2 - biosynthesis</topic><topic>Coronary artery disease</topic><topic>Cytokines</topic><topic>Cytoprotection - drug effects</topic><topic>Cytotoxicity</topic><topic>Diabetes</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Dipeptidyl Peptidase 4 - genetics</topic><topic>Dipeptidyl Peptidase 4 - metabolism</topic><topic>Dipeptidyl-Peptidase IV Inhibitors - pharmacology</topic><topic>Disease control</topic><topic>DPP-4</topic><topic>Gene Expression Regulation, Enzymologic - drug effects</topic><topic>H9C2 cells</topic><topic>Heart diseases</topic><topic>Heme Oxygenase (Decyclizing) - genetics</topic><topic>HMGB1 protein</topic><topic>HMGB1 Protein - genetics</topic><topic>Hypoxia</topic><topic>Hypoxia-inducible factors</topic><topic>Inflammation</topic><topic>Inhibitors</topic><topic>Interleukin 6</topic><topic>Interleukin-6 - biosynthesis</topic><topic>Membrane potential</topic><topic>Membrane Potential, Mitochondrial - drug effects</topic><topic>Mitochondria</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Morbidity</topic><topic>MyD88 protein</topic><topic>Myocytes</topic><topic>Myocytes, Cardiac - cytology</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Pharmacology</topic><topic>Pyrimidines - pharmacology</topic><topic>Rats</topic><topic>Toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ma, Yunxiang</creatorcontrib><creatorcontrib>Wang, Junkai</creatorcontrib><creatorcontrib>Wang, Changhua</creatorcontrib><creatorcontrib>Zhang, Qiong</creatorcontrib><creatorcontrib>Xu, Yannan</creatorcontrib><creatorcontrib>Liu, Huajin</creatorcontrib><creatorcontrib>Xiang, Xia</creatorcontrib><creatorcontrib>Ma, Jiangwei</creatorcontrib><collection>Taylor & Francis Open Access</collection><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><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Artificial cells, nanomedicine, and biotechnology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ma, Yunxiang</au><au>Wang, Junkai</au><au>Wang, Changhua</au><au>Zhang, Qiong</au><au>Xu, Yannan</au><au>Liu, Huajin</au><au>Xiang, Xia</au><au>Ma, Jiangwei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>DPP-4 inhibitor anagliptin protects against hypoxia-induced cytotoxicity in cardiac H9C2 cells</atitle><jtitle>Artificial cells, nanomedicine, and biotechnology</jtitle><addtitle>Artif Cells Nanomed Biotechnol</addtitle><date>2019-12-04</date><risdate>2019</risdate><volume>47</volume><issue>1</issue><spage>3823</spage><epage>3831</epage><pages>3823-3831</pages><issn>2169-1401</issn><eissn>2169-141X</eissn><abstract>Cardiovascular complications are the leading cause of mortality and morbidity in type 2 diabetes patients. Diabetes greatly increases the risk of heart disease; therefore, the management of diabetes often involves the prevention of heart disease. DPP-4 inhibitors have been proven to be the effective therapeutic agents of glycaemic control. Recent studies have shown that certain types of DPP-4 inhibitors could also have cardiovascular benefits. In this study, we examined the protective role of the newly developed DPP-4 inhibitor anagliptin in cultured cardiac myocytic cell line H9C2 cells. Our data show that exposure of H9C2 cells to hypoxic conditions induced higher expression of DPP-4, indicating that DPP-4 is a hypoxia-inducible factor. The inhibition of DPP-4 by anagliptin ameliorates hypoxia-induced cytotoxicity and induction of the pro-inflammatory cytokines IL-6 and MCP-1. Anagliptin also suppresses hypoxia-induced oxidative stress as revealed by the detected levels of cellular ROS and reduced GSH. Moreover, anagliptin protects myocytes from hypoxia-associated reduced mitochondrial membrane potential. Mechanistically, we show that anagliptin promotes hypoxia-induced NFR2/HO1 induction but suppresses HMGB1 and MyD88 generation. Collectively, our data indicate that anagliptin-mediated DPP-4 inhibition is a protective mechanism in cardiomyocytes and imply that the DDP-4 inhibitor anagliptin plays dual roles by lowering glucose and protecting cardiomyocytes.</abstract><cop>England</cop><pub>Taylor & Francis</pub><pmid>31556325</pmid><doi>10.1080/21691401.2019.1652624</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | anagliptin Animals Apoptosis - drug effects cardiomyocyte protection Cardiomyocytes Cardiovascular disease Cell Hypoxia - drug effects Cell Line Cell Survival - drug effects Chemical compounds Chemokine CCL2 - biosynthesis Coronary artery disease Cytokines Cytoprotection - drug effects Cytotoxicity Diabetes Diabetes mellitus (non-insulin dependent) Dipeptidyl Peptidase 4 - genetics Dipeptidyl Peptidase 4 - metabolism Dipeptidyl-Peptidase IV Inhibitors - pharmacology Disease control DPP-4 Gene Expression Regulation, Enzymologic - drug effects H9C2 cells Heart diseases Heme Oxygenase (Decyclizing) - genetics HMGB1 protein HMGB1 Protein - genetics Hypoxia Hypoxia-inducible factors Inflammation Inhibitors Interleukin 6 Interleukin-6 - biosynthesis Membrane potential Membrane Potential, Mitochondrial - drug effects Mitochondria Monocyte chemoattractant protein 1 Morbidity MyD88 protein Myocytes Myocytes, Cardiac - cytology Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Oxidative stress Oxidative Stress - drug effects Pharmacology Pyrimidines - pharmacology Rats Toxicity |
| title | DPP-4 inhibitor anagliptin protects against hypoxia-induced cytotoxicity in cardiac H9C2 cells |
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