Expression profile of mitrogen-activated protein kinase (MAPK) signaling genes in the skeletal muscle & liver of rat with type 2 diabetes: Role in disease pathology
Background & objectives: Type 2 diabetes (T2D) is characterized as hyperglycaemia caused by defects in insulin secretion, and it affects target tissues, such as skeletal muscle, liver and adipose tissue. Therefore, analyzing the changes of gene expression profiles in these tissues is important t...
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| Veröffentlicht in: | Indian journal of medical research (New Delhi, India : 1994) India : 1994), 2014-12, Vol.139 (6), p.744-755 |
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| container_title | Indian journal of medical research (New Delhi, India : 1994) |
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| creator | Tang, Xiaoli Deng, Libin Xiong, Huangui Li, Guilin Lin, Jiari Liu, Shuangmei Xie, Jinyan Liu, Jun Kong, Fanjun Tu, Guihua Peng, Haiying Liang, Shangdong |
| description | Background & objectives: Type 2 diabetes (T2D) is characterized as hyperglycaemia caused by defects in insulin secretion, and it affects target tissues, such as skeletal muscle, liver and adipose tissue. Therefore, analyzing the changes of gene expression profiles in these tissues is important to elucidate the pathogenesis of T2D. We, therefore, measured the gene transcript alterations in liver and skeletal muscle of rat with induced T2D, to detect differentially expressed genes in liver and skeletal muscle and perform gene-annotation enrichment analysis. Methods: In the present study, skeletal muscle and liver tissue from 10 streptozotocin-induced diabetic rats and 10 control rats were analyzed using gene expression microarrays. KEGG pathways enriched by differentially expressed genes (DEGs) were identified by WebGestalt Expander and GATHER software. DEGs were validated by the method of real-time PCR and western blot. Results: From the 9,929 expressed genes across the genome, 1,305 and 997 differentially expressed genes (DEGs, P |
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Therefore, analyzing the changes of gene expression profiles in these tissues is important to elucidate the pathogenesis of T2D. We, therefore, measured the gene transcript alterations in liver and skeletal muscle of rat with induced T2D, to detect differentially expressed genes in liver and skeletal muscle and perform gene-annotation enrichment analysis. Methods: In the present study, skeletal muscle and liver tissue from 10 streptozotocin-induced diabetic rats and 10 control rats were analyzed using gene expression microarrays. KEGG pathways enriched by differentially expressed genes (DEGs) were identified by WebGestalt Expander and GATHER software. DEGs were validated by the method of real-time PCR and western blot. Results: From the 9,929 expressed genes across the genome, 1,305 and 997 differentially expressed genes (DEGs, P<0.01) were identified in comparisons of skeletal muscle and liver, respectively. Large numbers of DEGs (200) were common in both comparisons, which was clearly more than the predicted number (131 genes, P<0.001). For further interpretation of the gene expression data, three over-representation analysis softwares (WebGestalt, Expander and GATHER) were used. All the tools detected one KEGG pathway (MAPK signaling) and two GO (gene ontology) biological processes (response to stress and cell death), with enrichment of DEGs in both tissues. In addition, PPI (protein-protein interaction) networks constructed using human homologues not only revealed the tendency of DEGs to form a highly connected module, but also suggested a "hub" role of p38-MAPK-related genes (such as MAPK14) in the pathogenesis of T2D. Interpretation & conclusions: Our results indicated the considerably aberrant MAPK signaling in both insulin-sensitive tissues of T2D rat, and that the p38 may play a role as a common "hub" in the gene module response to hyperglycaemia. Furthermore, our research pinpoints the role of several new T2D-associated genes (such as Srebf1 and Ppargc1) in the human population.</description><identifier>ISSN: 0971-5916</identifier><language>eng</language><publisher>New Delhi: Scientific Scholar</publisher><subject>Glucose ; Hyperglycemia ; Insulin resistance ; Kinases ; Rodents</subject><ispartof>Indian journal of medical research (New Delhi, India : 1994), 2014-12, Vol.139 (6), p.744-755</ispartof><rights>2014. This work is published under https://creativecommons.org/licenses/by-nc-sa/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></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids></links><search><creatorcontrib>Tang, Xiaoli</creatorcontrib><creatorcontrib>Deng, Libin</creatorcontrib><creatorcontrib>Xiong, Huangui</creatorcontrib><creatorcontrib>Li, Guilin</creatorcontrib><creatorcontrib>Lin, Jiari</creatorcontrib><creatorcontrib>Liu, Shuangmei</creatorcontrib><creatorcontrib>Xie, Jinyan</creatorcontrib><creatorcontrib>Liu, Jun</creatorcontrib><creatorcontrib>Kong, Fanjun</creatorcontrib><creatorcontrib>Tu, Guihua</creatorcontrib><creatorcontrib>Peng, Haiying</creatorcontrib><creatorcontrib>Liang, Shangdong</creatorcontrib><title>Expression profile of mitrogen-activated protein kinase (MAPK) signaling genes in the skeletal muscle & liver of rat with type 2 diabetes: Role in disease pathology</title><title>Indian journal of medical research (New Delhi, India : 1994)</title><description>Background & objectives: Type 2 diabetes (T2D) is characterized as hyperglycaemia caused by defects in insulin secretion, and it affects target tissues, such as skeletal muscle, liver and adipose tissue. Therefore, analyzing the changes of gene expression profiles in these tissues is important to elucidate the pathogenesis of T2D. We, therefore, measured the gene transcript alterations in liver and skeletal muscle of rat with induced T2D, to detect differentially expressed genes in liver and skeletal muscle and perform gene-annotation enrichment analysis. Methods: In the present study, skeletal muscle and liver tissue from 10 streptozotocin-induced diabetic rats and 10 control rats were analyzed using gene expression microarrays. KEGG pathways enriched by differentially expressed genes (DEGs) were identified by WebGestalt Expander and GATHER software. DEGs were validated by the method of real-time PCR and western blot. Results: From the 9,929 expressed genes across the genome, 1,305 and 997 differentially expressed genes (DEGs, P<0.01) were identified in comparisons of skeletal muscle and liver, respectively. Large numbers of DEGs (200) were common in both comparisons, which was clearly more than the predicted number (131 genes, P<0.001). For further interpretation of the gene expression data, three over-representation analysis softwares (WebGestalt, Expander and GATHER) were used. All the tools detected one KEGG pathway (MAPK signaling) and two GO (gene ontology) biological processes (response to stress and cell death), with enrichment of DEGs in both tissues. In addition, PPI (protein-protein interaction) networks constructed using human homologues not only revealed the tendency of DEGs to form a highly connected module, but also suggested a "hub" role of p38-MAPK-related genes (such as MAPK14) in the pathogenesis of T2D. Interpretation & conclusions: Our results indicated the considerably aberrant MAPK signaling in both insulin-sensitive tissues of T2D rat, and that the p38 may play a role as a common "hub" in the gene module response to hyperglycaemia. Furthermore, our research pinpoints the role of several new T2D-associated genes (such as Srebf1 and Ppargc1) in the human population.</description><subject>Glucose</subject><subject>Hyperglycemia</subject><subject>Insulin resistance</subject><subject>Kinases</subject><subject>Rodents</subject><issn>0971-5916</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNjt1Kw0AQhfdCwfrzDgOC6EUg2ZLUeCdSEUQQ8b6MzSSZdrsbdybVvo8P6gZ8AK_Oxfn4zjkys7xeFFlZF9WJORXZ5HlR20U9Mz_L7yGSCAcPQwwtO4LQwo41ho58hmvlPSo1U6vEHrbsUQiuX-5fn29AuPPo2HeQaBJIgPYEsiVHig52o6yT8goc7ylO6ogKX6w96GEgsNAwfpCS3MFbSGQSNCw0TQyofXChO5yb4xad0MVfnpnLx-X7w1OWPn2OJLrahDGmH7Kytry1VTmvivn_qF9mZlyX</recordid><startdate>20141201</startdate><enddate>20141201</enddate><creator>Tang, Xiaoli</creator><creator>Deng, Libin</creator><creator>Xiong, Huangui</creator><creator>Li, Guilin</creator><creator>Lin, Jiari</creator><creator>Liu, Shuangmei</creator><creator>Xie, Jinyan</creator><creator>Liu, Jun</creator><creator>Kong, Fanjun</creator><creator>Tu, Guihua</creator><creator>Peng, Haiying</creator><creator>Liang, Shangdong</creator><general>Scientific Scholar</general><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope></search><sort><creationdate>20141201</creationdate><title>Expression profile of mitrogen-activated protein kinase (MAPK) signaling genes in the skeletal muscle & liver of rat with type 2 diabetes: Role in disease pathology</title><author>Tang, Xiaoli ; Deng, Libin ; Xiong, Huangui ; Li, Guilin ; Lin, Jiari ; Liu, Shuangmei ; Xie, Jinyan ; Liu, Jun ; Kong, Fanjun ; Tu, Guihua ; Peng, Haiying ; Liang, Shangdong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-proquest_journals_22582653613</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Glucose</topic><topic>Hyperglycemia</topic><topic>Insulin resistance</topic><topic>Kinases</topic><topic>Rodents</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tang, Xiaoli</creatorcontrib><creatorcontrib>Deng, Libin</creatorcontrib><creatorcontrib>Xiong, Huangui</creatorcontrib><creatorcontrib>Li, Guilin</creatorcontrib><creatorcontrib>Lin, Jiari</creatorcontrib><creatorcontrib>Liu, Shuangmei</creatorcontrib><creatorcontrib>Xie, Jinyan</creatorcontrib><creatorcontrib>Liu, Jun</creatorcontrib><creatorcontrib>Kong, Fanjun</creatorcontrib><creatorcontrib>Tu, Guihua</creatorcontrib><creatorcontrib>Peng, Haiying</creatorcontrib><creatorcontrib>Liang, Shangdong</creatorcontrib><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest Research Library</collection><collection>ProQuest Science Journals</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><jtitle>Indian journal of medical research (New Delhi, India : 1994)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tang, Xiaoli</au><au>Deng, Libin</au><au>Xiong, Huangui</au><au>Li, Guilin</au><au>Lin, Jiari</au><au>Liu, Shuangmei</au><au>Xie, Jinyan</au><au>Liu, Jun</au><au>Kong, Fanjun</au><au>Tu, Guihua</au><au>Peng, Haiying</au><au>Liang, Shangdong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression profile of mitrogen-activated protein kinase (MAPK) signaling genes in the skeletal muscle & liver of rat with type 2 diabetes: Role in disease pathology</atitle><jtitle>Indian journal of medical research (New Delhi, India : 1994)</jtitle><date>2014-12-01</date><risdate>2014</risdate><volume>139</volume><issue>6</issue><spage>744</spage><epage>755</epage><pages>744-755</pages><issn>0971-5916</issn><abstract>Background & objectives: Type 2 diabetes (T2D) is characterized as hyperglycaemia caused by defects in insulin secretion, and it affects target tissues, such as skeletal muscle, liver and adipose tissue. Therefore, analyzing the changes of gene expression profiles in these tissues is important to elucidate the pathogenesis of T2D. We, therefore, measured the gene transcript alterations in liver and skeletal muscle of rat with induced T2D, to detect differentially expressed genes in liver and skeletal muscle and perform gene-annotation enrichment analysis. Methods: In the present study, skeletal muscle and liver tissue from 10 streptozotocin-induced diabetic rats and 10 control rats were analyzed using gene expression microarrays. KEGG pathways enriched by differentially expressed genes (DEGs) were identified by WebGestalt Expander and GATHER software. DEGs were validated by the method of real-time PCR and western blot. Results: From the 9,929 expressed genes across the genome, 1,305 and 997 differentially expressed genes (DEGs, P<0.01) were identified in comparisons of skeletal muscle and liver, respectively. Large numbers of DEGs (200) were common in both comparisons, which was clearly more than the predicted number (131 genes, P<0.001). For further interpretation of the gene expression data, three over-representation analysis softwares (WebGestalt, Expander and GATHER) were used. All the tools detected one KEGG pathway (MAPK signaling) and two GO (gene ontology) biological processes (response to stress and cell death), with enrichment of DEGs in both tissues. In addition, PPI (protein-protein interaction) networks constructed using human homologues not only revealed the tendency of DEGs to form a highly connected module, but also suggested a "hub" role of p38-MAPK-related genes (such as MAPK14) in the pathogenesis of T2D. Interpretation & conclusions: Our results indicated the considerably aberrant MAPK signaling in both insulin-sensitive tissues of T2D rat, and that the p38 may play a role as a common "hub" in the gene module response to hyperglycaemia. Furthermore, our research pinpoints the role of several new T2D-associated genes (such as Srebf1 and Ppargc1) in the human population.</abstract><cop>New Delhi</cop><pub>Scientific Scholar</pub><oa>free_for_read</oa></addata></record> |
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| subjects | Glucose Hyperglycemia Insulin resistance Kinases Rodents |
| title | Expression profile of mitrogen-activated protein kinase (MAPK) signaling genes in the skeletal muscle & liver of rat with type 2 diabetes: Role in disease pathology |
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