TDAG51-Deficiency Podocytes are Protected from High-Glucose-Induced Damage Through Nrf2 Activation via the AKT–GSK-3β Pathway
T cell death–associated gene 51 (TDAG51) has been implicated in the development of various pathological conditions. However, whether TDAG51 plays a role in diabetic renal disease remains unknown. The current work investigated the possible function of TDAG51 in diabetic renal disease using high-gluco...
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| Veröffentlicht in: | Inflammation 2022-08, Vol.45 (4), p.1520-1533 |
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| description | T cell death–associated gene 51 (TDAG51) has been implicated in the development of various pathological conditions. However, whether TDAG51 plays a role in diabetic renal disease remains unknown. The current work investigated the possible function of TDAG51 in diabetic renal disease using high-glucose (HG)-stimulated podocytes in vitro. The elevation of TDAG51 was observed in podocytes in response to HG exposure and the glomeruli of diabetic mice. The siRNAs targeting TDAG51 were applied to deplete TDAG51 in HG-stimulated podocytes. Crucially, TDAG51 deficiency was sufficient to decrease the apoptosis, oxidative stress, and inflammation caused by HG. Mechanically, the inhibition of TDAG51 was capable of enhancing the activation of nuclear factor E2-related factor 2 (Nrf2) associated with the upregulation of AKT-glycogen synthase kinase-3β (GSK-3β) pathway. The reduction of AKT abolished the activation of Nrf2 elicited by TDAG51 deficiency. Additionally, the reduction of Nrf2 diminished the anti-HG injury effect elicited by TDAG51 deficiency. Overall, these data demonstrate that TDAG51 deficiency defends against HG-induced podocyte damage through Nrf2 activation by regulating AKT-GSK-3β pathway. This study suggests that TDAG1 may have a potential role in diabetic renal disease by affecting HG-induced podocyte damage. |
| doi_str_mv | 10.1007/s10753-022-01638-9 |
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However, whether TDAG51 plays a role in diabetic renal disease remains unknown. The current work investigated the possible function of TDAG51 in diabetic renal disease using high-glucose (HG)-stimulated podocytes in vitro. The elevation of TDAG51 was observed in podocytes in response to HG exposure and the glomeruli of diabetic mice. The siRNAs targeting TDAG51 were applied to deplete TDAG51 in HG-stimulated podocytes. Crucially, TDAG51 deficiency was sufficient to decrease the apoptosis, oxidative stress, and inflammation caused by HG. Mechanically, the inhibition of TDAG51 was capable of enhancing the activation of nuclear factor E2-related factor 2 (Nrf2) associated with the upregulation of AKT-glycogen synthase kinase-3β (GSK-3β) pathway. The reduction of AKT abolished the activation of Nrf2 elicited by TDAG51 deficiency. Additionally, the reduction of Nrf2 diminished the anti-HG injury effect elicited by TDAG51 deficiency. Overall, these data demonstrate that TDAG51 deficiency defends against HG-induced podocyte damage through Nrf2 activation by regulating AKT-GSK-3β pathway. This study suggests that TDAG1 may have a potential role in diabetic renal disease by affecting HG-induced podocyte damage.</description><identifier>ISSN: 0360-3997</identifier><identifier>EISSN: 1573-2576</identifier><identifier>DOI: 10.1007/s10753-022-01638-9</identifier><identifier>PMID: 35175494</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>AKT protein ; Animals ; Apoptosis ; Biomedical and Life Sciences ; Biomedicine ; Cell death ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Experimental - metabolism ; Diabetic Nephropathies - metabolism ; Glucose - metabolism ; Glucose - toxicity ; Glycogen ; Glycogen synthase kinase 3 ; Glycogen Synthase Kinase 3 beta - metabolism ; Immunology ; Internal Medicine ; Kidney diseases ; Kinases ; Lymphocytes T ; Mice ; NF-E2-Related Factor 2 - metabolism ; Original Article ; Oxidative Stress ; Pathology ; Pharmacology/Toxicology ; Podocytes - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Rheumatology ; siRNA</subject><ispartof>Inflammation, 2022-08, Vol.45 (4), p.1520-1533</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022</rights><rights>2022. 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However, whether TDAG51 plays a role in diabetic renal disease remains unknown. The current work investigated the possible function of TDAG51 in diabetic renal disease using high-glucose (HG)-stimulated podocytes in vitro. The elevation of TDAG51 was observed in podocytes in response to HG exposure and the glomeruli of diabetic mice. The siRNAs targeting TDAG51 were applied to deplete TDAG51 in HG-stimulated podocytes. Crucially, TDAG51 deficiency was sufficient to decrease the apoptosis, oxidative stress, and inflammation caused by HG. Mechanically, the inhibition of TDAG51 was capable of enhancing the activation of nuclear factor E2-related factor 2 (Nrf2) associated with the upregulation of AKT-glycogen synthase kinase-3β (GSK-3β) pathway. The reduction of AKT abolished the activation of Nrf2 elicited by TDAG51 deficiency. Additionally, the reduction of Nrf2 diminished the anti-HG injury effect elicited by TDAG51 deficiency. Overall, these data demonstrate that TDAG51 deficiency defends against HG-induced podocyte damage through Nrf2 activation by regulating AKT-GSK-3β pathway. This study suggests that TDAG1 may have a potential role in diabetic renal disease by affecting HG-induced podocyte damage.</description><subject>AKT protein</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell death</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetic Nephropathies - metabolism</subject><subject>Glucose - metabolism</subject><subject>Glucose - toxicity</subject><subject>Glycogen</subject><subject>Glycogen synthase kinase 3</subject><subject>Glycogen Synthase Kinase 3 beta - metabolism</subject><subject>Immunology</subject><subject>Internal Medicine</subject><subject>Kidney diseases</subject><subject>Kinases</subject><subject>Lymphocytes T</subject><subject>Mice</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Original Article</subject><subject>Oxidative Stress</subject><subject>Pathology</subject><subject>Pharmacology/Toxicology</subject><subject>Podocytes - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rheumatology</subject><subject>siRNA</subject><issn>0360-3997</issn><issn>1573-2576</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kcFu1DAQhiMEotvCC3BAlrhwMYzt2E6Oq27ZVq1gJZZz5LXHm1SbuNhJ0d76DrxJH4SH4EkwbAGJA6c5zDf_jOYrihcM3jAA_TYx0FJQ4JwCU6Ki9aNixqQWlEutHhczEAqoqGt9VByndA0AVV2Jp8WRkEzLsi5nxd16MV9KRhfoO9vhYPdkFVyw-xETMRHJKoYR7YiO-Bh6ct5tW7rcTTYkpBeDm2zuLExvtkjWbQzTtiXvo-dkbsfu1oxdGMhtZ8jYIplfrr_ffV1-vKTi2z1ZmbH9YvbPiife7BI-f6gnxad3Z-vTc3r1YXlxOr-iVmg50tJr0IprDwzVprQOOHrrhZQOwCi34ZaXXoHCCpg0IErJndNeIHegHIiT4vUh9yaGzxOmsem7ZHG3MwOGKTVc8bqSMgdm9NU_6HWY4pCvy5RW-aFMVJniB8rGkFJE39zErjdx3zBofvppDn6a7Kf55aep89DLh-hp06P7M_JbSAbEAUi5NWwx_t39n9gfvtaa-Q</recordid><startdate>20220801</startdate><enddate>20220801</enddate><creator>Liu, Chuntian</creator><creator>Li, Yanling</creator><creator>Wang, Xiaojuan</creator><general>Springer US</general><general>Springer Nature 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>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-6970-6667</orcidid></search><sort><creationdate>20220801</creationdate><title>TDAG51-Deficiency Podocytes are Protected from High-Glucose-Induced Damage Through Nrf2 Activation via the AKT–GSK-3β Pathway</title><author>Liu, Chuntian ; Li, Yanling ; Wang, Xiaojuan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-4f707627f01e6b4cd02efcf355d00a6db2c24f606e8015a03452dd7f3e2d06d03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>AKT protein</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell death</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Diabetic Nephropathies - metabolism</topic><topic>Glucose - metabolism</topic><topic>Glucose - toxicity</topic><topic>Glycogen</topic><topic>Glycogen synthase kinase 3</topic><topic>Glycogen Synthase Kinase 3 beta - metabolism</topic><topic>Immunology</topic><topic>Internal Medicine</topic><topic>Kidney diseases</topic><topic>Kinases</topic><topic>Lymphocytes T</topic><topic>Mice</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>Original Article</topic><topic>Oxidative Stress</topic><topic>Pathology</topic><topic>Pharmacology/Toxicology</topic><topic>Podocytes - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Rheumatology</topic><topic>siRNA</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Chuntian</creatorcontrib><creatorcontrib>Li, Yanling</creatorcontrib><creatorcontrib>Wang, Xiaojuan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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>MEDLINE - Academic</collection><jtitle>Inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Chuntian</au><au>Li, Yanling</au><au>Wang, Xiaojuan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TDAG51-Deficiency Podocytes are Protected from High-Glucose-Induced Damage Through Nrf2 Activation via the AKT–GSK-3β Pathway</atitle><jtitle>Inflammation</jtitle><stitle>Inflammation</stitle><addtitle>Inflammation</addtitle><date>2022-08-01</date><risdate>2022</risdate><volume>45</volume><issue>4</issue><spage>1520</spage><epage>1533</epage><pages>1520-1533</pages><issn>0360-3997</issn><eissn>1573-2576</eissn><abstract>T cell death–associated gene 51 (TDAG51) has been implicated in the development of various pathological conditions. However, whether TDAG51 plays a role in diabetic renal disease remains unknown. The current work investigated the possible function of TDAG51 in diabetic renal disease using high-glucose (HG)-stimulated podocytes in vitro. The elevation of TDAG51 was observed in podocytes in response to HG exposure and the glomeruli of diabetic mice. The siRNAs targeting TDAG51 were applied to deplete TDAG51 in HG-stimulated podocytes. Crucially, TDAG51 deficiency was sufficient to decrease the apoptosis, oxidative stress, and inflammation caused by HG. Mechanically, the inhibition of TDAG51 was capable of enhancing the activation of nuclear factor E2-related factor 2 (Nrf2) associated with the upregulation of AKT-glycogen synthase kinase-3β (GSK-3β) pathway. The reduction of AKT abolished the activation of Nrf2 elicited by TDAG51 deficiency. Additionally, the reduction of Nrf2 diminished the anti-HG injury effect elicited by TDAG51 deficiency. Overall, these data demonstrate that TDAG51 deficiency defends against HG-induced podocyte damage through Nrf2 activation by regulating AKT-GSK-3β pathway. This study suggests that TDAG1 may have a potential role in diabetic renal disease by affecting HG-induced podocyte damage.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>35175494</pmid><doi>10.1007/s10753-022-01638-9</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0001-6970-6667</orcidid></addata></record> |
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| subjects | AKT protein Animals Apoptosis Biomedical and Life Sciences Biomedicine Cell death Diabetes Diabetes mellitus Diabetes Mellitus, Experimental - metabolism Diabetic Nephropathies - metabolism Glucose - metabolism Glucose - toxicity Glycogen Glycogen synthase kinase 3 Glycogen Synthase Kinase 3 beta - metabolism Immunology Internal Medicine Kidney diseases Kinases Lymphocytes T Mice NF-E2-Related Factor 2 - metabolism Original Article Oxidative Stress Pathology Pharmacology/Toxicology Podocytes - metabolism Proto-Oncogene Proteins c-akt - metabolism Rheumatology siRNA |
| title | TDAG51-Deficiency Podocytes are Protected from High-Glucose-Induced Damage Through Nrf2 Activation via the AKT–GSK-3β Pathway |
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