Local kallikrein–kinin system is involved in podocyte apoptosis under diabetic conditions
The kallikrein–kinin system (KKS) serves as the physiologic counterbalance to the renin-angiotensin system. This study was conducted to examine the changes in the expression of KKS components in podocytes under diabetic conditions and to elucidate the functional role of bradykinin (BK) in diabetes-a...
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| Veröffentlicht in: | Apoptosis (London) 2011-05, Vol.16 (5), p.478-490 |
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| creator | Kwak, Seung-Jae Paeng, Jisun Kim, Do Hee Lee, Sun Ha Nam, Bo-Young Kang, Hye Young Li, Jin Ji Jung, Dong-Sub Han, Seung Hyeok Ryu, Dong-Ryeol Park, Jung Tak Chang, Tae Ik Yoo, Tae-Hyun Han, Dae Suk Kang, Shin-Wook |
| description | The kallikrein–kinin system (KKS) serves as the physiologic counterbalance to the renin-angiotensin system. This study was conducted to examine the changes in the expression of KKS components in podocytes under diabetic conditions and to elucidate the functional role of bradykinin (BK) in diabetes-associated podocyte apoptosis. Thirty-two rats were injected with either diluent (
n
= 16, C) or with streptozotocin intraperitoneally (
n
= 16, DM), and 8 rats from each group were treated with BK infusion for 6 weeks. Immortalized mouse podocytes were cultured in media containing 5.6 mmol/l glucose (NG), NG + 10
−7
mol/l AII (AII), or 30 mmol/l glucose (HG) with or without 10
−8
mol/l BK. Urinary albumin excretion was significantly higher in DM rats, and this increase was ameliorated by BK. Not only kininogen, kallikrein, and BK B1- and B2-receptor expression but also BK levels were significantly decreased in DM glomeruli and in cultured podocytes exposed to HG. The changes in the expressions of apoptosis-related molecules and the increase in the number of apoptotic cells in DM glomeruli as well as in HG- and AII-stimulated podocytes were significantly abrogated by BK. The suppressed KSS within podocytes under diabetic condition was associated with podocyte apoptosis, suggesting that BK may be beneficial in preventing podocyte loss in diabetic nephropathy. |
| doi_str_mv | 10.1007/s10495-011-0585-1 |
| format | Article |
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n
= 16, C) or with streptozotocin intraperitoneally (
n
= 16, DM), and 8 rats from each group were treated with BK infusion for 6 weeks. Immortalized mouse podocytes were cultured in media containing 5.6 mmol/l glucose (NG), NG + 10
−7
mol/l AII (AII), or 30 mmol/l glucose (HG) with or without 10
−8
mol/l BK. Urinary albumin excretion was significantly higher in DM rats, and this increase was ameliorated by BK. Not only kininogen, kallikrein, and BK B1- and B2-receptor expression but also BK levels were significantly decreased in DM glomeruli and in cultured podocytes exposed to HG. The changes in the expressions of apoptosis-related molecules and the increase in the number of apoptotic cells in DM glomeruli as well as in HG- and AII-stimulated podocytes were significantly abrogated by BK. The suppressed KSS within podocytes under diabetic condition was associated with podocyte apoptosis, suggesting that BK may be beneficial in preventing podocyte loss in diabetic nephropathy.</description><identifier>ISSN: 1360-8185</identifier><identifier>EISSN: 1573-675X</identifier><identifier>DOI: 10.1007/s10495-011-0585-1</identifier><identifier>PMID: 21373934</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Animals ; Apoptosis - drug effects ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Bradykinin - pharmacology ; Bradykinin - physiology ; Cancer Research ; Cell Biology ; Cytoprotection ; Diabetes Mellitus, Experimental - chemically induced ; Diabetes Mellitus, Experimental - metabolism ; Diabetes Mellitus, Experimental - pathology ; Diabetic Nephropathies - metabolism ; Diabetic Nephropathies - pathology ; Gene Expression ; Glucose - metabolism ; Kallikrein-Kinin System ; Male ; Mice ; Oncology ; Original Paper ; Podocytes - drug effects ; Podocytes - metabolism ; Podocytes - pathology ; Rats ; Rats, Sprague-Dawley ; Virology</subject><ispartof>Apoptosis (London), 2011-05, Vol.16 (5), p.478-490</ispartof><rights>Springer Science+Business Media, LLC 2011</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c370t-6b849d17d82f494f427f279559c539924a47f4b56dd6324493392c952d8915b53</citedby><cites>FETCH-LOGICAL-c370t-6b849d17d82f494f427f279559c539924a47f4b56dd6324493392c952d8915b53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10495-011-0585-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10495-011-0585-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21373934$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kwak, Seung-Jae</creatorcontrib><creatorcontrib>Paeng, Jisun</creatorcontrib><creatorcontrib>Kim, Do Hee</creatorcontrib><creatorcontrib>Lee, Sun Ha</creatorcontrib><creatorcontrib>Nam, Bo-Young</creatorcontrib><creatorcontrib>Kang, Hye Young</creatorcontrib><creatorcontrib>Li, Jin Ji</creatorcontrib><creatorcontrib>Jung, Dong-Sub</creatorcontrib><creatorcontrib>Han, Seung Hyeok</creatorcontrib><creatorcontrib>Ryu, Dong-Ryeol</creatorcontrib><creatorcontrib>Park, Jung Tak</creatorcontrib><creatorcontrib>Chang, Tae Ik</creatorcontrib><creatorcontrib>Yoo, Tae-Hyun</creatorcontrib><creatorcontrib>Han, Dae Suk</creatorcontrib><creatorcontrib>Kang, Shin-Wook</creatorcontrib><title>Local kallikrein–kinin system is involved in podocyte apoptosis under diabetic conditions</title><title>Apoptosis (London)</title><addtitle>Apoptosis</addtitle><addtitle>Apoptosis</addtitle><description>The kallikrein–kinin system (KKS) serves as the physiologic counterbalance to the renin-angiotensin system. This study was conducted to examine the changes in the expression of KKS components in podocytes under diabetic conditions and to elucidate the functional role of bradykinin (BK) in diabetes-associated podocyte apoptosis. Thirty-two rats were injected with either diluent (
n
= 16, C) or with streptozotocin intraperitoneally (
n
= 16, DM), and 8 rats from each group were treated with BK infusion for 6 weeks. Immortalized mouse podocytes were cultured in media containing 5.6 mmol/l glucose (NG), NG + 10
−7
mol/l AII (AII), or 30 mmol/l glucose (HG) with or without 10
−8
mol/l BK. Urinary albumin excretion was significantly higher in DM rats, and this increase was ameliorated by BK. Not only kininogen, kallikrein, and BK B1- and B2-receptor expression but also BK levels were significantly decreased in DM glomeruli and in cultured podocytes exposed to HG. The changes in the expressions of apoptosis-related molecules and the increase in the number of apoptotic cells in DM glomeruli as well as in HG- and AII-stimulated podocytes were significantly abrogated by BK. The suppressed KSS within podocytes under diabetic condition was associated with podocyte apoptosis, suggesting that BK may be beneficial in preventing podocyte loss in diabetic nephropathy.</description><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Bradykinin - pharmacology</subject><subject>Bradykinin - physiology</subject><subject>Cancer Research</subject><subject>Cell Biology</subject><subject>Cytoprotection</subject><subject>Diabetes Mellitus, Experimental - chemically induced</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetes Mellitus, Experimental - pathology</subject><subject>Diabetic Nephropathies - metabolism</subject><subject>Diabetic Nephropathies - pathology</subject><subject>Gene Expression</subject><subject>Glucose - metabolism</subject><subject>Kallikrein-Kinin System</subject><subject>Male</subject><subject>Mice</subject><subject>Oncology</subject><subject>Original Paper</subject><subject>Podocytes - drug effects</subject><subject>Podocytes - metabolism</subject><subject>Podocytes - pathology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Virology</subject><issn>1360-8185</issn><issn>1573-675X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kMlKBDEQhoMojtsDeJHGi6fWrJ3kKOIGA14UBA-hO0lLZnqSNukW5uY7-IY-iRnGBQRPVVBf_VV8ABwieIog5GcJQSpZCREqIROsRBtgBzFOyoqzx83ckwqWAgk2AbspzSCERBC6DSYYEU4koTvgaRp03RXzuuvcPFrnP97e5847X6RlGuyicKlw_jV0r9bkpuiDCXo52KLuQz-ElMejNzYWxtWNHZwudPDGDS74tA-22rpL9uCr7oGHq8v7i5tyend9e3E-LTXhcCirRlBpEDcCt1TSlmLeYi4Zk5oRKTGtKW9pwypjKoIplYRIrCXDRkjEGkb2wMk6t4_hZbRpUAuXtO262tswJiUqwitBGcrk8R9yFsbo83MriHAmKpohtIZ0DClF26o-ukUdlwpBtfKu1t5V9q5W3tUq-OgreGwW1vxsfIvOAF4DKY_8s42_l_9P_QRtC43j</recordid><startdate>20110501</startdate><enddate>20110501</enddate><creator>Kwak, Seung-Jae</creator><creator>Paeng, Jisun</creator><creator>Kim, Do Hee</creator><creator>Lee, Sun Ha</creator><creator>Nam, Bo-Young</creator><creator>Kang, Hye Young</creator><creator>Li, Jin Ji</creator><creator>Jung, Dong-Sub</creator><creator>Han, Seung Hyeok</creator><creator>Ryu, Dong-Ryeol</creator><creator>Park, Jung Tak</creator><creator>Chang, Tae Ik</creator><creator>Yoo, Tae-Hyun</creator><creator>Han, Dae Suk</creator><creator>Kang, Shin-Wook</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>7QL</scope><scope>7QP</scope><scope>7RQ</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>20110501</creationdate><title>Local kallikrein–kinin system is involved in podocyte apoptosis under diabetic conditions</title><author>Kwak, Seung-Jae ; Paeng, Jisun ; Kim, Do Hee ; Lee, Sun Ha ; Nam, Bo-Young ; Kang, Hye Young ; Li, Jin Ji ; Jung, Dong-Sub ; Han, Seung Hyeok ; Ryu, Dong-Ryeol ; Park, Jung Tak ; Chang, Tae Ik ; Yoo, Tae-Hyun ; Han, Dae Suk ; Kang, Shin-Wook</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c370t-6b849d17d82f494f427f279559c539924a47f4b56dd6324493392c952d8915b53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Bradykinin - pharmacology</topic><topic>Bradykinin - physiology</topic><topic>Cancer Research</topic><topic>Cell Biology</topic><topic>Cytoprotection</topic><topic>Diabetes Mellitus, Experimental - chemically induced</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Diabetes Mellitus, Experimental - pathology</topic><topic>Diabetic Nephropathies - metabolism</topic><topic>Diabetic Nephropathies - pathology</topic><topic>Gene Expression</topic><topic>Glucose - metabolism</topic><topic>Kallikrein-Kinin System</topic><topic>Male</topic><topic>Mice</topic><topic>Oncology</topic><topic>Original Paper</topic><topic>Podocytes - drug effects</topic><topic>Podocytes - metabolism</topic><topic>Podocytes - pathology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Virology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kwak, Seung-Jae</creatorcontrib><creatorcontrib>Paeng, Jisun</creatorcontrib><creatorcontrib>Kim, Do Hee</creatorcontrib><creatorcontrib>Lee, Sun Ha</creatorcontrib><creatorcontrib>Nam, Bo-Young</creatorcontrib><creatorcontrib>Kang, Hye Young</creatorcontrib><creatorcontrib>Li, Jin Ji</creatorcontrib><creatorcontrib>Jung, Dong-Sub</creatorcontrib><creatorcontrib>Han, Seung Hyeok</creatorcontrib><creatorcontrib>Ryu, Dong-Ryeol</creatorcontrib><creatorcontrib>Park, Jung Tak</creatorcontrib><creatorcontrib>Chang, Tae Ik</creatorcontrib><creatorcontrib>Yoo, Tae-Hyun</creatorcontrib><creatorcontrib>Han, Dae Suk</creatorcontrib><creatorcontrib>Kang, Shin-Wook</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Career & Technical Education Database</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech 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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</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>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science 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 Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Apoptosis (London)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kwak, Seung-Jae</au><au>Paeng, Jisun</au><au>Kim, Do Hee</au><au>Lee, Sun Ha</au><au>Nam, Bo-Young</au><au>Kang, Hye Young</au><au>Li, Jin Ji</au><au>Jung, Dong-Sub</au><au>Han, Seung Hyeok</au><au>Ryu, Dong-Ryeol</au><au>Park, Jung Tak</au><au>Chang, Tae Ik</au><au>Yoo, Tae-Hyun</au><au>Han, Dae Suk</au><au>Kang, Shin-Wook</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Local kallikrein–kinin system is involved in podocyte apoptosis under diabetic conditions</atitle><jtitle>Apoptosis (London)</jtitle><stitle>Apoptosis</stitle><addtitle>Apoptosis</addtitle><date>2011-05-01</date><risdate>2011</risdate><volume>16</volume><issue>5</issue><spage>478</spage><epage>490</epage><pages>478-490</pages><issn>1360-8185</issn><eissn>1573-675X</eissn><abstract>The kallikrein–kinin system (KKS) serves as the physiologic counterbalance to the renin-angiotensin system. This study was conducted to examine the changes in the expression of KKS components in podocytes under diabetic conditions and to elucidate the functional role of bradykinin (BK) in diabetes-associated podocyte apoptosis. Thirty-two rats were injected with either diluent (
n
= 16, C) or with streptozotocin intraperitoneally (
n
= 16, DM), and 8 rats from each group were treated with BK infusion for 6 weeks. Immortalized mouse podocytes were cultured in media containing 5.6 mmol/l glucose (NG), NG + 10
−7
mol/l AII (AII), or 30 mmol/l glucose (HG) with or without 10
−8
mol/l BK. Urinary albumin excretion was significantly higher in DM rats, and this increase was ameliorated by BK. Not only kininogen, kallikrein, and BK B1- and B2-receptor expression but also BK levels were significantly decreased in DM glomeruli and in cultured podocytes exposed to HG. The changes in the expressions of apoptosis-related molecules and the increase in the number of apoptotic cells in DM glomeruli as well as in HG- and AII-stimulated podocytes were significantly abrogated by BK. The suppressed KSS within podocytes under diabetic condition was associated with podocyte apoptosis, suggesting that BK may be beneficial in preventing podocyte loss in diabetic nephropathy.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>21373934</pmid><doi>10.1007/s10495-011-0585-1</doi><tpages>13</tpages></addata></record> |
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| ispartof | Apoptosis (London), 2011-05, Vol.16 (5), p.478-490 |
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| subjects | Animals Apoptosis - drug effects Biochemistry Biomedical and Life Sciences Biomedicine Bradykinin - pharmacology Bradykinin - physiology Cancer Research Cell Biology Cytoprotection Diabetes Mellitus, Experimental - chemically induced Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Experimental - pathology Diabetic Nephropathies - metabolism Diabetic Nephropathies - pathology Gene Expression Glucose - metabolism Kallikrein-Kinin System Male Mice Oncology Original Paper Podocytes - drug effects Podocytes - metabolism Podocytes - pathology Rats Rats, Sprague-Dawley Virology |
| title | Local kallikrein–kinin system is involved in podocyte apoptosis under diabetic conditions |
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