Prolonged Endoplasmic Reticulum Stress Induces Apoptotic Cell Death in an Experimental Model of Chronic Cyclosporine Nephropathy
Background/Aims: Apoptosis contributes to cyclosporine (CsA)-induced renal cell death. This study tested the effects of CsA-induced endoplasmic reticulum (ER) stress on apoptotic cell death in an experimental model of chronic CsA nephropathy. Methods: CsA (15 mg/kg per day) was given to rats for 7 o...
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| Veröffentlicht in: | American journal of nephrology 2008-01, Vol.28 (5), p.707-714 |
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| creator | Han, Sang Woo Li, Can Ahn, Kyung Ohk Lim, Sun Woo Song, Hyun Guk Jang, Yoon Sung Cho, Yoon Mi Jang, Young Min Ghee, Jung Yeon Kim, Jin Young Kim, Su Hyun Kim, Jin Kwon, Oh Joo Yang, Chul Woo |
| description | Background/Aims: Apoptosis contributes to cyclosporine (CsA)-induced renal cell death. This study tested the effects of CsA-induced endoplasmic reticulum (ER) stress on apoptotic cell death in an experimental model of chronic CsA nephropathy. Methods: CsA (15 mg/kg per day) was given to rats for 7 or 28 days. The ER stress response was evaluated with BiP expression, and the proapoptotic response was assessed with CHOP and caspase 12 expression. ER structure was evaluated by transmission electron microscopy, and apoptotic cell death was detected with TUNEL staining. Results: Short-term treatment of CsA for 7 days activated both the ER stress response (induction of BiP mRNA and protein) and the proapoptotic response (upregulation of caspase 12 and CHOP mRNAs and proteins). However, long-term treatment with CsA for 28 days decreased BiP and further increased CHOP. The imbalance between the two responses coincided with the timing of the appearance of apoptotic cell death and the disruption of the ER structure. Conclusion: Prolonged CsA-induced ER stress causes apoptotic cell death by depleting molecular chaperones and activating the proapoptotic pathway. |
| doi_str_mv | 10.1159/000127432 |
| format | Article |
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This study tested the effects of CsA-induced endoplasmic reticulum (ER) stress on apoptotic cell death in an experimental model of chronic CsA nephropathy. Methods: CsA (15 mg/kg per day) was given to rats for 7 or 28 days. The ER stress response was evaluated with BiP expression, and the proapoptotic response was assessed with CHOP and caspase 12 expression. ER structure was evaluated by transmission electron microscopy, and apoptotic cell death was detected with TUNEL staining. Results: Short-term treatment of CsA for 7 days activated both the ER stress response (induction of BiP mRNA and protein) and the proapoptotic response (upregulation of caspase 12 and CHOP mRNAs and proteins). However, long-term treatment with CsA for 28 days decreased BiP and further increased CHOP. The imbalance between the two responses coincided with the timing of the appearance of apoptotic cell death and the disruption of the ER structure. Conclusion: Prolonged CsA-induced ER stress causes apoptotic cell death by depleting molecular chaperones and activating the proapoptotic pathway.</description><identifier>ISSN: 0250-8095</identifier><identifier>EISSN: 1421-9670</identifier><identifier>DOI: 10.1159/000127432</identifier><identifier>PMID: 18434710</identifier><identifier>CODEN: AJNED9</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Animals ; Apoptosis ; Blotting, Northern ; Caspase 12 - analysis ; Cell Death ; Cyclosporine ; Endoplasmic Reticulum - drug effects ; Immunohistochemistry ; In Situ Nick-End Labeling ; Kidney Diseases - chemically induced ; Kidney Diseases - pathology ; Male ; Original Report: Laboratory Investigation ; Rats ; Rats, Sprague-Dawley ; Transcription Factor CHOP - analysis</subject><ispartof>American journal of nephrology, 2008-01, Vol.28 (5), p.707-714</ispartof><rights>2008 S. Karger AG, Basel</rights><rights>Copyright 2008 S. Karger AG, Basel.</rights><rights>Copyright (c) 2008 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c397t-e54508446f783ec20d5d1ed5908e0b3b5271ebcf40057759592df4a810359de73</citedby><cites>FETCH-LOGICAL-c397t-e54508446f783ec20d5d1ed5908e0b3b5271ebcf40057759592df4a810359de73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,2423,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18434710$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Han, Sang Woo</creatorcontrib><creatorcontrib>Li, Can</creatorcontrib><creatorcontrib>Ahn, Kyung Ohk</creatorcontrib><creatorcontrib>Lim, Sun Woo</creatorcontrib><creatorcontrib>Song, Hyun Guk</creatorcontrib><creatorcontrib>Jang, Yoon Sung</creatorcontrib><creatorcontrib>Cho, Yoon Mi</creatorcontrib><creatorcontrib>Jang, Young Min</creatorcontrib><creatorcontrib>Ghee, Jung Yeon</creatorcontrib><creatorcontrib>Kim, Jin Young</creatorcontrib><creatorcontrib>Kim, Su Hyun</creatorcontrib><creatorcontrib>Kim, Jin</creatorcontrib><creatorcontrib>Kwon, Oh Joo</creatorcontrib><creatorcontrib>Yang, Chul Woo</creatorcontrib><title>Prolonged Endoplasmic Reticulum Stress Induces Apoptotic Cell Death in an Experimental Model of Chronic Cyclosporine Nephropathy</title><title>American journal of nephrology</title><addtitle>Am J Nephrol</addtitle><description>Background/Aims: Apoptosis contributes to cyclosporine (CsA)-induced renal cell death. This study tested the effects of CsA-induced endoplasmic reticulum (ER) stress on apoptotic cell death in an experimental model of chronic CsA nephropathy. Methods: CsA (15 mg/kg per day) was given to rats for 7 or 28 days. The ER stress response was evaluated with BiP expression, and the proapoptotic response was assessed with CHOP and caspase 12 expression. ER structure was evaluated by transmission electron microscopy, and apoptotic cell death was detected with TUNEL staining. Results: Short-term treatment of CsA for 7 days activated both the ER stress response (induction of BiP mRNA and protein) and the proapoptotic response (upregulation of caspase 12 and CHOP mRNAs and proteins). However, long-term treatment with CsA for 28 days decreased BiP and further increased CHOP. The imbalance between the two responses coincided with the timing of the appearance of apoptotic cell death and the disruption of the ER structure. Conclusion: Prolonged CsA-induced ER stress causes apoptotic cell death by depleting molecular chaperones and activating the proapoptotic pathway.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Blotting, Northern</subject><subject>Caspase 12 - analysis</subject><subject>Cell Death</subject><subject>Cyclosporine</subject><subject>Endoplasmic Reticulum - drug effects</subject><subject>Immunohistochemistry</subject><subject>In Situ Nick-End Labeling</subject><subject>Kidney Diseases - chemically induced</subject><subject>Kidney Diseases - pathology</subject><subject>Male</subject><subject>Original Report: Laboratory Investigation</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Transcription Factor CHOP - analysis</subject><issn>0250-8095</issn><issn>1421-9670</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpF0D1PwzAQBmALgaAUBnaELDaGwDmx63hEpUAlvsTHHKXxpQRc29iJRDd-OqlawWTp_Nyd7iXkiME5Y0JdAABLJc_SLTJgPGWJGknYJgNIBSQ5KLFH9mP8WKkc5C7ZYznPuGQwID9PwRln56jpxGrnTRkXTUWfsW2qznQL-tIGjJFOre4qjPTSO9-6_pOO0Rh6hWX7ThtLS0sn3x5Ds0DblobeO42GupqO34OzK76sjIvehcYifUDfl33fuzwgO3VpIh5u3iF5u568jm-Tu8eb6fjyLqkyJdsEBReQcz6qZZ5hlYIWmqEWCnKEWTYTqWQ4q2oOIKQUSqhU17zMGWRCaZTZkJyu5_rgvjqMbfHhumD7lUWajZQAAaMena1RFVyMAevC9xeVYVkwKFZRF39R9_ZkM7CbLVD_y022PTheg88yzDH8g3X_LxswglU</recordid><startdate>20080101</startdate><enddate>20080101</enddate><creator>Han, Sang Woo</creator><creator>Li, Can</creator><creator>Ahn, Kyung Ohk</creator><creator>Lim, Sun Woo</creator><creator>Song, Hyun Guk</creator><creator>Jang, Yoon Sung</creator><creator>Cho, Yoon Mi</creator><creator>Jang, Young Min</creator><creator>Ghee, Jung Yeon</creator><creator>Kim, Jin Young</creator><creator>Kim, Su Hyun</creator><creator>Kim, Jin</creator><creator>Kwon, Oh Joo</creator><creator>Yang, Chul Woo</creator><general>S. 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This study tested the effects of CsA-induced endoplasmic reticulum (ER) stress on apoptotic cell death in an experimental model of chronic CsA nephropathy. Methods: CsA (15 mg/kg per day) was given to rats for 7 or 28 days. The ER stress response was evaluated with BiP expression, and the proapoptotic response was assessed with CHOP and caspase 12 expression. ER structure was evaluated by transmission electron microscopy, and apoptotic cell death was detected with TUNEL staining. Results: Short-term treatment of CsA for 7 days activated both the ER stress response (induction of BiP mRNA and protein) and the proapoptotic response (upregulation of caspase 12 and CHOP mRNAs and proteins). However, long-term treatment with CsA for 28 days decreased BiP and further increased CHOP. The imbalance between the two responses coincided with the timing of the appearance of apoptotic cell death and the disruption of the ER structure. Conclusion: Prolonged CsA-induced ER stress causes apoptotic cell death by depleting molecular chaperones and activating the proapoptotic pathway.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>18434710</pmid><doi>10.1159/000127432</doi><tpages>8</tpages></addata></record> |
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| subjects | Animals Apoptosis Blotting, Northern Caspase 12 - analysis Cell Death Cyclosporine Endoplasmic Reticulum - drug effects Immunohistochemistry In Situ Nick-End Labeling Kidney Diseases - chemically induced Kidney Diseases - pathology Male Original Report: Laboratory Investigation Rats Rats, Sprague-Dawley Transcription Factor CHOP - analysis |
| title | Prolonged Endoplasmic Reticulum Stress Induces Apoptotic Cell Death in an Experimental Model of Chronic Cyclosporine Nephropathy |
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