Resolvin D1 reduces ER stress-induced apoptosis and triglyceride accumulation through JNK pathway in HepG2 cells
•Resolvin D1 suppresses palmitate-mediated ER stress-induced cellular dysfunction.•Resolvin D1 selctively reduced JNK phosphorylation through PPAR-g in hepatocytes.•Resolvin D1 does not affect expression change of ER stress markers and chaperones.•ALX/FPR2 and GPR32 are not involved in the effects o...
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| Veröffentlicht in: | Molecular and cellular endocrinology 2014-06, Vol.391 (1-2), p.30-40 |
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| creator | Jung, Tae Woo Hwang, Hwan-Jin Hong, Ho Cheol Choi, Hae Yoon Yoo, Hye Jin Baik, Sei Hyun Choi, Kyung Mook |
| description | •Resolvin D1 suppresses palmitate-mediated ER stress-induced cellular dysfunction.•Resolvin D1 selctively reduced JNK phosphorylation through PPAR-g in hepatocytes.•Resolvin D1 does not affect expression change of ER stress markers and chaperones.•ALX/FPR2 and GPR32 are not involved in the effects of Resolvin D1.
Research has indicated that stress on the endoplasmic reticulum (ER) of a cell affects the pathogenesis of metabolic disorders such as obesity, type 2 diabetes mellitus, and non-alcoholic fatty liver disease (NAFLD). Resolvins, a novel family derived from ω-3 polyunsaturated fatty acids, have anti-inflammatory and insulin sensitizing properties, and it has been suggested that they play a role in the amelioration of obesity-related metabolic dysfunctions. This study showed that pretreatment with resolvin D1 (RvD1) attenuated ER stress-induced apoptosis and also decreased caspase 3 activity in HepG2 cells. Furthermore, RvD1 significantly decreased tunicamycin-induced triglycerides accumulation as well as SREBP-1 expression. However, tunicamycin-induced ER stress markers were not significantly affected by RvD1 treatment. Moreover, RvD1 treatment did not affect the tunicamycin-induced expression of chaperones that assist protein folding in the ER. These results suggest that RvD1-conferred cellular protection may occur downstream of the ER stress. This was supported by the finding that RvD1 significantly inhibited tunicamycin-induced c-Jun N-terminal kinase (JNK) expression, although P38 and ERK1/2 phosphorylation were not affected. In addition, anisomycin, a JNK activator, increased caspase 3 activity and apoptosis as well as triglycerides accumulation and SREBP1 expression, and RvD1 treatment reversed these changes. In conclusion, RvD1 attenuated ER stress-induced hepatic steatosis and apoptosis via the JNK-mediated pathway. This study may provide insight into a novel underlying mechanism and a strategy for treating NAFLD. |
| doi_str_mv | 10.1016/j.mce.2014.04.012 |
| format | Article |
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Research has indicated that stress on the endoplasmic reticulum (ER) of a cell affects the pathogenesis of metabolic disorders such as obesity, type 2 diabetes mellitus, and non-alcoholic fatty liver disease (NAFLD). Resolvins, a novel family derived from ω-3 polyunsaturated fatty acids, have anti-inflammatory and insulin sensitizing properties, and it has been suggested that they play a role in the amelioration of obesity-related metabolic dysfunctions. This study showed that pretreatment with resolvin D1 (RvD1) attenuated ER stress-induced apoptosis and also decreased caspase 3 activity in HepG2 cells. Furthermore, RvD1 significantly decreased tunicamycin-induced triglycerides accumulation as well as SREBP-1 expression. However, tunicamycin-induced ER stress markers were not significantly affected by RvD1 treatment. Moreover, RvD1 treatment did not affect the tunicamycin-induced expression of chaperones that assist protein folding in the ER. These results suggest that RvD1-conferred cellular protection may occur downstream of the ER stress. This was supported by the finding that RvD1 significantly inhibited tunicamycin-induced c-Jun N-terminal kinase (JNK) expression, although P38 and ERK1/2 phosphorylation were not affected. In addition, anisomycin, a JNK activator, increased caspase 3 activity and apoptosis as well as triglycerides accumulation and SREBP1 expression, and RvD1 treatment reversed these changes. In conclusion, RvD1 attenuated ER stress-induced hepatic steatosis and apoptosis via the JNK-mediated pathway. This study may provide insight into a novel underlying mechanism and a strategy for treating NAFLD.</description><identifier>ISSN: 0303-7207</identifier><identifier>EISSN: 1872-8057</identifier><identifier>DOI: 10.1016/j.mce.2014.04.012</identifier><identifier>PMID: 24784707</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>Anisomycin - pharmacology ; Anti-Inflammatory Agents, Non-Steroidal - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - genetics ; Attenuation ; c-Jun N-terminal kinase ; Caspase 3 - genetics ; Caspase 3 - metabolism ; Cellular ; Docosahexaenoic Acids - pharmacology ; Endoplasmic Reticulum - drug effects ; Endoplasmic Reticulum Stress - drug effects ; ER stress ; Gene Expression Regulation ; Hep G2 Cells ; Humans ; JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors ; JNK Mitogen-Activated Protein Kinases - genetics ; JNK Mitogen-Activated Protein Kinases - metabolism ; Kinases ; Mitogen-Activated Protein Kinase 1 - genetics ; Mitogen-Activated Protein Kinase 1 - metabolism ; Mitogen-Activated Protein Kinase 3 - genetics ; Mitogen-Activated Protein Kinase 3 - metabolism ; Non-alcoholic fatty liver ; p38 Mitogen-Activated Protein Kinases - genetics ; p38 Mitogen-Activated Protein Kinases - metabolism ; Pathways ; Phosphorylation ; Proliferator-activated receptor-γ ; Resolvin D1 ; Signal Transduction ; Sterol Regulatory Element Binding Protein 1 - genetics ; Sterol Regulatory Element Binding Protein 1 - metabolism ; Stresses ; Triglycerides ; Triglycerides - antagonists & inhibitors ; Triglycerides - biosynthesis ; Tunicamycin - pharmacology</subject><ispartof>Molecular and cellular endocrinology, 2014-06, Vol.391 (1-2), p.30-40</ispartof><rights>2014 Elsevier Ireland Ltd</rights><rights>Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c386t-7ab3bf9f70ac2a923fd9f3e5bdc7ddb7eee85a06403d88d29b355c2c520deabb3</citedby><cites>FETCH-LOGICAL-c386t-7ab3bf9f70ac2a923fd9f3e5bdc7ddb7eee85a06403d88d29b355c2c520deabb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0303720714001300$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24784707$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jung, Tae Woo</creatorcontrib><creatorcontrib>Hwang, Hwan-Jin</creatorcontrib><creatorcontrib>Hong, Ho Cheol</creatorcontrib><creatorcontrib>Choi, Hae Yoon</creatorcontrib><creatorcontrib>Yoo, Hye Jin</creatorcontrib><creatorcontrib>Baik, Sei Hyun</creatorcontrib><creatorcontrib>Choi, Kyung Mook</creatorcontrib><title>Resolvin D1 reduces ER stress-induced apoptosis and triglyceride accumulation through JNK pathway in HepG2 cells</title><title>Molecular and cellular endocrinology</title><addtitle>Mol Cell Endocrinol</addtitle><description>•Resolvin D1 suppresses palmitate-mediated ER stress-induced cellular dysfunction.•Resolvin D1 selctively reduced JNK phosphorylation through PPAR-g in hepatocytes.•Resolvin D1 does not affect expression change of ER stress markers and chaperones.•ALX/FPR2 and GPR32 are not involved in the effects of Resolvin D1.
Research has indicated that stress on the endoplasmic reticulum (ER) of a cell affects the pathogenesis of metabolic disorders such as obesity, type 2 diabetes mellitus, and non-alcoholic fatty liver disease (NAFLD). Resolvins, a novel family derived from ω-3 polyunsaturated fatty acids, have anti-inflammatory and insulin sensitizing properties, and it has been suggested that they play a role in the amelioration of obesity-related metabolic dysfunctions. This study showed that pretreatment with resolvin D1 (RvD1) attenuated ER stress-induced apoptosis and also decreased caspase 3 activity in HepG2 cells. Furthermore, RvD1 significantly decreased tunicamycin-induced triglycerides accumulation as well as SREBP-1 expression. However, tunicamycin-induced ER stress markers were not significantly affected by RvD1 treatment. Moreover, RvD1 treatment did not affect the tunicamycin-induced expression of chaperones that assist protein folding in the ER. These results suggest that RvD1-conferred cellular protection may occur downstream of the ER stress. This was supported by the finding that RvD1 significantly inhibited tunicamycin-induced c-Jun N-terminal kinase (JNK) expression, although P38 and ERK1/2 phosphorylation were not affected. In addition, anisomycin, a JNK activator, increased caspase 3 activity and apoptosis as well as triglycerides accumulation and SREBP1 expression, and RvD1 treatment reversed these changes. In conclusion, RvD1 attenuated ER stress-induced hepatic steatosis and apoptosis via the JNK-mediated pathway. This study may provide insight into a novel underlying mechanism and a strategy for treating NAFLD.</description><subject>Anisomycin - pharmacology</subject><subject>Anti-Inflammatory Agents, Non-Steroidal - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>Attenuation</subject><subject>c-Jun N-terminal kinase</subject><subject>Caspase 3 - genetics</subject><subject>Caspase 3 - metabolism</subject><subject>Cellular</subject><subject>Docosahexaenoic Acids - pharmacology</subject><subject>Endoplasmic Reticulum - drug effects</subject><subject>Endoplasmic Reticulum Stress - drug effects</subject><subject>ER stress</subject><subject>Gene Expression Regulation</subject><subject>Hep G2 Cells</subject><subject>Humans</subject><subject>JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors</subject><subject>JNK Mitogen-Activated Protein Kinases - genetics</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>Kinases</subject><subject>Mitogen-Activated Protein Kinase 1 - genetics</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Mitogen-Activated Protein Kinase 3 - genetics</subject><subject>Mitogen-Activated Protein Kinase 3 - metabolism</subject><subject>Non-alcoholic fatty liver</subject><subject>p38 Mitogen-Activated Protein Kinases - genetics</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Pathways</subject><subject>Phosphorylation</subject><subject>Proliferator-activated receptor-γ</subject><subject>Resolvin D1</subject><subject>Signal Transduction</subject><subject>Sterol Regulatory Element Binding Protein 1 - genetics</subject><subject>Sterol Regulatory Element Binding Protein 1 - metabolism</subject><subject>Stresses</subject><subject>Triglycerides</subject><subject>Triglycerides - antagonists & inhibitors</subject><subject>Triglycerides - biosynthesis</subject><subject>Tunicamycin - pharmacology</subject><issn>0303-7207</issn><issn>1872-8057</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkUFv1DAQhS0EokvhB3BBPnLJMrbjOBEn1JYWqECq4Gw59qTrVRIH2ynaf49XWzgipJFGGn3vafQeIa8ZbBmw5t1-O1nccmD1Fsow_oRsWKt41YJUT8kGBIhKcVBn5EVKewBQkrfPyRmvVVsrUBuy3GEK44Of6SWjEd1qMdGrO5pyxJQqPx8vjpolLDkkn6iZHc3R348Hi9E7pMbadVpHk32Yad7FsN7v6OevX-hi8u6XOdDifYPLNacWxzG9JM8GMyZ89bjPyY-PV98vbqrbb9efLj7cVla0Ta6U6UU_dIMCY7npuBhcNwiUvbPKuV4hYisNNDUI17aOd72Q0nIrOTg0fS_OyduT7xLDzxVT1pNPxw_MjGFNmknJoG6gY_-B8q4VXcPqgrITamNIKeKgl-gnEw-agT52ove6dKKPnWgow3jRvHm0X_sJ3V_FnxIK8P4EYMnjwWPUyXqcS-4-os3aBf8P-9_bxp3c</recordid><startdate>20140625</startdate><enddate>20140625</enddate><creator>Jung, Tae Woo</creator><creator>Hwang, Hwan-Jin</creator><creator>Hong, Ho Cheol</creator><creator>Choi, Hae Yoon</creator><creator>Yoo, Hye Jin</creator><creator>Baik, Sei Hyun</creator><creator>Choi, Kyung Mook</creator><general>Elsevier Ireland Ltd</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>7X8</scope><scope>7U5</scope><scope>8FD</scope><scope>L7M</scope></search><sort><creationdate>20140625</creationdate><title>Resolvin D1 reduces ER stress-induced apoptosis and triglyceride accumulation through JNK pathway in HepG2 cells</title><author>Jung, Tae Woo ; Hwang, Hwan-Jin ; Hong, Ho Cheol ; Choi, Hae Yoon ; Yoo, Hye Jin ; Baik, Sei Hyun ; Choi, Kyung Mook</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c386t-7ab3bf9f70ac2a923fd9f3e5bdc7ddb7eee85a06403d88d29b355c2c520deabb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Anisomycin - pharmacology</topic><topic>Anti-Inflammatory Agents, Non-Steroidal - pharmacology</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - genetics</topic><topic>Attenuation</topic><topic>c-Jun N-terminal kinase</topic><topic>Caspase 3 - genetics</topic><topic>Caspase 3 - metabolism</topic><topic>Cellular</topic><topic>Docosahexaenoic Acids - pharmacology</topic><topic>Endoplasmic Reticulum - drug effects</topic><topic>Endoplasmic Reticulum Stress - drug effects</topic><topic>ER stress</topic><topic>Gene Expression Regulation</topic><topic>Hep G2 Cells</topic><topic>Humans</topic><topic>JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors</topic><topic>JNK Mitogen-Activated Protein Kinases - genetics</topic><topic>JNK Mitogen-Activated Protein Kinases - metabolism</topic><topic>Kinases</topic><topic>Mitogen-Activated Protein Kinase 1 - genetics</topic><topic>Mitogen-Activated Protein Kinase 1 - metabolism</topic><topic>Mitogen-Activated Protein Kinase 3 - genetics</topic><topic>Mitogen-Activated Protein Kinase 3 - metabolism</topic><topic>Non-alcoholic fatty liver</topic><topic>p38 Mitogen-Activated Protein Kinases - genetics</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Pathways</topic><topic>Phosphorylation</topic><topic>Proliferator-activated receptor-γ</topic><topic>Resolvin D1</topic><topic>Signal Transduction</topic><topic>Sterol Regulatory Element Binding Protein 1 - genetics</topic><topic>Sterol Regulatory Element Binding Protein 1 - metabolism</topic><topic>Stresses</topic><topic>Triglycerides</topic><topic>Triglycerides - antagonists & inhibitors</topic><topic>Triglycerides - biosynthesis</topic><topic>Tunicamycin - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jung, Tae Woo</creatorcontrib><creatorcontrib>Hwang, Hwan-Jin</creatorcontrib><creatorcontrib>Hong, Ho Cheol</creatorcontrib><creatorcontrib>Choi, Hae Yoon</creatorcontrib><creatorcontrib>Yoo, Hye Jin</creatorcontrib><creatorcontrib>Baik, Sei Hyun</creatorcontrib><creatorcontrib>Choi, Kyung Mook</creatorcontrib><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>Solid State and Superconductivity Abstracts</collection><collection>Technology Research Database</collection><collection>Advanced Technologies Database with Aerospace</collection><jtitle>Molecular and cellular endocrinology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jung, Tae Woo</au><au>Hwang, Hwan-Jin</au><au>Hong, Ho Cheol</au><au>Choi, Hae Yoon</au><au>Yoo, Hye Jin</au><au>Baik, Sei Hyun</au><au>Choi, Kyung Mook</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Resolvin D1 reduces ER stress-induced apoptosis and triglyceride accumulation through JNK pathway in HepG2 cells</atitle><jtitle>Molecular and cellular endocrinology</jtitle><addtitle>Mol Cell Endocrinol</addtitle><date>2014-06-25</date><risdate>2014</risdate><volume>391</volume><issue>1-2</issue><spage>30</spage><epage>40</epage><pages>30-40</pages><issn>0303-7207</issn><eissn>1872-8057</eissn><abstract>•Resolvin D1 suppresses palmitate-mediated ER stress-induced cellular dysfunction.•Resolvin D1 selctively reduced JNK phosphorylation through PPAR-g in hepatocytes.•Resolvin D1 does not affect expression change of ER stress markers and chaperones.•ALX/FPR2 and GPR32 are not involved in the effects of Resolvin D1.
Research has indicated that stress on the endoplasmic reticulum (ER) of a cell affects the pathogenesis of metabolic disorders such as obesity, type 2 diabetes mellitus, and non-alcoholic fatty liver disease (NAFLD). Resolvins, a novel family derived from ω-3 polyunsaturated fatty acids, have anti-inflammatory and insulin sensitizing properties, and it has been suggested that they play a role in the amelioration of obesity-related metabolic dysfunctions. This study showed that pretreatment with resolvin D1 (RvD1) attenuated ER stress-induced apoptosis and also decreased caspase 3 activity in HepG2 cells. Furthermore, RvD1 significantly decreased tunicamycin-induced triglycerides accumulation as well as SREBP-1 expression. However, tunicamycin-induced ER stress markers were not significantly affected by RvD1 treatment. Moreover, RvD1 treatment did not affect the tunicamycin-induced expression of chaperones that assist protein folding in the ER. These results suggest that RvD1-conferred cellular protection may occur downstream of the ER stress. This was supported by the finding that RvD1 significantly inhibited tunicamycin-induced c-Jun N-terminal kinase (JNK) expression, although P38 and ERK1/2 phosphorylation were not affected. In addition, anisomycin, a JNK activator, increased caspase 3 activity and apoptosis as well as triglycerides accumulation and SREBP1 expression, and RvD1 treatment reversed these changes. In conclusion, RvD1 attenuated ER stress-induced hepatic steatosis and apoptosis via the JNK-mediated pathway. This study may provide insight into a novel underlying mechanism and a strategy for treating NAFLD.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>24784707</pmid><doi>10.1016/j.mce.2014.04.012</doi><tpages>11</tpages></addata></record> |
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| ispartof | Molecular and cellular endocrinology, 2014-06, Vol.391 (1-2), p.30-40 |
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| subjects | Anisomycin - pharmacology Anti-Inflammatory Agents, Non-Steroidal - pharmacology Apoptosis Apoptosis - drug effects Apoptosis - genetics Attenuation c-Jun N-terminal kinase Caspase 3 - genetics Caspase 3 - metabolism Cellular Docosahexaenoic Acids - pharmacology Endoplasmic Reticulum - drug effects Endoplasmic Reticulum Stress - drug effects ER stress Gene Expression Regulation Hep G2 Cells Humans JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors JNK Mitogen-Activated Protein Kinases - genetics JNK Mitogen-Activated Protein Kinases - metabolism Kinases Mitogen-Activated Protein Kinase 1 - genetics Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 - genetics Mitogen-Activated Protein Kinase 3 - metabolism Non-alcoholic fatty liver p38 Mitogen-Activated Protein Kinases - genetics p38 Mitogen-Activated Protein Kinases - metabolism Pathways Phosphorylation Proliferator-activated receptor-γ Resolvin D1 Signal Transduction Sterol Regulatory Element Binding Protein 1 - genetics Sterol Regulatory Element Binding Protein 1 - metabolism Stresses Triglycerides Triglycerides - antagonists & inhibitors Triglycerides - biosynthesis Tunicamycin - pharmacology |
| title | Resolvin D1 reduces ER stress-induced apoptosis and triglyceride accumulation through JNK pathway in HepG2 cells |
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