Peroxisome proliferator‐activated receptor delta protects against obesity‐related glomerulopathy through the P38 MAPK pathway
Objective: Obesity is a prominent component of metabolic syndrome and a major risk factor for renal disease. The aim of this study was to explore the effect of cross‐talk between peroxisome proliferator‐activated receptor (PPAR)δ and p38 mitogen‐activated protein kinase (p38 MAPK) on obesity‐related...
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| Veröffentlicht in: | Obesity (Silver Spring, Md.) Md.), 2013-03, Vol.21 (3), p.538-545 |
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| container_title | Obesity (Silver Spring, Md.) |
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| creator | Yan, Zhencheng Ni, Yinxing Wang, Peijian Chen, Jian He, Hongbo Sun, Jing Cao, Tingbing Chen, Jing Zhao, Zhigang Luo, Zhidan Chen, Lin Liu, Daoyan Zhu, Zhiming |
| description | Objective:
Obesity is a prominent component of metabolic syndrome and a major risk factor for renal disease. The aim of this study was to explore the effect of cross‐talk between peroxisome proliferator‐activated receptor (PPAR)δ and p38 mitogen‐activated protein kinase (p38 MAPK) on obesity‐related glomerulopathy.
Design and Methods:
Male Wistar rats were randomly assigned to standard laboratory chow or a high‐fat diet for 32 weeks. Glomerular mesangial cells HBZY‐1 and mature differentiation 3T3‐L1 cells were cocultured and were transfected with PPARδ‐expressing vectors or treated with agonist or inhibitor of PPARδ or p38 MAPK.
Results:
Rats on a high‐fat diet showed typical characteristics of metabolic syndrome including obesity, dyslipidemia, insulin resistance, and hypertension. Rats on a high‐fat diet also had significant glomerular hypertrophy and extracellular matrix accumulation, which were accompanied by increased p38 MAPK phosphorylation and decreased PPARδ expression in the kidney tissue. The roles of p38 MAPK and PPARδ in a coculture system of mesangial cells and mature differentiation 3T3‐L1 cells were further explored. PPARδ suppression promoted laminin and type IV collagen secretion through p38 MAPK phosphorylation in mesangial cells, whereas PPARδ overexpression or PPARδ agonist attenuated phosphorylation of p38 MAPK and laminin and type IV collagen secretion.
Conclusions:
The characteristics of obesity‐related glomerulopathy, which might be partly caused by PPARδ suppression‐induced p38 MAPK activation and laminin and type IV collagen secretion was demonstrated. |
| doi_str_mv | 10.1002/oby.20103 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1328545636</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1328545636</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4543-aed7a0ad87295f8ebb96b4028b76e72ff221603e02516cba4b1244166151fce3</originalsourceid><addsrcrecordid>eNp1kc9OGzEQh60KRChw6AsgS1zKIeB_6909AiqlahA55NCeLHt3NtnIiYPtLd1b-wZ9xj4JDgk5IHEay_7m04x_CH2i5IISwi6d6S8YoYR_QIe05GSY8_LH3u5c0AH6GMKcECFJRg_QgPGsZFLSQ_R3DN79boNbAF55Z9sGvI7O___zT1ex_aUj1NhDBat0iWuwUa-5CFUMWE91uwwROwOhjX3q8WBfOqY2CX1n3UrHWY_jzLtuOksV8JgX-P5q_B2vn550f4z2G20DnGzrEZrcfpnc3A1HD1-_3VyNhpXIBB9qqHNNdF3krMyaAowppRGEFSaXkLOmYYxKwoGwjMrKaGEoE4KmJTPaVMCP0OeNNk3_2EGIatGGCqzVS3BdUJSzIhOZ5DKhZ2_Quev8Mg2nqMxF-lwp1tT5hqq8C8FDo1a-XWjfK0rUOhaVYlEvsST2dGvszALqHfmaQwIuN8BTa6F_36Qern9ulM9GiJqc</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1674739646</pqid></control><display><type>article</type><title>Peroxisome proliferator‐activated receptor delta protects against obesity‐related glomerulopathy through the P38 MAPK pathway</title><source>Wiley-Blackwell Journals</source><source>MEDLINE</source><source>Wiley Free Archive</source><creator>Yan, Zhencheng ; Ni, Yinxing ; Wang, Peijian ; Chen, Jian ; He, Hongbo ; Sun, Jing ; Cao, Tingbing ; Chen, Jing ; Zhao, Zhigang ; Luo, Zhidan ; Chen, Lin ; Liu, Daoyan ; Zhu, Zhiming</creator><creatorcontrib>Yan, Zhencheng ; Ni, Yinxing ; Wang, Peijian ; Chen, Jian ; He, Hongbo ; Sun, Jing ; Cao, Tingbing ; Chen, Jing ; Zhao, Zhigang ; Luo, Zhidan ; Chen, Lin ; Liu, Daoyan ; Zhu, Zhiming</creatorcontrib><description>Objective:
Obesity is a prominent component of metabolic syndrome and a major risk factor for renal disease. The aim of this study was to explore the effect of cross‐talk between peroxisome proliferator‐activated receptor (PPAR)δ and p38 mitogen‐activated protein kinase (p38 MAPK) on obesity‐related glomerulopathy.
Design and Methods:
Male Wistar rats were randomly assigned to standard laboratory chow or a high‐fat diet for 32 weeks. Glomerular mesangial cells HBZY‐1 and mature differentiation 3T3‐L1 cells were cocultured and were transfected with PPARδ‐expressing vectors or treated with agonist or inhibitor of PPARδ or p38 MAPK.
Results:
Rats on a high‐fat diet showed typical characteristics of metabolic syndrome including obesity, dyslipidemia, insulin resistance, and hypertension. Rats on a high‐fat diet also had significant glomerular hypertrophy and extracellular matrix accumulation, which were accompanied by increased p38 MAPK phosphorylation and decreased PPARδ expression in the kidney tissue. The roles of p38 MAPK and PPARδ in a coculture system of mesangial cells and mature differentiation 3T3‐L1 cells were further explored. PPARδ suppression promoted laminin and type IV collagen secretion through p38 MAPK phosphorylation in mesangial cells, whereas PPARδ overexpression or PPARδ agonist attenuated phosphorylation of p38 MAPK and laminin and type IV collagen secretion.
Conclusions:
The characteristics of obesity‐related glomerulopathy, which might be partly caused by PPARδ suppression‐induced p38 MAPK activation and laminin and type IV collagen secretion was demonstrated.</description><identifier>ISSN: 1930-7381</identifier><identifier>EISSN: 1930-739X</identifier><identifier>DOI: 10.1002/oby.20103</identifier><identifier>PMID: 23592661</identifier><language>eng</language><publisher>Hoboken, USA: John Wiley & Sons, Inc</publisher><subject>3T3-L1 Cells ; Animals ; Blotting, Western ; Cell Differentiation ; Collagen - antagonists & inhibitors ; Collagen - metabolism ; Diet, High-Fat ; Glomerular Mesangium - cytology ; Glomerular Mesangium - pathology ; Glucose ; Immunohistochemistry ; Insulin ; Kidney - metabolism ; Kidney - pathology ; Kidney Diseases - etiology ; Kidney Diseases - pathology ; Kinases ; Laminin - antagonists & inhibitors ; Laminin - metabolism ; Male ; MAP Kinase Signaling System ; Mesangial Cells - metabolism ; Mesangial Cells - pathology ; Metabolic Syndrome - complications ; Metabolic Syndrome - physiopathology ; Mice ; Mitogen-Activated Protein Kinase 14 - genetics ; Mitogen-Activated Protein Kinase 14 - metabolism ; Obesity ; Obesity - complications ; Obesity - physiopathology ; Phosphorylation ; PPAR delta - genetics ; PPAR delta - metabolism ; Rats ; Rats, Wistar ; Rodents</subject><ispartof>Obesity (Silver Spring, Md.), 2013-03, Vol.21 (3), p.538-545</ispartof><rights>Copyright © 2013 The Obesity Society</rights><rights>Copyright © 2013 The Obesity Society.</rights><rights>Copyright Blackwell Publishing Ltd. Mar 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4543-aed7a0ad87295f8ebb96b4028b76e72ff221603e02516cba4b1244166151fce3</citedby><cites>FETCH-LOGICAL-c4543-aed7a0ad87295f8ebb96b4028b76e72ff221603e02516cba4b1244166151fce3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Foby.20103$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Foby.20103$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,1433,27924,27925,45574,45575,46409,46833</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23592661$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yan, Zhencheng</creatorcontrib><creatorcontrib>Ni, Yinxing</creatorcontrib><creatorcontrib>Wang, Peijian</creatorcontrib><creatorcontrib>Chen, Jian</creatorcontrib><creatorcontrib>He, Hongbo</creatorcontrib><creatorcontrib>Sun, Jing</creatorcontrib><creatorcontrib>Cao, Tingbing</creatorcontrib><creatorcontrib>Chen, Jing</creatorcontrib><creatorcontrib>Zhao, Zhigang</creatorcontrib><creatorcontrib>Luo, Zhidan</creatorcontrib><creatorcontrib>Chen, Lin</creatorcontrib><creatorcontrib>Liu, Daoyan</creatorcontrib><creatorcontrib>Zhu, Zhiming</creatorcontrib><title>Peroxisome proliferator‐activated receptor delta protects against obesity‐related glomerulopathy through the P38 MAPK pathway</title><title>Obesity (Silver Spring, Md.)</title><addtitle>Obesity (Silver Spring)</addtitle><description>Objective:
Obesity is a prominent component of metabolic syndrome and a major risk factor for renal disease. The aim of this study was to explore the effect of cross‐talk between peroxisome proliferator‐activated receptor (PPAR)δ and p38 mitogen‐activated protein kinase (p38 MAPK) on obesity‐related glomerulopathy.
Design and Methods:
Male Wistar rats were randomly assigned to standard laboratory chow or a high‐fat diet for 32 weeks. Glomerular mesangial cells HBZY‐1 and mature differentiation 3T3‐L1 cells were cocultured and were transfected with PPARδ‐expressing vectors or treated with agonist or inhibitor of PPARδ or p38 MAPK.
Results:
Rats on a high‐fat diet showed typical characteristics of metabolic syndrome including obesity, dyslipidemia, insulin resistance, and hypertension. Rats on a high‐fat diet also had significant glomerular hypertrophy and extracellular matrix accumulation, which were accompanied by increased p38 MAPK phosphorylation and decreased PPARδ expression in the kidney tissue. The roles of p38 MAPK and PPARδ in a coculture system of mesangial cells and mature differentiation 3T3‐L1 cells were further explored. PPARδ suppression promoted laminin and type IV collagen secretion through p38 MAPK phosphorylation in mesangial cells, whereas PPARδ overexpression or PPARδ agonist attenuated phosphorylation of p38 MAPK and laminin and type IV collagen secretion.
Conclusions:
The characteristics of obesity‐related glomerulopathy, which might be partly caused by PPARδ suppression‐induced p38 MAPK activation and laminin and type IV collagen secretion was demonstrated.</description><subject>3T3-L1 Cells</subject><subject>Animals</subject><subject>Blotting, Western</subject><subject>Cell Differentiation</subject><subject>Collagen - antagonists & inhibitors</subject><subject>Collagen - metabolism</subject><subject>Diet, High-Fat</subject><subject>Glomerular Mesangium - cytology</subject><subject>Glomerular Mesangium - pathology</subject><subject>Glucose</subject><subject>Immunohistochemistry</subject><subject>Insulin</subject><subject>Kidney - metabolism</subject><subject>Kidney - pathology</subject><subject>Kidney Diseases - etiology</subject><subject>Kidney Diseases - pathology</subject><subject>Kinases</subject><subject>Laminin - antagonists & inhibitors</subject><subject>Laminin - metabolism</subject><subject>Male</subject><subject>MAP Kinase Signaling System</subject><subject>Mesangial Cells - metabolism</subject><subject>Mesangial Cells - pathology</subject><subject>Metabolic Syndrome - complications</subject><subject>Metabolic Syndrome - physiopathology</subject><subject>Mice</subject><subject>Mitogen-Activated Protein Kinase 14 - genetics</subject><subject>Mitogen-Activated Protein Kinase 14 - metabolism</subject><subject>Obesity</subject><subject>Obesity - complications</subject><subject>Obesity - physiopathology</subject><subject>Phosphorylation</subject><subject>PPAR delta - genetics</subject><subject>PPAR delta - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Rodents</subject><issn>1930-7381</issn><issn>1930-739X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc9OGzEQh60KRChw6AsgS1zKIeB_6909AiqlahA55NCeLHt3NtnIiYPtLd1b-wZ9xj4JDgk5IHEay_7m04x_CH2i5IISwi6d6S8YoYR_QIe05GSY8_LH3u5c0AH6GMKcECFJRg_QgPGsZFLSQ_R3DN79boNbAF55Z9sGvI7O___zT1ex_aUj1NhDBat0iWuwUa-5CFUMWE91uwwROwOhjX3q8WBfOqY2CX1n3UrHWY_jzLtuOksV8JgX-P5q_B2vn550f4z2G20DnGzrEZrcfpnc3A1HD1-_3VyNhpXIBB9qqHNNdF3krMyaAowppRGEFSaXkLOmYYxKwoGwjMrKaGEoE4KmJTPaVMCP0OeNNk3_2EGIatGGCqzVS3BdUJSzIhOZ5DKhZ2_Quev8Mg2nqMxF-lwp1tT5hqq8C8FDo1a-XWjfK0rUOhaVYlEvsST2dGvszALqHfmaQwIuN8BTa6F_36Qern9ulM9GiJqc</recordid><startdate>201303</startdate><enddate>201303</enddate><creator>Yan, Zhencheng</creator><creator>Ni, Yinxing</creator><creator>Wang, Peijian</creator><creator>Chen, Jian</creator><creator>He, Hongbo</creator><creator>Sun, Jing</creator><creator>Cao, Tingbing</creator><creator>Chen, Jing</creator><creator>Zhao, Zhigang</creator><creator>Luo, Zhidan</creator><creator>Chen, Lin</creator><creator>Liu, Daoyan</creator><creator>Zhu, Zhiming</creator><general>John Wiley & Sons, Inc</general><general>Blackwell Publishing 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>K9.</scope><scope>7X8</scope></search><sort><creationdate>201303</creationdate><title>Peroxisome proliferator‐activated receptor delta protects against obesity‐related glomerulopathy through the P38 MAPK pathway</title><author>Yan, Zhencheng ; Ni, Yinxing ; Wang, Peijian ; Chen, Jian ; He, Hongbo ; Sun, Jing ; Cao, Tingbing ; Chen, Jing ; Zhao, Zhigang ; Luo, Zhidan ; Chen, Lin ; Liu, Daoyan ; Zhu, Zhiming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4543-aed7a0ad87295f8ebb96b4028b76e72ff221603e02516cba4b1244166151fce3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>3T3-L1 Cells</topic><topic>Animals</topic><topic>Blotting, Western</topic><topic>Cell Differentiation</topic><topic>Collagen - antagonists & inhibitors</topic><topic>Collagen - metabolism</topic><topic>Diet, High-Fat</topic><topic>Glomerular Mesangium - cytology</topic><topic>Glomerular Mesangium - pathology</topic><topic>Glucose</topic><topic>Immunohistochemistry</topic><topic>Insulin</topic><topic>Kidney - metabolism</topic><topic>Kidney - pathology</topic><topic>Kidney Diseases - etiology</topic><topic>Kidney Diseases - pathology</topic><topic>Kinases</topic><topic>Laminin - antagonists & inhibitors</topic><topic>Laminin - metabolism</topic><topic>Male</topic><topic>MAP Kinase Signaling System</topic><topic>Mesangial Cells - metabolism</topic><topic>Mesangial Cells - pathology</topic><topic>Metabolic Syndrome - complications</topic><topic>Metabolic Syndrome - physiopathology</topic><topic>Mice</topic><topic>Mitogen-Activated Protein Kinase 14 - genetics</topic><topic>Mitogen-Activated Protein Kinase 14 - metabolism</topic><topic>Obesity</topic><topic>Obesity - complications</topic><topic>Obesity - physiopathology</topic><topic>Phosphorylation</topic><topic>PPAR delta - genetics</topic><topic>PPAR delta - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Rodents</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yan, Zhencheng</creatorcontrib><creatorcontrib>Ni, Yinxing</creatorcontrib><creatorcontrib>Wang, Peijian</creatorcontrib><creatorcontrib>Chen, Jian</creatorcontrib><creatorcontrib>He, Hongbo</creatorcontrib><creatorcontrib>Sun, Jing</creatorcontrib><creatorcontrib>Cao, Tingbing</creatorcontrib><creatorcontrib>Chen, Jing</creatorcontrib><creatorcontrib>Zhao, Zhigang</creatorcontrib><creatorcontrib>Luo, Zhidan</creatorcontrib><creatorcontrib>Chen, Lin</creatorcontrib><creatorcontrib>Liu, Daoyan</creatorcontrib><creatorcontrib>Zhu, Zhiming</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 Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Obesity (Silver Spring, Md.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yan, Zhencheng</au><au>Ni, Yinxing</au><au>Wang, Peijian</au><au>Chen, Jian</au><au>He, Hongbo</au><au>Sun, Jing</au><au>Cao, Tingbing</au><au>Chen, Jing</au><au>Zhao, Zhigang</au><au>Luo, Zhidan</au><au>Chen, Lin</au><au>Liu, Daoyan</au><au>Zhu, Zhiming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Peroxisome proliferator‐activated receptor delta protects against obesity‐related glomerulopathy through the P38 MAPK pathway</atitle><jtitle>Obesity (Silver Spring, Md.)</jtitle><addtitle>Obesity (Silver Spring)</addtitle><date>2013-03</date><risdate>2013</risdate><volume>21</volume><issue>3</issue><spage>538</spage><epage>545</epage><pages>538-545</pages><issn>1930-7381</issn><eissn>1930-739X</eissn><abstract>Objective:
Obesity is a prominent component of metabolic syndrome and a major risk factor for renal disease. The aim of this study was to explore the effect of cross‐talk between peroxisome proliferator‐activated receptor (PPAR)δ and p38 mitogen‐activated protein kinase (p38 MAPK) on obesity‐related glomerulopathy.
Design and Methods:
Male Wistar rats were randomly assigned to standard laboratory chow or a high‐fat diet for 32 weeks. Glomerular mesangial cells HBZY‐1 and mature differentiation 3T3‐L1 cells were cocultured and were transfected with PPARδ‐expressing vectors or treated with agonist or inhibitor of PPARδ or p38 MAPK.
Results:
Rats on a high‐fat diet showed typical characteristics of metabolic syndrome including obesity, dyslipidemia, insulin resistance, and hypertension. Rats on a high‐fat diet also had significant glomerular hypertrophy and extracellular matrix accumulation, which were accompanied by increased p38 MAPK phosphorylation and decreased PPARδ expression in the kidney tissue. The roles of p38 MAPK and PPARδ in a coculture system of mesangial cells and mature differentiation 3T3‐L1 cells were further explored. PPARδ suppression promoted laminin and type IV collagen secretion through p38 MAPK phosphorylation in mesangial cells, whereas PPARδ overexpression or PPARδ agonist attenuated phosphorylation of p38 MAPK and laminin and type IV collagen secretion.
Conclusions:
The characteristics of obesity‐related glomerulopathy, which might be partly caused by PPARδ suppression‐induced p38 MAPK activation and laminin and type IV collagen secretion was demonstrated.</abstract><cop>Hoboken, USA</cop><pub>John Wiley & Sons, Inc</pub><pmid>23592661</pmid><doi>10.1002/oby.20103</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Obesity (Silver Spring, Md.), 2013-03, Vol.21 (3), p.538-545 |
| issn | 1930-7381 1930-739X |
| language | eng |
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| source | Wiley-Blackwell Journals; MEDLINE; Wiley Free Archive |
| subjects | 3T3-L1 Cells Animals Blotting, Western Cell Differentiation Collagen - antagonists & inhibitors Collagen - metabolism Diet, High-Fat Glomerular Mesangium - cytology Glomerular Mesangium - pathology Glucose Immunohistochemistry Insulin Kidney - metabolism Kidney - pathology Kidney Diseases - etiology Kidney Diseases - pathology Kinases Laminin - antagonists & inhibitors Laminin - metabolism Male MAP Kinase Signaling System Mesangial Cells - metabolism Mesangial Cells - pathology Metabolic Syndrome - complications Metabolic Syndrome - physiopathology Mice Mitogen-Activated Protein Kinase 14 - genetics Mitogen-Activated Protein Kinase 14 - metabolism Obesity Obesity - complications Obesity - physiopathology Phosphorylation PPAR delta - genetics PPAR delta - metabolism Rats Rats, Wistar Rodents |
| title | Peroxisome proliferator‐activated receptor delta protects against obesity‐related glomerulopathy through the P38 MAPK pathway |
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