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A natural PPAR-γ agonist, 15-deoxy-delta 12,14-prostaglandin J2, may act as an enhancer of PAI-1 in human proximal renal tubular cells under hypoxic and inflammatory conditions

Background. Hypoxia and inflammation, an unavoidable milieu for renal tubular cells during the development of renal fibrosis, reportedly up-regulate production of plasminogen activator inhibitor-1 (PAI-1), a promoter of tissue fibrosis. Peroxisome proliferator-activated receptor (PPAR)-γ agonists ma...

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Published in:Nephrology, dialysis, transplantation dialysis, transplantation, 2008-08, Vol.23 (8), p.2496-2503
Main Authors: Kimura, Hideki, Li, Xuan, Torii, Kunio, Okada, Toshiharu, Takahashi, Naoki, Fujii, Hiroshi, Ishihara, Shunji, Yoshida, Haruyoshi
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container_issue 8
container_start_page 2496
container_title Nephrology, dialysis, transplantation
container_volume 23
creator Kimura, Hideki
Li, Xuan
Torii, Kunio
Okada, Toshiharu
Takahashi, Naoki
Fujii, Hiroshi
Ishihara, Shunji
Yoshida, Haruyoshi
description Background. Hypoxia and inflammation, an unavoidable milieu for renal tubular cells during the development of renal fibrosis, reportedly up-regulate production of plasminogen activator inhibitor-1 (PAI-1), a promoter of tissue fibrosis. Peroxisome proliferator-activated receptor (PPAR)-γ agonists may modulate renal fibrosis progression via their anti-inflammatory effects in a PPAR-γ-dependent or -independent manner. However, no information is known about the effects of PPAR-γ agonists on PAI-1 expression in human proximal renal tubular cells (HPTECs) under hypoxia and/or inflammation. Methods. Confluent HPTECs were exposed to normoxia (18% O2), hypoxia (1% O2) and/or TNF-α at 10 ng/mL for up to 48 h. The cells were incubated with two PPAR-γ ago- nists, 15-deoxy-delta 12,14-prostaglandin J2 (15d-PGJ2) and pioglitazone. Precise amounts of PAI-1 mRNA and protein were measured by TaqMan quantitative PCR and immunoassay, respectively. PPAR response element (PPRE) activity induced by 15d-PGJ2 was measured by transfection with PPRE-luciferase construct. Results. Basal PAI-1 was significantly increased, in a dose-dependent manner, by 15d-PGJ2. It also enhanced hypoxia-, TNF-α- and hypoxia plus TNF-α-stimulated PAI-1 expression at the mRNA and protein levels. Pioglitazone had no influence on PAI-1 protein production. Although 15d-PGJ2 enhanced PPRE activity significantly in the HPTECs expressing PPAR-γ, a specific inhibitor for PPAR-γ, GW9662, did not diminish 15d-PGJ2-induced PAI-1 expression. In contrast, a non-selective tyrosine kinase (TK) inhibitor, genisteine or a MEK1 (MAPK kinase) inhibitor, PD98059, inhibited 15d-PGJ2-induced PAI-1 production completely. Conclusions. The endogenous PPAR-γ agonist, 15d-PGJ2, increased PAI-1 expression independently of PPAR-γ via the activation of TK or MAP kinase in HPTECs and may act as an enhancer of PAI-1 production in the kidney under hypoxic and inflammatory conditions.
doi_str_mv 10.1093/ndt/gfn139
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Hypoxia and inflammation, an unavoidable milieu for renal tubular cells during the development of renal fibrosis, reportedly up-regulate production of plasminogen activator inhibitor-1 (PAI-1), a promoter of tissue fibrosis. Peroxisome proliferator-activated receptor (PPAR)-γ agonists may modulate renal fibrosis progression via their anti-inflammatory effects in a PPAR-γ-dependent or -independent manner. However, no information is known about the effects of PPAR-γ agonists on PAI-1 expression in human proximal renal tubular cells (HPTECs) under hypoxia and/or inflammation. Methods. Confluent HPTECs were exposed to normoxia (18% O2), hypoxia (1% O2) and/or TNF-α at 10 ng/mL for up to 48 h. The cells were incubated with two PPAR-γ ago- nists, 15-deoxy-delta 12,14-prostaglandin J2 (15d-PGJ2) and pioglitazone. Precise amounts of PAI-1 mRNA and protein were measured by TaqMan quantitative PCR and immunoassay, respectively. PPAR response element (PPRE) activity induced by 15d-PGJ2 was measured by transfection with PPRE-luciferase construct. Results. Basal PAI-1 was significantly increased, in a dose-dependent manner, by 15d-PGJ2. It also enhanced hypoxia-, TNF-α- and hypoxia plus TNF-α-stimulated PAI-1 expression at the mRNA and protein levels. Pioglitazone had no influence on PAI-1 protein production. Although 15d-PGJ2 enhanced PPRE activity significantly in the HPTECs expressing PPAR-γ, a specific inhibitor for PPAR-γ, GW9662, did not diminish 15d-PGJ2-induced PAI-1 expression. In contrast, a non-selective tyrosine kinase (TK) inhibitor, genisteine or a MEK1 (MAPK kinase) inhibitor, PD98059, inhibited 15d-PGJ2-induced PAI-1 production completely. Conclusions. The endogenous PPAR-γ agonist, 15d-PGJ2, increased PAI-1 expression independently of PPAR-γ via the activation of TK or MAP kinase in HPTECs and may act as an enhancer of PAI-1 production in the kidney under hypoxic and inflammatory conditions.</description><identifier>ISSN: 0931-0509</identifier><identifier>EISSN: 1460-2385</identifier><identifier>DOI: 10.1093/ndt/gfn139</identifier><identifier>PMID: 18367541</identifier><identifier>CODEN: NDTREA</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>15d-PGJ2 ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Biological and medical sciences ; Cell Hypoxia ; Cells, Cultured ; Emergency and intensive care: renal failure. Dialysis management ; Flavonoids - pharmacology ; Genistein - pharmacology ; human proximal tubular cells ; Humans ; hypoxia ; Inflammation - metabolism ; Inflammation - pathology ; Intensive care medicine ; Kidney Tubules, Proximal - drug effects ; Kidney Tubules, Proximal - metabolism ; Kidney Tubules, Proximal - pathology ; MAP Kinase Kinase 1 - antagonists &amp; inhibitors ; Medical sciences ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; PAI-1 ; Plasminogen Activator Inhibitor 1 - biosynthesis ; Plasminogen Activator Inhibitor 1 - genetics ; PPAR gamma - agonists ; PPAR-γ ; Prostaglandin D2 - analogs &amp; derivatives ; Prostaglandin D2 - pharmacology ; Protein Kinase Inhibitors - pharmacology ; Protein-Tyrosine Kinases - antagonists &amp; inhibitors ; Renal failure ; Thiazolidinediones - pharmacology ; Tumor Necrosis Factor-alpha - pharmacology</subject><ispartof>Nephrology, dialysis, transplantation, 2008-08, Vol.23 (8), p.2496-2503</ispartof><rights>Oxford University Press © The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org 2008</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=20577776$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18367541$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kimura, Hideki</creatorcontrib><creatorcontrib>Li, Xuan</creatorcontrib><creatorcontrib>Torii, Kunio</creatorcontrib><creatorcontrib>Okada, Toshiharu</creatorcontrib><creatorcontrib>Takahashi, Naoki</creatorcontrib><creatorcontrib>Fujii, Hiroshi</creatorcontrib><creatorcontrib>Ishihara, Shunji</creatorcontrib><creatorcontrib>Yoshida, Haruyoshi</creatorcontrib><title>A natural PPAR-γ agonist, 15-deoxy-delta 12,14-prostaglandin J2, may act as an enhancer of PAI-1 in human proximal renal tubular cells under hypoxic and inflammatory conditions</title><title>Nephrology, dialysis, transplantation</title><addtitle>Nephrol Dial Transplant</addtitle><addtitle>Nephrol Dial Transplant</addtitle><description>Background. Hypoxia and inflammation, an unavoidable milieu for renal tubular cells during the development of renal fibrosis, reportedly up-regulate production of plasminogen activator inhibitor-1 (PAI-1), a promoter of tissue fibrosis. Peroxisome proliferator-activated receptor (PPAR)-γ agonists may modulate renal fibrosis progression via their anti-inflammatory effects in a PPAR-γ-dependent or -independent manner. However, no information is known about the effects of PPAR-γ agonists on PAI-1 expression in human proximal renal tubular cells (HPTECs) under hypoxia and/or inflammation. Methods. Confluent HPTECs were exposed to normoxia (18% O2), hypoxia (1% O2) and/or TNF-α at 10 ng/mL for up to 48 h. The cells were incubated with two PPAR-γ ago- nists, 15-deoxy-delta 12,14-prostaglandin J2 (15d-PGJ2) and pioglitazone. Precise amounts of PAI-1 mRNA and protein were measured by TaqMan quantitative PCR and immunoassay, respectively. PPAR response element (PPRE) activity induced by 15d-PGJ2 was measured by transfection with PPRE-luciferase construct. Results. Basal PAI-1 was significantly increased, in a dose-dependent manner, by 15d-PGJ2. It also enhanced hypoxia-, TNF-α- and hypoxia plus TNF-α-stimulated PAI-1 expression at the mRNA and protein levels. Pioglitazone had no influence on PAI-1 protein production. Although 15d-PGJ2 enhanced PPRE activity significantly in the HPTECs expressing PPAR-γ, a specific inhibitor for PPAR-γ, GW9662, did not diminish 15d-PGJ2-induced PAI-1 expression. In contrast, a non-selective tyrosine kinase (TK) inhibitor, genisteine or a MEK1 (MAPK kinase) inhibitor, PD98059, inhibited 15d-PGJ2-induced PAI-1 production completely. Conclusions. The endogenous PPAR-γ agonist, 15d-PGJ2, increased PAI-1 expression independently of PPAR-γ via the activation of TK or MAP kinase in HPTECs and may act as an enhancer of PAI-1 production in the kidney under hypoxic and inflammatory conditions.</description><subject>15d-PGJ2</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Biological and medical sciences</subject><subject>Cell Hypoxia</subject><subject>Cells, Cultured</subject><subject>Emergency and intensive care: renal failure. Dialysis management</subject><subject>Flavonoids - pharmacology</subject><subject>Genistein - pharmacology</subject><subject>human proximal tubular cells</subject><subject>Humans</subject><subject>hypoxia</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - pathology</subject><subject>Intensive care medicine</subject><subject>Kidney Tubules, Proximal - drug effects</subject><subject>Kidney Tubules, Proximal - metabolism</subject><subject>Kidney Tubules, Proximal - pathology</subject><subject>MAP Kinase Kinase 1 - antagonists &amp; inhibitors</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>PAI-1</subject><subject>Plasminogen Activator Inhibitor 1 - biosynthesis</subject><subject>Plasminogen Activator Inhibitor 1 - genetics</subject><subject>PPAR gamma - agonists</subject><subject>PPAR-γ</subject><subject>Prostaglandin D2 - analogs &amp; derivatives</subject><subject>Prostaglandin D2 - pharmacology</subject><subject>Protein Kinase Inhibitors - pharmacology</subject><subject>Protein-Tyrosine Kinases - antagonists &amp; inhibitors</subject><subject>Renal failure</subject><subject>Thiazolidinediones - pharmacology</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><issn>0931-0509</issn><issn>1460-2385</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><recordid>eNpFkc1u1DAQxyMEokvhwgMgX-C0puM4juPjqny0qIgVFKniYk0SZzeQONvYkTaPhXgPnompdml9GB_m95-vf5K8FPBWgJFnvo5nm8YLaR4lC5HlwFNZqMfJgpKCgwJzkjwL4ScAmFTrp8mJKGSuVSYWye8V8xinETu2Xq--8r9_GG4G34a4ZELx2g37mWIXkYl0KTK-G4cQcdOhr1vPPqVL1uPMsIoMA0PPnN-ir9zIhoatV5dcMMK2U08pku7bnjqNzlOMUzl1OLLKdV1gk69JtJ13xFRUqCZd02HfYxzGmVUD9Yvt4MPz5EmDXXAvjv9p8v3D--vzC3715ePl-eqKtxJ05JVrcsiVUaKRUouyUcLUKVSp0VAYXWQFVlIbrTQWaQMG6qIEKF0GRqAshDxN3hzq0ti3kwvR9m24mxW9G6ZgcyOVMQIIfHUEp7J3td2NtOQ42_9HJuD1EcBQYdeMdKA23HMpKE0vf-CGafdQBeydyZZMtgeTieMHjlxy-3sSx18211Ire3Hzw36-1vIbvNP2Rv4DGBWmuQ</recordid><startdate>20080801</startdate><enddate>20080801</enddate><creator>Kimura, Hideki</creator><creator>Li, Xuan</creator><creator>Torii, Kunio</creator><creator>Okada, Toshiharu</creator><creator>Takahashi, Naoki</creator><creator>Fujii, Hiroshi</creator><creator>Ishihara, Shunji</creator><creator>Yoshida, Haruyoshi</creator><general>Oxford University Press</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20080801</creationdate><title>A natural PPAR-γ agonist, 15-deoxy-delta 12,14-prostaglandin J2, may act as an enhancer of PAI-1 in human proximal renal tubular cells under hypoxic and inflammatory conditions</title><author>Kimura, Hideki ; Li, Xuan ; Torii, Kunio ; Okada, Toshiharu ; Takahashi, Naoki ; Fujii, Hiroshi ; Ishihara, Shunji ; Yoshida, Haruyoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-i307t-cef6065951f3371bf519d20c2970897848ac379757a82f090d8b00be4091a3813</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>15d-PGJ2</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Biological and medical sciences</topic><topic>Cell Hypoxia</topic><topic>Cells, Cultured</topic><topic>Emergency and intensive care: renal failure. Dialysis management</topic><topic>Flavonoids - pharmacology</topic><topic>Genistein - pharmacology</topic><topic>human proximal tubular cells</topic><topic>Humans</topic><topic>hypoxia</topic><topic>Inflammation - metabolism</topic><topic>Inflammation - pathology</topic><topic>Intensive care medicine</topic><topic>Kidney Tubules, Proximal - drug effects</topic><topic>Kidney Tubules, Proximal - metabolism</topic><topic>Kidney Tubules, Proximal - pathology</topic><topic>MAP Kinase Kinase 1 - antagonists &amp; inhibitors</topic><topic>Medical sciences</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>PAI-1</topic><topic>Plasminogen Activator Inhibitor 1 - biosynthesis</topic><topic>Plasminogen Activator Inhibitor 1 - genetics</topic><topic>PPAR gamma - agonists</topic><topic>PPAR-γ</topic><topic>Prostaglandin D2 - analogs &amp; derivatives</topic><topic>Prostaglandin D2 - pharmacology</topic><topic>Protein Kinase Inhibitors - pharmacology</topic><topic>Protein-Tyrosine Kinases - antagonists &amp; inhibitors</topic><topic>Renal failure</topic><topic>Thiazolidinediones - pharmacology</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kimura, Hideki</creatorcontrib><creatorcontrib>Li, Xuan</creatorcontrib><creatorcontrib>Torii, Kunio</creatorcontrib><creatorcontrib>Okada, Toshiharu</creatorcontrib><creatorcontrib>Takahashi, Naoki</creatorcontrib><creatorcontrib>Fujii, Hiroshi</creatorcontrib><creatorcontrib>Ishihara, Shunji</creatorcontrib><creatorcontrib>Yoshida, Haruyoshi</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Nephrology, dialysis, transplantation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kimura, Hideki</au><au>Li, Xuan</au><au>Torii, Kunio</au><au>Okada, Toshiharu</au><au>Takahashi, Naoki</au><au>Fujii, Hiroshi</au><au>Ishihara, Shunji</au><au>Yoshida, Haruyoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A natural PPAR-γ agonist, 15-deoxy-delta 12,14-prostaglandin J2, may act as an enhancer of PAI-1 in human proximal renal tubular cells under hypoxic and inflammatory conditions</atitle><jtitle>Nephrology, dialysis, transplantation</jtitle><stitle>Nephrol Dial Transplant</stitle><addtitle>Nephrol Dial Transplant</addtitle><date>2008-08-01</date><risdate>2008</risdate><volume>23</volume><issue>8</issue><spage>2496</spage><epage>2503</epage><pages>2496-2503</pages><issn>0931-0509</issn><eissn>1460-2385</eissn><coden>NDTREA</coden><abstract>Background. Hypoxia and inflammation, an unavoidable milieu for renal tubular cells during the development of renal fibrosis, reportedly up-regulate production of plasminogen activator inhibitor-1 (PAI-1), a promoter of tissue fibrosis. Peroxisome proliferator-activated receptor (PPAR)-γ agonists may modulate renal fibrosis progression via their anti-inflammatory effects in a PPAR-γ-dependent or -independent manner. However, no information is known about the effects of PPAR-γ agonists on PAI-1 expression in human proximal renal tubular cells (HPTECs) under hypoxia and/or inflammation. Methods. Confluent HPTECs were exposed to normoxia (18% O2), hypoxia (1% O2) and/or TNF-α at 10 ng/mL for up to 48 h. The cells were incubated with two PPAR-γ ago- nists, 15-deoxy-delta 12,14-prostaglandin J2 (15d-PGJ2) and pioglitazone. Precise amounts of PAI-1 mRNA and protein were measured by TaqMan quantitative PCR and immunoassay, respectively. PPAR response element (PPRE) activity induced by 15d-PGJ2 was measured by transfection with PPRE-luciferase construct. Results. Basal PAI-1 was significantly increased, in a dose-dependent manner, by 15d-PGJ2. It also enhanced hypoxia-, TNF-α- and hypoxia plus TNF-α-stimulated PAI-1 expression at the mRNA and protein levels. Pioglitazone had no influence on PAI-1 protein production. Although 15d-PGJ2 enhanced PPRE activity significantly in the HPTECs expressing PPAR-γ, a specific inhibitor for PPAR-γ, GW9662, did not diminish 15d-PGJ2-induced PAI-1 expression. In contrast, a non-selective tyrosine kinase (TK) inhibitor, genisteine or a MEK1 (MAPK kinase) inhibitor, PD98059, inhibited 15d-PGJ2-induced PAI-1 production completely. Conclusions. The endogenous PPAR-γ agonist, 15d-PGJ2, increased PAI-1 expression independently of PPAR-γ via the activation of TK or MAP kinase in HPTECs and may act as an enhancer of PAI-1 production in the kidney under hypoxic and inflammatory conditions.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>18367541</pmid><doi>10.1093/ndt/gfn139</doi><tpages>8</tpages></addata></record>
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subjects 15d-PGJ2
Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy
Biological and medical sciences
Cell Hypoxia
Cells, Cultured
Emergency and intensive care: renal failure. Dialysis management
Flavonoids - pharmacology
Genistein - pharmacology
human proximal tubular cells
Humans
hypoxia
Inflammation - metabolism
Inflammation - pathology
Intensive care medicine
Kidney Tubules, Proximal - drug effects
Kidney Tubules, Proximal - metabolism
Kidney Tubules, Proximal - pathology
MAP Kinase Kinase 1 - antagonists & inhibitors
Medical sciences
Nephrology. Urinary tract diseases
Nephropathies. Renovascular diseases. Renal failure
PAI-1
Plasminogen Activator Inhibitor 1 - biosynthesis
Plasminogen Activator Inhibitor 1 - genetics
PPAR gamma - agonists
PPAR-γ
Prostaglandin D2 - analogs & derivatives
Prostaglandin D2 - pharmacology
Protein Kinase Inhibitors - pharmacology
Protein-Tyrosine Kinases - antagonists & inhibitors
Renal failure
Thiazolidinediones - pharmacology
Tumor Necrosis Factor-alpha - pharmacology
title A natural PPAR-γ agonist, 15-deoxy-delta 12,14-prostaglandin J2, may act as an enhancer of PAI-1 in human proximal renal tubular cells under hypoxic and inflammatory conditions
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