Chronic blockade of 20-HETE synthesis reduces polycystic kidney disease in an orthologous rat model of ARPKD
1 Department of Medicine, Division of Nephrology, Departments of 2 Physiology, 3 Pediatrics, 4 Children's Research Institute, and 5 Kidney Disease Center, Medical College of Wisconsin, Milwaukee, Wisconsin; and 6 Department of Biochemistry, University of Texas-Southwestern, Dallas, Texas Submit...
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| Veröffentlicht in: | American journal of physiology. Renal physiology 2009-03, Vol.296 (3), p.F575-F582 |
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| container_title | American journal of physiology. Renal physiology |
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| creator | Park, Frank Sweeney, William E., Jr Jia, Guangfu Akbulut, Talha Mueller, Benjamin Falck, J. Russell Birudaraju, Saritha Roman, Richard J Avner, Ellis D |
| description | 1 Department of Medicine, Division of Nephrology, Departments of 2 Physiology, 3 Pediatrics, 4 Children's Research Institute, and 5 Kidney Disease Center, Medical College of Wisconsin, Milwaukee, Wisconsin; and 6 Department of Biochemistry, University of Texas-Southwestern, Dallas, Texas
Submitted 24 November 2008
; accepted in final form 5 January 2009
20-Hydroxyeicosatetraenoic acid (20-HETE) has been implicated as a potential mediator in epithelial cell proliferation and cyst formation in polycystic kidney disease (PKD). In the present study, we studied the effects of chronic blockade of 20-HETE synthesis in an orthologous rodent model of autosomal recessive polycystic kidney disease (ARPKD), the PCK rat. RT-PCR analysis indicated that the expression of CYP4A1, CYP4A2, CYP4A3, and CYP4A8 mRNA was increased two- to fourfold in cystic PCK compared with noncystic Sprague-Dawley rat kidneys. Daily administration of a 20-HETE synthesis inhibitor, HET-0016 (10 mg·kg –1 ·day –1 ip) for 4–7 wk significantly reduced kidney size by 24% from 4.95 ± 0.19 g in vehicle-treated PCK rats to 3.76 ± 0.15 g ( n = 4). Collecting tubule morphometric cystic indices were reduced in HET-0016-treated PCK rats (2.1 ± 0.2; n = 4) compared with vehicle-treated PCK rats (4.4 ± 0.1; n = 4). The cellular mechanism by which 20-HETE may play a role in cyst formation has not been well characterized, but there was a significantly lower ( P < 0.05) level of intracellular cAMP and decreased phosphorylation (activation) of ERK1/2 protein in PCK rat kidneys ( n = 3) treated with HET-0016 . These studies indicate a potential role of 20-HETE in cyst formation in the orthologous rodent PCK model of ARPKD.
cytochrome P -450; HET-0016; epithelial cell proliferation; polycystic kidney rat; pck; autosomal recessive polycystic kidney mouse
Address for reprint requests and other correspondence: F. Park, Medical College of Wisconsin, 8701 Watertown Plank Rd., HRC 4100, Milwaukee, WI 53226 (e-mail: fpark{at}mcw.edu ) |
| doi_str_mv | 10.1152/ajprenal.90705.2008 |
| format | Article |
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Submitted 24 November 2008
; accepted in final form 5 January 2009
20-Hydroxyeicosatetraenoic acid (20-HETE) has been implicated as a potential mediator in epithelial cell proliferation and cyst formation in polycystic kidney disease (PKD). In the present study, we studied the effects of chronic blockade of 20-HETE synthesis in an orthologous rodent model of autosomal recessive polycystic kidney disease (ARPKD), the PCK rat. RT-PCR analysis indicated that the expression of CYP4A1, CYP4A2, CYP4A3, and CYP4A8 mRNA was increased two- to fourfold in cystic PCK compared with noncystic Sprague-Dawley rat kidneys. Daily administration of a 20-HETE synthesis inhibitor, HET-0016 (10 mg·kg –1 ·day –1 ip) for 4–7 wk significantly reduced kidney size by 24% from 4.95 ± 0.19 g in vehicle-treated PCK rats to 3.76 ± 0.15 g ( n = 4). Collecting tubule morphometric cystic indices were reduced in HET-0016-treated PCK rats (2.1 ± 0.2; n = 4) compared with vehicle-treated PCK rats (4.4 ± 0.1; n = 4). The cellular mechanism by which 20-HETE may play a role in cyst formation has not been well characterized, but there was a significantly lower ( P < 0.05) level of intracellular cAMP and decreased phosphorylation (activation) of ERK1/2 protein in PCK rat kidneys ( n = 3) treated with HET-0016 . These studies indicate a potential role of 20-HETE in cyst formation in the orthologous rodent PCK model of ARPKD.
cytochrome P -450; HET-0016; epithelial cell proliferation; polycystic kidney rat; pck; autosomal recessive polycystic kidney mouse
Address for reprint requests and other correspondence: F. Park, Medical College of Wisconsin, 8701 Watertown Plank Rd., HRC 4100, Milwaukee, WI 53226 (e-mail: fpark{at}mcw.edu )</description><identifier>ISSN: 0363-6127</identifier><identifier>ISSN: 1931-857X</identifier><identifier>EISSN: 2161-1157</identifier><identifier>EISSN: 1522-1466</identifier><identifier>DOI: 10.1152/ajprenal.90705.2008</identifier><identifier>PMID: 19129252</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>8,11,14-Eicosatrienoic Acid - analogs & derivatives ; 8,11,14-Eicosatrienoic Acid - metabolism ; Acids ; Amidines - pharmacology ; Animals ; Cyclic AMP - metabolism ; Cytochrome P-450 CYP4A - antagonists & inhibitors ; Disease Models, Animal ; Enzyme Activation ; Epoxy Compounds - metabolism ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Hydroxyeicosatetraenoic Acids - metabolism ; Kidney - pathology ; Kidney diseases ; Kidneys ; Male ; Microsomes - metabolism ; Nephrology ; Organ Size ; Polycystic Kidney, Autosomal Recessive - metabolism ; Polycystic Kidney, Autosomal Recessive - pathology ; Protein Isoforms - metabolism ; Rats ; Rats, Sprague-Dawley ; RNA, Messenger - metabolism ; Rodents</subject><ispartof>American journal of physiology. Renal physiology, 2009-03, Vol.296 (3), p.F575-F582</ispartof><rights>Copyright American Physiological Society Mar 2009</rights><rights>Copyright © 2009 the American Physiological Society 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c535t-d32c31ac0887d328b86ac94dd1eb3534e78a310fe3a03247e76405570f43d4d43</citedby><cites>FETCH-LOGICAL-c535t-d32c31ac0887d328b86ac94dd1eb3534e78a310fe3a03247e76405570f43d4d43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,778,782,883,3028,27911,27912</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19129252$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Park, Frank</creatorcontrib><creatorcontrib>Sweeney, William E., Jr</creatorcontrib><creatorcontrib>Jia, Guangfu</creatorcontrib><creatorcontrib>Akbulut, Talha</creatorcontrib><creatorcontrib>Mueller, Benjamin</creatorcontrib><creatorcontrib>Falck, J. Russell</creatorcontrib><creatorcontrib>Birudaraju, Saritha</creatorcontrib><creatorcontrib>Roman, Richard J</creatorcontrib><creatorcontrib>Avner, Ellis D</creatorcontrib><title>Chronic blockade of 20-HETE synthesis reduces polycystic kidney disease in an orthologous rat model of ARPKD</title><title>American journal of physiology. Renal physiology</title><addtitle>Am J Physiol Renal Physiol</addtitle><description>1 Department of Medicine, Division of Nephrology, Departments of 2 Physiology, 3 Pediatrics, 4 Children's Research Institute, and 5 Kidney Disease Center, Medical College of Wisconsin, Milwaukee, Wisconsin; and 6 Department of Biochemistry, University of Texas-Southwestern, Dallas, Texas
Submitted 24 November 2008
; accepted in final form 5 January 2009
20-Hydroxyeicosatetraenoic acid (20-HETE) has been implicated as a potential mediator in epithelial cell proliferation and cyst formation in polycystic kidney disease (PKD). In the present study, we studied the effects of chronic blockade of 20-HETE synthesis in an orthologous rodent model of autosomal recessive polycystic kidney disease (ARPKD), the PCK rat. RT-PCR analysis indicated that the expression of CYP4A1, CYP4A2, CYP4A3, and CYP4A8 mRNA was increased two- to fourfold in cystic PCK compared with noncystic Sprague-Dawley rat kidneys. Daily administration of a 20-HETE synthesis inhibitor, HET-0016 (10 mg·kg –1 ·day –1 ip) for 4–7 wk significantly reduced kidney size by 24% from 4.95 ± 0.19 g in vehicle-treated PCK rats to 3.76 ± 0.15 g ( n = 4). Collecting tubule morphometric cystic indices were reduced in HET-0016-treated PCK rats (2.1 ± 0.2; n = 4) compared with vehicle-treated PCK rats (4.4 ± 0.1; n = 4). The cellular mechanism by which 20-HETE may play a role in cyst formation has not been well characterized, but there was a significantly lower ( P < 0.05) level of intracellular cAMP and decreased phosphorylation (activation) of ERK1/2 protein in PCK rat kidneys ( n = 3) treated with HET-0016 . These studies indicate a potential role of 20-HETE in cyst formation in the orthologous rodent PCK model of ARPKD.
cytochrome P -450; HET-0016; epithelial cell proliferation; polycystic kidney rat; pck; autosomal recessive polycystic kidney mouse
Address for reprint requests and other correspondence: F. Park, Medical College of Wisconsin, 8701 Watertown Plank Rd., HRC 4100, Milwaukee, WI 53226 (e-mail: fpark{at}mcw.edu )</description><subject>8,11,14-Eicosatrienoic Acid - analogs & derivatives</subject><subject>8,11,14-Eicosatrienoic Acid - metabolism</subject><subject>Acids</subject><subject>Amidines - pharmacology</subject><subject>Animals</subject><subject>Cyclic AMP - metabolism</subject><subject>Cytochrome P-450 CYP4A - antagonists & inhibitors</subject><subject>Disease Models, Animal</subject><subject>Enzyme Activation</subject><subject>Epoxy Compounds - metabolism</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Hydroxyeicosatetraenoic Acids - metabolism</subject><subject>Kidney - pathology</subject><subject>Kidney diseases</subject><subject>Kidneys</subject><subject>Male</subject><subject>Microsomes - metabolism</subject><subject>Nephrology</subject><subject>Organ Size</subject><subject>Polycystic Kidney, Autosomal Recessive - metabolism</subject><subject>Polycystic Kidney, Autosomal Recessive - pathology</subject><subject>Protein Isoforms - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>RNA, Messenger - metabolism</subject><subject>Rodents</subject><issn>0363-6127</issn><issn>1931-857X</issn><issn>2161-1157</issn><issn>1522-1466</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkV1v0zAUhi0EYt3gFyAhiwvuUvyR2MkN0tR1G2ISCI1ry7VPGnduHOwElH-PSwsDrmzJz_vaxw9CryhZUlqxd3o3ROi1XzZEkmrJCKmfoAWjghb5XD5FC8IFLwRl8gydp7QjhDFRi-fojDaUNaxiC-RXXQy9M3jjg3nQFnBoMSPF7fp-jdPcjx0kl3AEOxlIeAh-NnMac-DB2R5mbF0CnQC7Husehzh2wYdtmHJGj3gfLPhD5eWXzx-vXqBnrfYJXp7WC_T1en2_ui3uPt18WF3eFabi1VhYzgyn2pC6lnlfb2qhTVNaS2HDK16CrDWnpAWuCWelBClKUlWStCW3pS35BXp_7B2mzR6sgX6M2qshur2OswraqX9PetepbfiumBCENnUueHsqiOHbBGlUe5cMeK97yKMpIRqe75QZfPMfuAtTzFKSYpxQxinlGeJHyMSQUoT2z0soUQeV6rdK9UulOqjMqdd_D_GYObnLwPIIdG7b_XAR1NDNyR2-f35sZI1QXF1XsuI_AVSArSM</recordid><startdate>20090301</startdate><enddate>20090301</enddate><creator>Park, Frank</creator><creator>Sweeney, William E., Jr</creator><creator>Jia, Guangfu</creator><creator>Akbulut, Talha</creator><creator>Mueller, Benjamin</creator><creator>Falck, J. Russell</creator><creator>Birudaraju, Saritha</creator><creator>Roman, Richard J</creator><creator>Avner, Ellis D</creator><general>American Physiological Society</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>5PM</scope></search><sort><creationdate>20090301</creationdate><title>Chronic blockade of 20-HETE synthesis reduces polycystic kidney disease in an orthologous rat model of ARPKD</title><author>Park, Frank ; Sweeney, William E., Jr ; Jia, Guangfu ; Akbulut, Talha ; Mueller, Benjamin ; Falck, J. Russell ; Birudaraju, Saritha ; Roman, Richard J ; Avner, Ellis D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c535t-d32c31ac0887d328b86ac94dd1eb3534e78a310fe3a03247e76405570f43d4d43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>8,11,14-Eicosatrienoic Acid - analogs & derivatives</topic><topic>8,11,14-Eicosatrienoic Acid - metabolism</topic><topic>Acids</topic><topic>Amidines - pharmacology</topic><topic>Animals</topic><topic>Cyclic AMP - metabolism</topic><topic>Cytochrome P-450 CYP4A - antagonists & inhibitors</topic><topic>Disease Models, Animal</topic><topic>Enzyme Activation</topic><topic>Epoxy Compounds - metabolism</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>Hydroxyeicosatetraenoic Acids - metabolism</topic><topic>Kidney - pathology</topic><topic>Kidney diseases</topic><topic>Kidneys</topic><topic>Male</topic><topic>Microsomes - metabolism</topic><topic>Nephrology</topic><topic>Organ Size</topic><topic>Polycystic Kidney, Autosomal Recessive - metabolism</topic><topic>Polycystic Kidney, Autosomal Recessive - pathology</topic><topic>Protein Isoforms - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>RNA, Messenger - metabolism</topic><topic>Rodents</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Park, Frank</creatorcontrib><creatorcontrib>Sweeney, William E., Jr</creatorcontrib><creatorcontrib>Jia, Guangfu</creatorcontrib><creatorcontrib>Akbulut, Talha</creatorcontrib><creatorcontrib>Mueller, Benjamin</creatorcontrib><creatorcontrib>Falck, J. Russell</creatorcontrib><creatorcontrib>Birudaraju, Saritha</creatorcontrib><creatorcontrib>Roman, Richard J</creatorcontrib><creatorcontrib>Avner, Ellis D</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>PubMed Central (Full Participant titles)</collection><jtitle>American journal of physiology. Renal physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Park, Frank</au><au>Sweeney, William E., Jr</au><au>Jia, Guangfu</au><au>Akbulut, Talha</au><au>Mueller, Benjamin</au><au>Falck, J. Russell</au><au>Birudaraju, Saritha</au><au>Roman, Richard J</au><au>Avner, Ellis D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chronic blockade of 20-HETE synthesis reduces polycystic kidney disease in an orthologous rat model of ARPKD</atitle><jtitle>American journal of physiology. Renal physiology</jtitle><addtitle>Am J Physiol Renal Physiol</addtitle><date>2009-03-01</date><risdate>2009</risdate><volume>296</volume><issue>3</issue><spage>F575</spage><epage>F582</epage><pages>F575-F582</pages><issn>0363-6127</issn><issn>1931-857X</issn><eissn>2161-1157</eissn><eissn>1522-1466</eissn><abstract>1 Department of Medicine, Division of Nephrology, Departments of 2 Physiology, 3 Pediatrics, 4 Children's Research Institute, and 5 Kidney Disease Center, Medical College of Wisconsin, Milwaukee, Wisconsin; and 6 Department of Biochemistry, University of Texas-Southwestern, Dallas, Texas
Submitted 24 November 2008
; accepted in final form 5 January 2009
20-Hydroxyeicosatetraenoic acid (20-HETE) has been implicated as a potential mediator in epithelial cell proliferation and cyst formation in polycystic kidney disease (PKD). In the present study, we studied the effects of chronic blockade of 20-HETE synthesis in an orthologous rodent model of autosomal recessive polycystic kidney disease (ARPKD), the PCK rat. RT-PCR analysis indicated that the expression of CYP4A1, CYP4A2, CYP4A3, and CYP4A8 mRNA was increased two- to fourfold in cystic PCK compared with noncystic Sprague-Dawley rat kidneys. Daily administration of a 20-HETE synthesis inhibitor, HET-0016 (10 mg·kg –1 ·day –1 ip) for 4–7 wk significantly reduced kidney size by 24% from 4.95 ± 0.19 g in vehicle-treated PCK rats to 3.76 ± 0.15 g ( n = 4). Collecting tubule morphometric cystic indices were reduced in HET-0016-treated PCK rats (2.1 ± 0.2; n = 4) compared with vehicle-treated PCK rats (4.4 ± 0.1; n = 4). The cellular mechanism by which 20-HETE may play a role in cyst formation has not been well characterized, but there was a significantly lower ( P < 0.05) level of intracellular cAMP and decreased phosphorylation (activation) of ERK1/2 protein in PCK rat kidneys ( n = 3) treated with HET-0016 . These studies indicate a potential role of 20-HETE in cyst formation in the orthologous rodent PCK model of ARPKD.
cytochrome P -450; HET-0016; epithelial cell proliferation; polycystic kidney rat; pck; autosomal recessive polycystic kidney mouse
Address for reprint requests and other correspondence: F. Park, Medical College of Wisconsin, 8701 Watertown Plank Rd., HRC 4100, Milwaukee, WI 53226 (e-mail: fpark{at}mcw.edu )</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>19129252</pmid><doi>10.1152/ajprenal.90705.2008</doi><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0363-6127 |
| ispartof | American journal of physiology. Renal physiology, 2009-03, Vol.296 (3), p.F575-F582 |
| issn | 0363-6127 1931-857X 2161-1157 1522-1466 |
| language | eng |
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| source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | 8,11,14-Eicosatrienoic Acid - analogs & derivatives 8,11,14-Eicosatrienoic Acid - metabolism Acids Amidines - pharmacology Animals Cyclic AMP - metabolism Cytochrome P-450 CYP4A - antagonists & inhibitors Disease Models, Animal Enzyme Activation Epoxy Compounds - metabolism Extracellular Signal-Regulated MAP Kinases - metabolism Hydroxyeicosatetraenoic Acids - metabolism Kidney - pathology Kidney diseases Kidneys Male Microsomes - metabolism Nephrology Organ Size Polycystic Kidney, Autosomal Recessive - metabolism Polycystic Kidney, Autosomal Recessive - pathology Protein Isoforms - metabolism Rats Rats, Sprague-Dawley RNA, Messenger - metabolism Rodents |
| title | Chronic blockade of 20-HETE synthesis reduces polycystic kidney disease in an orthologous rat model of ARPKD |
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