Role of heat shock protein 47 on tubulointerstitium in experimental radiation nephropathy
Identifieur interne : 000471 ( Istex/Corpus ); précédent : 000470; suivant : 000472Role of heat shock protein 47 on tubulointerstitium in experimental radiation nephropathy
Auteurs : Diange Liu ; Mohammed S. Razzaque ; Arifa Nazneen ; Takashi Naito ; Takashi TaguchiSource :
- Pathology International [ 1320-5463 ] ; 2002-05.
English descriptors
- Teeft :
- Actin, Arterial pressure, Blood urea nitrogen, Brosis, Brotic, Brotic areas, Cell tissue, Cellular basis, Collagen, Collagen synthesis, Collagen type, Colocalization, Control rats, Creatinine, Double immunostaining, Double staining, Epithelial, Experimental radiation nephropathy, Glomerular, Glomerular cells, Glomerular lesions, Glomerulus, Glomerulus time, Heat shock protein, High dose, Histological, Histological changes, Histological lesion, Immunohistochemical examination, Immunohistochemical staining, Immunostaining, Interstitial, Interstitial cells, Interstitial collagens, Kidney, Lesion, Molecular chaperone, Nagasaki university school, Nephropathy, Ninth month, Present study, Previous studies, Primary antibodies, Radiation exposure, Radiation nephritis, Radiation nephropathy, Radiation procedures, Rat, Razzaque, Recent studies, Renal, Renal cells, Renal dysfunction, Renal injury, Renal lesions, Scant attention, Sclerotic area, Sclerotic glomeruli, Second staining, Serum creatinine, Single exposure, Sixth month, Smooth muscle, Smooth muscle actin, Stress protein, Stressgene biotechnologies, Taguchi, Takashi taguchi, Time course, Transcriptional activation, Tubular, Tubular basement membrane, Tubular epithelial cells, Tubulointerstitial, Tubulointerstitial injuries, Tubulointerstitium vessel, Vascular wall, Vimentin.
Abstract
The molecular mechanisms of fibrosis in radiation nephropathy have received scant attention. Heat shock protein 47 (HSP47), a collagen‐binding stress protein, helps in the intracellular processing of procollagen molecules during collagen synthesis. We investigated the role of HSP47 in the progression of radiation nephropathy using experimental radiation nephropathy. Experimental rat groups were as follows: (i) group I, sham operated (n = 12); (ii) group II, single doses of irradiation, either 7, 15 or 25 Gy to left kidney (n = 60); and (iii) group III, a similar irradiation procedure as group II after right nephrectomy (n = 60). The rats were followed up until 9 months after renal exposure to radiation. Renal dysfunction (as determined by serum creatinine and blood urea nitrogen) and hypertension were noted in group III rats, along with inflammatory cell infiltration and interstitial fibrosis (as determined by increased deposition of collagens). Compared to control rat kidneys, an increased expression of HSP47 was noted in kidneys obtained from irradiated rats. By double immunostaining, HSP47‐expressing cells were identified as α‐smooth muscle actin‐positive myofibroblasts and vimentin‐positive tubular epithelial cells. Increased expression of HSP47 was closely associated with increased deposition of collagens in the widened interstitium of irradiated rats. Overexpression of HSP47 by phenotypically altered tubulointerstitial cells might play a role in excessive assembly/synthesis of collagens and could contribute to tubulointerstitial fibrosis in radiation nephropathy.
Url:
DOI: 10.1046/j.1440-1827.2002.01362.x
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ISTEX:11218936D4EBF6D2495C6C0A35020D3C6071A4EELe document en format XML
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Razzaque</name><affiliation><mods:affiliation>Second Department of Pathology, Nagasaki University School of Medicine, Nagasaki, Japan</mods:affiliation></affiliation></author><author><name sortKey="Nazneen, Arifa" sort="Nazneen, Arifa" uniqKey="Nazneen A" first="Arifa" last="Nazneen">Arifa Nazneen</name><affiliation><mods:affiliation>Second Department of Pathology, Nagasaki University School of Medicine, Nagasaki, Japan</mods:affiliation></affiliation></author><author><name sortKey="Naito, Takashi" sort="Naito, Takashi" uniqKey="Naito T" first="Takashi" last="Naito">Takashi Naito</name><affiliation><mods:affiliation>Second Department of Pathology, Nagasaki University School of Medicine, Nagasaki, Japan</mods:affiliation></affiliation></author><author><name sortKey="Taguchi, Takashi" sort="Taguchi, Takashi" uniqKey="Taguchi T" first="Takashi" last="Taguchi">Takashi Taguchi</name><affiliation><mods:affiliation>Second Department of Pathology, Nagasaki University School of Medicine, Nagasaki, Japan</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:11218936D4EBF6D2495C6C0A35020D3C6071A4EE</idno><date when="2002" year="2002">2002</date><idno type="doi">10.1046/j.1440-1827.2002.01362.x</idno><idno type="url">https://api.istex.fr/ark:/67375/WNG-BP569W16-Z/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000471</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000471</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main">Role of heat shock protein 47 on tubulointerstitium in experimental radiation nephropathy</title><author><name sortKey="Liu, Diange" sort="Liu, Diange" uniqKey="Liu D" first="Diange" last="Liu">Diange Liu</name><affiliation><mods:affiliation>Second Department of Pathology, Nagasaki University School of Medicine, Nagasaki, Japan</mods:affiliation></affiliation></author><author><name sortKey="Razzaque, Mohammed S" sort="Razzaque, Mohammed S" uniqKey="Razzaque M" first="Mohammed S." last="Razzaque">Mohammed S. Razzaque</name><affiliation><mods:affiliation>Second Department of Pathology, Nagasaki University School of Medicine, Nagasaki, Japan</mods:affiliation></affiliation></author><author><name sortKey="Nazneen, Arifa" sort="Nazneen, Arifa" uniqKey="Nazneen A" first="Arifa" last="Nazneen">Arifa Nazneen</name><affiliation><mods:affiliation>Second Department of Pathology, Nagasaki University School of Medicine, Nagasaki, Japan</mods:affiliation></affiliation></author><author><name sortKey="Naito, Takashi" sort="Naito, Takashi" uniqKey="Naito T" first="Takashi" last="Naito">Takashi Naito</name><affiliation><mods:affiliation>Second Department of Pathology, Nagasaki University School of Medicine, Nagasaki, Japan</mods:affiliation></affiliation></author><author><name sortKey="Taguchi, Takashi" sort="Taguchi, Takashi" uniqKey="Taguchi T" first="Takashi" last="Taguchi">Takashi Taguchi</name><affiliation><mods:affiliation>Second Department of Pathology, Nagasaki University School of Medicine, Nagasaki, Japan</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Pathology International</title><title level="j" type="alt">PATHOLOGY INTERNATIONAL</title><idno type="ISSN">1320-5463</idno><idno type="eISSN">1440-1827</idno><imprint><biblScope unit="vol">52</biblScope><biblScope unit="issue">5‐6</biblScope><biblScope unit="page" from="340">340</biblScope><biblScope unit="page" to="347">347</biblScope><biblScope unit="page-count">8</biblScope><publisher>Blackwell Science Pty</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2002-05">2002-05</date></imprint><idno type="ISSN">1320-5463</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1320-5463</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Actin</term><term>Arterial pressure</term><term>Blood urea nitrogen</term><term>Brosis</term><term>Brotic</term><term>Brotic areas</term><term>Cell tissue</term><term>Cellular basis</term><term>Collagen</term><term>Collagen synthesis</term><term>Collagen type</term><term>Colocalization</term><term>Control rats</term><term>Creatinine</term><term>Double immunostaining</term><term>Double staining</term><term>Epithelial</term><term>Experimental radiation nephropathy</term><term>Glomerular</term><term>Glomerular cells</term><term>Glomerular lesions</term><term>Glomerulus</term><term>Glomerulus time</term><term>Heat shock protein</term><term>High dose</term><term>Histological</term><term>Histological changes</term><term>Histological lesion</term><term>Immunohistochemical examination</term><term>Immunohistochemical staining</term><term>Immunostaining</term><term>Interstitial</term><term>Interstitial cells</term><term>Interstitial collagens</term><term>Kidney</term><term>Lesion</term><term>Molecular chaperone</term><term>Nagasaki university school</term><term>Nephropathy</term><term>Ninth month</term><term>Present study</term><term>Previous studies</term><term>Primary antibodies</term><term>Radiation exposure</term><term>Radiation nephritis</term><term>Radiation nephropathy</term><term>Radiation procedures</term><term>Rat</term><term>Razzaque</term><term>Recent studies</term><term>Renal</term><term>Renal cells</term><term>Renal dysfunction</term><term>Renal injury</term><term>Renal lesions</term><term>Scant attention</term><term>Sclerotic area</term><term>Sclerotic glomeruli</term><term>Second staining</term><term>Serum creatinine</term><term>Single exposure</term><term>Sixth month</term><term>Smooth muscle</term><term>Smooth muscle actin</term><term>Stress protein</term><term>Stressgene biotechnologies</term><term>Taguchi</term><term>Takashi taguchi</term><term>Time course</term><term>Transcriptional activation</term><term>Tubular</term><term>Tubular basement membrane</term><term>Tubular epithelial cells</term><term>Tubulointerstitial</term><term>Tubulointerstitial injuries</term><term>Tubulointerstitium vessel</term><term>Vascular wall</term><term>Vimentin</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The molecular mechanisms of fibrosis in radiation nephropathy have received scant attention. Heat shock protein 47 (HSP47), a collagen‐binding stress protein, helps in the intracellular processing of procollagen molecules during collagen synthesis. We investigated the role of HSP47 in the progression of radiation nephropathy using experimental radiation nephropathy. Experimental rat groups were as follows: (i) group I, sham operated (n = 12); (ii) group II, single doses of irradiation, either 7, 15 or 25 Gy to left kidney (n = 60); and (iii) group III, a similar irradiation procedure as group II after right nephrectomy (n = 60). The rats were followed up until 9 months after renal exposure to radiation. Renal dysfunction (as determined by serum creatinine and blood urea nitrogen) and hypertension were noted in group III rats, along with inflammatory cell infiltration and interstitial fibrosis (as determined by increased deposition of collagens). Compared to control rat kidneys, an increased expression of HSP47 was noted in kidneys obtained from irradiated rats. By double immunostaining, HSP47‐expressing cells were identified as α‐smooth muscle actin‐positive myofibroblasts and vimentin‐positive tubular epithelial cells. Increased expression of HSP47 was closely associated with increased deposition of collagens in the widened interstitium of irradiated rats. Overexpression of HSP47 by phenotypically altered tubulointerstitial cells might play a role in excessive assembly/synthesis of collagens and could contribute to tubulointerstitial fibrosis in radiation nephropathy.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>nephropathy</json:string><json:string>radiation nephropathy</json:string><json:string>brosis</json:string><json:string>epithelial</json:string><json:string>tubulointerstitial</json:string><json:string>tubular epithelial cells</json:string><json:string>heat shock protein</json:string><json:string>brotic</json:string><json:string>renal</json:string><json:string>glomerulus</json:string><json:string>histological</json:string><json:string>razzaque</json:string><json:string>taguchi</json:string><json:string>actin</json:string><json:string>vimentin</json:string><json:string>creatinine</json:string><json:string>immunostaining</json:string><json:string>smooth muscle actin</json:string><json:string>serum creatinine</json:string><json:string>colocalization</json:string><json:string>collagen</json:string><json:string>interstitial cells</json:string><json:string>interstitial</json:string><json:string>kidney</json:string><json:string>tubulointerstitial injuries</json:string><json:string>collagen synthesis</json:string><json:string>double immunostaining</json:string><json:string>lesion</json:string><json:string>radiation nephritis</json:string><json:string>present study</json:string><json:string>primary antibodies</json:string><json:string>renal cells</json:string><json:string>sclerotic area</json:string><json:string>control rats</json:string><json:string>renal injury</json:string><json:string>ninth month</json:string><json:string>collagen type</json:string><json:string>stress protein</json:string><json:string>rat</json:string><json:string>tubular</json:string><json:string>glomerular</json:string><json:string>immunohistochemical staining</json:string><json:string>recent studies</json:string><json:string>glomerular cells</json:string><json:string>immunohistochemical examination</json:string><json:string>radiation procedures</json:string><json:string>stressgene biotechnologies</json:string><json:string>second staining</json:string><json:string>sixth month</json:string><json:string>histological changes</json:string><json:string>blood urea nitrogen</json:string><json:string>glomerular lesions</json:string><json:string>time course</json:string><json:string>tubular basement membrane</json:string><json:string>histological lesion</json:string><json:string>glomerulus time</json:string><json:string>tubulointerstitium vessel</json:string><json:string>sclerotic glomeruli</json:string><json:string>arterial pressure</json:string><json:string>renal dysfunction</json:string><json:string>vascular wall</json:string><json:string>experimental radiation nephropathy</json:string><json:string>smooth muscle</json:string><json:string>double staining</json:string><json:string>scant attention</json:string><json:string>renal lesions</json:string><json:string>single exposure</json:string><json:string>nagasaki university school</json:string><json:string>brotic areas</json:string><json:string>radiation exposure</json:string><json:string>interstitial collagens</json:string><json:string>molecular chaperone</json:string><json:string>previous studies</json:string><json:string>transcriptional activation</json:string><json:string>cellular basis</json:string><json:string>cell tissue</json:string><json:string>takashi taguchi</json:string><json:string>high dose</json:string></teeft></keywords><author><json:item><name>Diange Liu</name><affiliations><json:string>Second Department of Pathology, Nagasaki University School of Medicine, Nagasaki, Japan</json:string></affiliations></json:item><json:item><name>Mohammed S. Razzaque</name><affiliations><json:string>Second Department of Pathology, Nagasaki University School of Medicine, Nagasaki, Japan</json:string></affiliations></json:item><json:item><name>Arifa Nazneen</name><affiliations><json:string>Second Department of Pathology, Nagasaki University School of Medicine, Nagasaki, Japan</json:string></affiliations></json:item><json:item><name>Takashi Naito</name><affiliations><json:string>Second Department of Pathology, Nagasaki University School of Medicine, Nagasaki, Japan</json:string></affiliations></json:item><json:item><name>Takashi Taguchi</name><affiliations><json:string>Second Department of Pathology, Nagasaki University School of Medicine, Nagasaki, Japan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>collagen</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>heat shock protein</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>HSP47</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>immunohistochemistry</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>radiation nephropathy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>tubulointerstitial fibrosis</value></json:item></subject><articleId><json:string>PIN1362</json:string></articleId><arkIstex>ark:/67375/WNG-BP569W16-Z</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>The molecular mechanisms of fibrosis in radiation nephropathy have received scant attention. Heat shock protein 47 (HSP47), a collagen‐binding stress protein, helps in the intracellular processing of procollagen molecules during collagen synthesis. We investigated the role of HSP47 in the progression of radiation nephropathy using experimental radiation nephropathy. Experimental rat groups were as follows: (i) group I, sham operated (n = 12); (ii) group II, single doses of irradiation, either 7, 15 or 25 Gy to left kidney (n = 60); and (iii) group III, a similar irradiation procedure as group II after right nephrectomy (n = 60). The rats were followed up until 9 months after renal exposure to radiation. Renal dysfunction (as determined by serum creatinine and blood urea nitrogen) and hypertension were noted in group III rats, along with inflammatory cell infiltration and interstitial fibrosis (as determined by increased deposition of collagens). Compared to control rat kidneys, an increased expression of HSP47 was noted in kidneys obtained from irradiated rats. By double immunostaining, HSP47‐expressing cells were identified as α‐smooth muscle actin‐positive myofibroblasts and vimentin‐positive tubular epithelial cells. Increased expression of HSP47 was closely associated with increased deposition of collagens in the widened interstitium of irradiated rats. Overexpression of HSP47 by phenotypically altered tubulointerstitial cells might play a role in excessive assembly/synthesis of collagens and could contribute to tubulointerstitial fibrosis in radiation nephropathy.</abstract><qualityIndicators><score>8.323</score><pdfWordCount>3719</pdfWordCount><pdfCharCount>24920</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>8</pdfPageCount><pdfPageSize>595 x 842 pts (A4)</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>217</abstractWordCount><abstractCharCount>1595</abstractCharCount><keywordCount>6</keywordCount></qualityIndicators><title>Role of heat shock protein 47 on tubulointerstitium in experimental radiation nephropathy</title><pmid><json:string>12100516</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Pathology 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osteoarticulaire</json:string></inist></categories><publicationDate>2002</publicationDate><copyrightDate>2002</copyrightDate><doi><json:string>10.1046/j.1440-1827.2002.01362.x</json:string></doi><id>11218936D4EBF6D2495C6C0A35020D3C6071A4EE</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-BP569W16-Z/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-BP569W16-Z/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/WNG-BP569W16-Z/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main">Role of heat shock protein 47 on tubulointerstitium in experimental radiation nephropathy</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Science Pty</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2002-05"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main">Role of heat shock protein 47 on tubulointerstitium in experimental radiation nephropathy</title><title level="a" type="short">HSP47 in radiation nephropathy</title><author xml:id="author-0000"><persName><forename type="first">Diange</forename><surname>Liu</surname></persName><affiliation><orgName type="department">Second Department of Pathology</orgName><orgName type="institution">Nagasaki University School of Medicine</orgName><address><addrLine>Nagasaki</addrLine><country key="JP">JAPAN</country><country key="JP"></country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Mohammed S.</forename><surname>Razzaque</surname></persName><affiliation><orgName type="department">Second Department of Pathology</orgName><orgName type="institution">Nagasaki University School of Medicine</orgName><address><addrLine>Nagasaki</addrLine><country key="JP">JAPAN</country><country key="JP"></country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Arifa</forename><surname>Nazneen</surname></persName><affiliation><orgName type="department">Second Department of Pathology</orgName><orgName type="institution">Nagasaki University School of Medicine</orgName><address><addrLine>Nagasaki</addrLine><country key="JP">JAPAN</country><country key="JP"></country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Takashi</forename><surname>Naito</surname></persName><affiliation><orgName type="department">Second Department of Pathology</orgName><orgName type="institution">Nagasaki University School of Medicine</orgName><address><addrLine>Nagasaki</addrLine><country key="JP">JAPAN</country><country key="JP"></country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Takashi</forename><surname>Taguchi</surname></persName><affiliation><orgName type="department">Second Department of Pathology</orgName><orgName type="institution">Nagasaki University School of Medicine</orgName><address><addrLine>Nagasaki</addrLine><country key="JP">JAPAN</country><country key="JP"></country></address></affiliation></author><idno type="istex">11218936D4EBF6D2495C6C0A35020D3C6071A4EE</idno><idno type="ark">ark:/67375/WNG-BP569W16-Z</idno><idno type="DOI">10.1046/j.1440-1827.2002.01362.x</idno><idno type="unit">PIN1362</idno><idno type="toTypesetVersion">file:PIN.PIN1362.pdf</idno></analytic><monogr><title level="j" type="main">Pathology International</title><title level="j" type="alt">PATHOLOGY INTERNATIONAL</title><idno type="pISSN">1320-5463</idno><idno type="eISSN">1440-1827</idno><idno type="book-DOI">10.1111/(ISSN)1440-1827</idno><idno type="book-part-DOI">10.1111/pin.2002.52.issue-5-6</idno><idno type="product">PIN</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">52</biblScope><biblScope unit="issue">5‐6</biblScope><biblScope unit="page" from="340">340</biblScope><biblScope unit="page" to="347">347</biblScope><biblScope unit="page-count">8</biblScope><publisher>Blackwell Science Pty</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2002-05"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><p>The molecular mechanisms of fibrosis in radiation nephropathy have received scant attention. Heat shock protein 47 (HSP47), a collagen‐binding stress protein, helps in the intracellular processing of procollagen molecules during collagen synthesis. We investigated the role of HSP47 in the progression of radiation nephropathy using experimental radiation nephropathy. Experimental rat groups were as follows: (i) group I, sham operated (<hi rend="italic">n</hi> = 12); (ii) group II, single doses of irradiation, either 7, 15 or 25 Gy to left kidney (<hi rend="italic">n</hi> = 60); and (iii) group III, a similar irradiation procedure as group II after right nephrectomy (<hi rend="italic">n</hi> = 60). The rats were followed up until 9 months after renal exposure to radiation. Renal dysfunction (as determined by serum creatinine and blood urea nitrogen) and hypertension were noted in group III rats, along with inflammatory cell infiltration and interstitial fibrosis (as determined by increased deposition of collagens). Compared to control rat kidneys, an increased expression of HSP47 was noted in kidneys obtained from irradiated rats. By double immunostaining, HSP47‐expressing cells were identified as α‐smooth muscle actin‐positive myofibroblasts and vimentin‐positive tubular epithelial cells. Increased expression of HSP47 was closely associated with increased deposition of collagens in the widened interstitium of irradiated rats. Overexpression of HSP47 by phenotypically altered tubulointerstitial cells might play a role in excessive assembly/synthesis of collagens and could contribute to tubulointerstitial fibrosis in radiation nephropathy.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">collagen</term><term xml:id="k2">heat shock protein</term><term xml:id="k3">HSP47</term><term xml:id="k4">immunohistochemistry</term><term xml:id="k5">radiation nephropathy</term><term xml:id="k6">tubulointerstitial fibrosis </term></keywords><keywords rend="tocHeading1"><term>ORIGINAL ARTICLES</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-BP569W16-Z/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Science Pty</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1440-1827</doi><issn type="print">1320-5463</issn><issn type="electronic">1440-1827</issn><idGroup><id type="product" value="PIN"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="PATHOLOGY INTERNATIONAL">Pathology International</title></titleGroup></publicationMeta><publicationMeta level="part" position="05005"><doi origin="wiley">10.1111/pin.2002.52.issue-5-6</doi><numberingGroup><numbering type="journalVolume" number="52">52</numbering><numbering type="journalIssue">5‐6</numbering></numberingGroup><coverDate startDate="2002-05">May 2002</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="0034000" status="forIssue"><doi origin="wiley">10.1046/j.1440-1827.2002.01362.x</doi><idGroup><id type="unit" value="PIN1362"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="tocHeading1">ORIGINAL ARTICLES</title></titleGroup><eventGroup><event type="firstOnline" date="2002-07-11"></event><event type="publishedOnlineFinalForm" date="2002-07-11"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-02"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-06"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-11-03"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="340">340</numbering><numbering type="pageLast" number="347">347</numbering></numberingGroup><correspondenceTo> Takashi Taguchi, MD, PhD, Second Department of Pathology, Nagasaki University School of Medicine, Sakamoto 1‐12‐4, Nagasaki 852‐8523, Japan. Email: <email normalForm="taguchi@net.nagasaki-u.ac.jp">taguchi@net.nagasaki‐u.ac.jp</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:PIN.PIN1362.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 1 November 2001. Accepted for publication 30 January 2002.</unparsedEditorialHistory><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="3"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="35"></count><count type="wordTotal" number="3384"></count><count type="linksPubMed" number="2"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Role of heat shock protein 47 on tubulointerstitium in experimental radiation nephropathy</title><title type="shortAuthors">D. Liu</title><title type="short">HSP47 in radiation nephropathy</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Diange</givenNames><familyName>Liu</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>Mohammed S.</givenNames><familyName>Razzaque</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Arifa</givenNames><familyName>Nazneen</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>Takashi</givenNames><familyName>Naito</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>Takashi</givenNames><familyName>Taguchi</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="JP"><unparsedAffiliation>Second Department of Pathology, Nagasaki University School of Medicine, Nagasaki, Japan</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">collagen</keyword><keyword xml:id="k2">heat shock protein</keyword><keyword xml:id="k3">HSP47</keyword><keyword xml:id="k4">immunohistochemistry</keyword><keyword xml:id="k5">radiation nephropathy</keyword><keyword xml:id="k6">tubulointerstitial fibrosis </keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>The molecular mechanisms of fibrosis in radiation nephropathy have received scant attention. Heat shock protein 47 (HSP47), a collagen‐binding stress protein, helps in the intracellular processing of procollagen molecules during collagen synthesis. We investigated the role of HSP47 in the progression of radiation nephropathy using experimental radiation nephropathy. Experimental rat groups were as follows: (i) group I, sham operated (<i>n</i> = 12); (ii) group II, single doses of irradiation, either 7, 15 or 25 Gy to left kidney (<i>n</i> = 60); and (iii) group III, a similar irradiation procedure as group II after right nephrectomy (<i>n</i> = 60). The rats were followed up until 9 months after renal exposure to radiation. Renal dysfunction (as determined by serum creatinine and blood urea nitrogen) and hypertension were noted in group III rats, along with inflammatory cell infiltration and interstitial fibrosis (as determined by increased deposition of collagens). Compared to control rat kidneys, an increased expression of HSP47 was noted in kidneys obtained from irradiated rats. By double immunostaining, HSP47‐expressing cells were identified as α‐smooth muscle actin‐positive myofibroblasts and vimentin‐positive tubular epithelial cells. Increased expression of HSP47 was closely associated with increased deposition of collagens in the widened interstitium of irradiated rats. Overexpression of HSP47 by phenotypically altered tubulointerstitial cells might play a role in excessive assembly/synthesis of collagens and could contribute to tubulointerstitial fibrosis in radiation nephropathy.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Role of heat shock protein 47 on tubulointerstitium in experimental radiation nephropathy</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>HSP47 in radiation nephropathy</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Role of heat shock protein 47 on tubulointerstitium in experimental radiation nephropathy</title></titleInfo><name type="personal"><namePart type="given">Diange</namePart><namePart type="family">Liu</namePart><affiliation>Second Department of Pathology, Nagasaki University School of Medicine, Nagasaki, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mohammed S.</namePart><namePart type="family">Razzaque</namePart><affiliation>Second Department of Pathology, Nagasaki University School of Medicine, Nagasaki, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Arifa</namePart><namePart type="family">Nazneen</namePart><affiliation>Second Department of Pathology, Nagasaki University School of Medicine, Nagasaki, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Takashi</namePart><namePart type="family">Naito</namePart><affiliation>Second Department of Pathology, Nagasaki University School of Medicine, Nagasaki, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Takashi</namePart><namePart type="family">Taguchi</namePart><affiliation>Second Department of Pathology, Nagasaki University School of Medicine, Nagasaki, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Science Pty</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2002-05</dateIssued><edition>Received 1 November 2001. Accepted for publication 30 January 2002.</edition><copyrightDate encoding="w3cdtf">2002</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">0</extent><extent unit="tables">3</extent><extent unit="formulas">0</extent><extent unit="references">35</extent><extent unit="linksCrossRef">0</extent><extent unit="words">3384</extent></physicalDescription><abstract lang="en">The molecular mechanisms of fibrosis in radiation nephropathy have received scant attention. Heat shock protein 47 (HSP47), a collagen‐binding stress protein, helps in the intracellular processing of procollagen molecules during collagen synthesis. We investigated the role of HSP47 in the progression of radiation nephropathy using experimental radiation nephropathy. Experimental rat groups were as follows: (i) group I, sham operated (n = 12); (ii) group II, single doses of irradiation, either 7, 15 or 25 Gy to left kidney (n = 60); and (iii) group III, a similar irradiation procedure as group II after right nephrectomy (n = 60). The rats were followed up until 9 months after renal exposure to radiation. Renal dysfunction (as determined by serum creatinine and blood urea nitrogen) and hypertension were noted in group III rats, along with inflammatory cell infiltration and interstitial fibrosis (as determined by increased deposition of collagens). Compared to control rat kidneys, an increased expression of HSP47 was noted in kidneys obtained from irradiated rats. By double immunostaining, HSP47‐expressing cells were identified as α‐smooth muscle actin‐positive myofibroblasts and vimentin‐positive tubular epithelial cells. Increased expression of HSP47 was closely associated with increased deposition of collagens in the widened interstitium of irradiated rats. Overexpression of HSP47 by phenotypically altered tubulointerstitial cells might play a role in excessive assembly/synthesis of collagens and could contribute to tubulointerstitial fibrosis in radiation nephropathy.</abstract><subject lang="en"><genre>keywords</genre><topic>collagen</topic><topic>heat shock protein</topic><topic>HSP47</topic><topic>immunohistochemistry</topic><topic>radiation nephropathy</topic><topic>tubulointerstitial fibrosis</topic></subject><relatedItem type="host"><titleInfo><title>Pathology International</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><identifier type="ISSN">1320-5463</identifier><identifier type="eISSN">1440-1827</identifier><identifier type="DOI">10.1111/(ISSN)1440-1827</identifier><identifier type="PublisherID">PIN</identifier><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>52</number></detail><detail type="issue"><caption>no.</caption><number>5‐6</number></detail><extent unit="pages"><start>340</start><end>347</end><total>8</total></extent></part></relatedItem><identifier type="istex">11218936D4EBF6D2495C6C0A35020D3C6071A4EE</identifier><identifier type="ark">ark:/67375/WNG-BP569W16-Z</identifier><identifier type="DOI">10.1046/j.1440-1827.2002.01362.x</identifier><identifier type="ArticleID">PIN1362</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-L0C46X92-X">wiley</recordContentSource><recordOrigin>Blackwell Science Pty</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-BP569W16-Z/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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