Hematopoietic stem cells contribute to the regeneration of renal tubules after renal ischemia-reperfusion injury in mice
Ischemia-reperfusion injury (I/R injury) is a common cause of acute renal failure. Recovery from I/R injury requires renal tubular regeneration. Hematopoietic stem cells (HSC) have been shown to be capable of differentiating into hepatocytes, cardiac myocytes, gastrointestinal epithelial cells, and...
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| Veröffentlicht in: | Journal of the American Society of Nephrology 2003-05, Vol.14 (5), p.1188-1199 |
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| container_title | Journal of the American Society of Nephrology |
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| creator | FANGMING LIN CORDES, Kimberly LINHENG LI HOOD, Leroy COUSER, William G SHANKLAND, Stuart J IGARASHI, Peter |
| description | Ischemia-reperfusion injury (I/R injury) is a common cause of acute renal failure. Recovery from I/R injury requires renal tubular regeneration. Hematopoietic stem cells (HSC) have been shown to be capable of differentiating into hepatocytes, cardiac myocytes, gastrointestinal epithelial cells, and vascular endothelial cells during tissue repair. The current study tested the hypothesis that murine HSC can contribute to the regeneration of renal tubular epithelial cells after I/R injury. HSC isolated from male Rosa26 mice that express beta-galactosidase constitutively were transplanted into female nontransgenic mice after unilateral renal I/R injury. Four weeks after HSC transplantation, beta-galactosidase-positive cells were detected in renal tubules of the recipients by X-Gal staining. PCR analysis of the male-specific Sry gene and Y chromosome fluorescence in situ hybridization confirmed the presence of male-derived cells in the kidneys of female recipients. Antibody co-staining showed that beta-galactosidase was primarily expressed in renal proximal tubules. This is the first report to show that HSC can differentiate into renal tubular cells after I/R injury. Because of their availability, HSC may be useful for cell replacement therapy of acute renal failure. |
| doi_str_mv | 10.1097/01.asn.0000061595.28546.a0 |
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Recovery from I/R injury requires renal tubular regeneration. Hematopoietic stem cells (HSC) have been shown to be capable of differentiating into hepatocytes, cardiac myocytes, gastrointestinal epithelial cells, and vascular endothelial cells during tissue repair. The current study tested the hypothesis that murine HSC can contribute to the regeneration of renal tubular epithelial cells after I/R injury. HSC isolated from male Rosa26 mice that express beta-galactosidase constitutively were transplanted into female nontransgenic mice after unilateral renal I/R injury. Four weeks after HSC transplantation, beta-galactosidase-positive cells were detected in renal tubules of the recipients by X-Gal staining. PCR analysis of the male-specific Sry gene and Y chromosome fluorescence in situ hybridization confirmed the presence of male-derived cells in the kidneys of female recipients. Antibody co-staining showed that beta-galactosidase was primarily expressed in renal proximal tubules. This is the first report to show that HSC can differentiate into renal tubular cells after I/R injury. Because of their availability, HSC may be useful for cell replacement therapy of acute renal failure.</description><identifier>ISSN: 1046-6673</identifier><identifier>EISSN: 1533-3450</identifier><identifier>DOI: 10.1097/01.asn.0000061595.28546.a0</identifier><identifier>PMID: 12707389</identifier><identifier>CODEN: JASNEU</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Animals ; Antibodies ; Antigens, Ly - analysis ; beta-Galactosidase - immunology ; Biological and medical sciences ; Biomarkers ; Cell Death ; Cell Differentiation ; Cell Separation - methods ; Epithelial Cells - cytology ; Female ; Galactosides ; Genes, sry ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells - chemistry ; Hematopoietic Stem Cells - cytology ; In Situ Hybridization, Fluorescence ; Indoles ; Kidney Tubules - cytology ; Kidney Tubules - physiology ; Male ; Medical sciences ; Membrane Proteins - analysis ; Mice ; Mice, Inbred Strains ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; Proto-Oncogene Proteins c-kit - analysis ; Regeneration ; Renal failure ; Reperfusion Injury - pathology ; Reperfusion Injury - physiopathology ; Reperfusion Injury - therapy ; Staining and Labeling ; Y Chromosome</subject><ispartof>Journal of the American Society of Nephrology, 2003-05, Vol.14 (5), p.1188-1199</ispartof><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-f4676360baca86af7e4bcab9ceb5a542d22c7584ac69d9627b8979c09c9cab103</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27929,27930</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14756579$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12707389$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>FANGMING LIN</creatorcontrib><creatorcontrib>CORDES, Kimberly</creatorcontrib><creatorcontrib>LINHENG LI</creatorcontrib><creatorcontrib>HOOD, Leroy</creatorcontrib><creatorcontrib>COUSER, William G</creatorcontrib><creatorcontrib>SHANKLAND, Stuart J</creatorcontrib><creatorcontrib>IGARASHI, Peter</creatorcontrib><title>Hematopoietic stem cells contribute to the regeneration of renal tubules after renal ischemia-reperfusion injury in mice</title><title>Journal of the American Society of Nephrology</title><addtitle>J Am Soc Nephrol</addtitle><description>Ischemia-reperfusion injury (I/R injury) is a common cause of acute renal failure. Recovery from I/R injury requires renal tubular regeneration. Hematopoietic stem cells (HSC) have been shown to be capable of differentiating into hepatocytes, cardiac myocytes, gastrointestinal epithelial cells, and vascular endothelial cells during tissue repair. The current study tested the hypothesis that murine HSC can contribute to the regeneration of renal tubular epithelial cells after I/R injury. HSC isolated from male Rosa26 mice that express beta-galactosidase constitutively were transplanted into female nontransgenic mice after unilateral renal I/R injury. Four weeks after HSC transplantation, beta-galactosidase-positive cells were detected in renal tubules of the recipients by X-Gal staining. PCR analysis of the male-specific Sry gene and Y chromosome fluorescence in situ hybridization confirmed the presence of male-derived cells in the kidneys of female recipients. Antibody co-staining showed that beta-galactosidase was primarily expressed in renal proximal tubules. This is the first report to show that HSC can differentiate into renal tubular cells after I/R injury. Because of their availability, HSC may be useful for cell replacement therapy of acute renal failure.</description><subject>Animals</subject><subject>Antibodies</subject><subject>Antigens, Ly - analysis</subject><subject>beta-Galactosidase - immunology</subject><subject>Biological and medical sciences</subject><subject>Biomarkers</subject><subject>Cell Death</subject><subject>Cell Differentiation</subject><subject>Cell Separation - methods</subject><subject>Epithelial Cells - cytology</subject><subject>Female</subject><subject>Galactosides</subject><subject>Genes, sry</subject><subject>Hematopoietic Stem Cell Transplantation</subject><subject>Hematopoietic Stem Cells - chemistry</subject><subject>Hematopoietic Stem Cells - cytology</subject><subject>In Situ Hybridization, Fluorescence</subject><subject>Indoles</subject><subject>Kidney Tubules - cytology</subject><subject>Kidney Tubules - physiology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Proteins - analysis</subject><subject>Mice</subject><subject>Mice, Inbred Strains</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>Proto-Oncogene Proteins c-kit - analysis</subject><subject>Regeneration</subject><subject>Renal failure</subject><subject>Reperfusion Injury - pathology</subject><subject>Reperfusion Injury - physiopathology</subject><subject>Reperfusion Injury - therapy</subject><subject>Staining and Labeling</subject><subject>Y Chromosome</subject><issn>1046-6673</issn><issn>1533-3450</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkEtv1DAQxy0EoqXwFZCFRG8JfjvmtqoKRarooXC2Jt4JdZXEi-1I7bcnSyPtXOah37z-hHzirOXM2S-Mt1Dmlh3NcO10KzqtTAvsFTnnWspGKs1erzFTpjHGyjPyrpRHxrgW1r4lZ1xYZmXnzsnTDU5Q0yFFrDHQUnGiAcex0JDmmmO_VKQ10fqANOMfnDFDjWmmaVjzGUZal34ZsVAYKuatFkt4wClCk_GAeVjKsSPOj0t-Xh2dYsD35M0AY8EPm78gv79d_7q6aW7vvv-42t02QRlZm0EZa6RhPQToDAwWVR-gdwF7DVqJvRDB6k5BMG7vjLB956wLzAW3YpzJC3L5MveQ098FS_XTet36IcyYluKtFKJTTKzg1xcw5FRKxsEfcpwgP3vO_FF3z7jf3f_0J939f9397rjl47Zl6Sfcn1o3oVfg8wZACTAOGeYQy4lTVhttnfwHSWmPew</recordid><startdate>20030501</startdate><enddate>20030501</enddate><creator>FANGMING LIN</creator><creator>CORDES, Kimberly</creator><creator>LINHENG LI</creator><creator>HOOD, Leroy</creator><creator>COUSER, William G</creator><creator>SHANKLAND, Stuart J</creator><creator>IGARASHI, Peter</creator><general>Lippincott Williams & Wilkins</general><scope>IQODW</scope><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></search><sort><creationdate>20030501</creationdate><title>Hematopoietic stem cells contribute to the regeneration of renal tubules after renal ischemia-reperfusion injury in mice</title><author>FANGMING LIN ; CORDES, Kimberly ; LINHENG LI ; HOOD, Leroy ; COUSER, William G ; SHANKLAND, Stuart J ; IGARASHI, Peter</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c463t-f4676360baca86af7e4bcab9ceb5a542d22c7584ac69d9627b8979c09c9cab103</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Antibodies</topic><topic>Antigens, Ly - analysis</topic><topic>beta-Galactosidase - immunology</topic><topic>Biological and medical sciences</topic><topic>Biomarkers</topic><topic>Cell Death</topic><topic>Cell Differentiation</topic><topic>Cell Separation - methods</topic><topic>Epithelial Cells - cytology</topic><topic>Female</topic><topic>Galactosides</topic><topic>Genes, sry</topic><topic>Hematopoietic Stem Cell Transplantation</topic><topic>Hematopoietic Stem Cells - chemistry</topic><topic>Hematopoietic Stem Cells - cytology</topic><topic>In Situ Hybridization, Fluorescence</topic><topic>Indoles</topic><topic>Kidney Tubules - cytology</topic><topic>Kidney Tubules - physiology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Proteins - analysis</topic><topic>Mice</topic><topic>Mice, Inbred Strains</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>Proto-Oncogene Proteins c-kit - analysis</topic><topic>Regeneration</topic><topic>Renal failure</topic><topic>Reperfusion Injury - pathology</topic><topic>Reperfusion Injury - physiopathology</topic><topic>Reperfusion Injury - therapy</topic><topic>Staining and Labeling</topic><topic>Y Chromosome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>FANGMING LIN</creatorcontrib><creatorcontrib>CORDES, Kimberly</creatorcontrib><creatorcontrib>LINHENG LI</creatorcontrib><creatorcontrib>HOOD, Leroy</creatorcontrib><creatorcontrib>COUSER, William G</creatorcontrib><creatorcontrib>SHANKLAND, Stuart J</creatorcontrib><creatorcontrib>IGARASHI, Peter</creatorcontrib><collection>Pascal-Francis</collection><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><jtitle>Journal of the American Society of Nephrology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>FANGMING LIN</au><au>CORDES, Kimberly</au><au>LINHENG LI</au><au>HOOD, Leroy</au><au>COUSER, William G</au><au>SHANKLAND, Stuart J</au><au>IGARASHI, Peter</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hematopoietic stem cells contribute to the regeneration of renal tubules after renal ischemia-reperfusion injury in mice</atitle><jtitle>Journal of the American Society of Nephrology</jtitle><addtitle>J Am Soc Nephrol</addtitle><date>2003-05-01</date><risdate>2003</risdate><volume>14</volume><issue>5</issue><spage>1188</spage><epage>1199</epage><pages>1188-1199</pages><issn>1046-6673</issn><eissn>1533-3450</eissn><coden>JASNEU</coden><abstract>Ischemia-reperfusion injury (I/R injury) is a common cause of acute renal failure. Recovery from I/R injury requires renal tubular regeneration. Hematopoietic stem cells (HSC) have been shown to be capable of differentiating into hepatocytes, cardiac myocytes, gastrointestinal epithelial cells, and vascular endothelial cells during tissue repair. The current study tested the hypothesis that murine HSC can contribute to the regeneration of renal tubular epithelial cells after I/R injury. HSC isolated from male Rosa26 mice that express beta-galactosidase constitutively were transplanted into female nontransgenic mice after unilateral renal I/R injury. Four weeks after HSC transplantation, beta-galactosidase-positive cells were detected in renal tubules of the recipients by X-Gal staining. PCR analysis of the male-specific Sry gene and Y chromosome fluorescence in situ hybridization confirmed the presence of male-derived cells in the kidneys of female recipients. Antibody co-staining showed that beta-galactosidase was primarily expressed in renal proximal tubules. This is the first report to show that HSC can differentiate into renal tubular cells after I/R injury. Because of their availability, HSC may be useful for cell replacement therapy of acute renal failure.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>12707389</pmid><doi>10.1097/01.asn.0000061595.28546.a0</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antibodies Antigens, Ly - analysis beta-Galactosidase - immunology Biological and medical sciences Biomarkers Cell Death Cell Differentiation Cell Separation - methods Epithelial Cells - cytology Female Galactosides Genes, sry Hematopoietic Stem Cell Transplantation Hematopoietic Stem Cells - chemistry Hematopoietic Stem Cells - cytology In Situ Hybridization, Fluorescence Indoles Kidney Tubules - cytology Kidney Tubules - physiology Male Medical sciences Membrane Proteins - analysis Mice Mice, Inbred Strains Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure Proto-Oncogene Proteins c-kit - analysis Regeneration Renal failure Reperfusion Injury - pathology Reperfusion Injury - physiopathology Reperfusion Injury - therapy Staining and Labeling Y Chromosome |
| title | Hematopoietic stem cells contribute to the regeneration of renal tubules after renal ischemia-reperfusion injury in mice |
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