N-cadherin is depleted from proximal tubules in experimental and human acute kidney injury
Ischemia remains the most common cause of acute kidney injury (AKI). Decreased intercellular adhesion and alterations in adhesion molecules may contribute to the loss of renal function observed in AKI. In the present study, we evaluated the distribution of adhesion molecules in the human kidney and...
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| Veröffentlicht in: | Histochemistry and cell biology 2010-06, Vol.133 (6), p.641-649 |
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| creator | Nürnberger, Jens Feldkamp, Thorsten Kavapurackal, Rosmaria Opazo Saez, Anabelle Becker, Jan Hörbelt, Markus Kribben, Andreas |
| description | Ischemia remains the most common cause of acute kidney injury (AKI). Decreased intercellular adhesion and alterations in adhesion molecules may contribute to the loss of renal function observed in AKI. In the present study, we evaluated the distribution of adhesion molecules in the human kidney and analyzed their expression in human and experimental AKI. Specimens of human kidneys obtained from patients with and without AKI were stained for the cell adhesion molecules E-cadherin, N-cadherin and β-catenin. Experimental AKI in rats was induced by renal artery clamping. Immunostaining and immunoblotting were carried out for E-cadherin, N-cadherin and β-catenin. Proximal tubule cells from opossum kidneys (OKs) were used to analyze the effect of chemical hypoxia (ATP depletion) in vitro. In the adult human kidney, N-cadherin was expressed in proximal tubules, while E-cadherin was expressed in other nephron segments. β-Catenin was expressed in both proximal and distal tubules. In human AKI and in ischemic rat kidneys, N-cadherin immunostaining was depleted from proximal tubules. There was no change in E-cadherin or β-catenin. In vitro, OK cells expressed N-cadherin only in the presence of collagen, and ATP depletion led to a depletion of N-cadherin. Collagen IV staining was reduced in ischemic rat kidneys compared to controls. The results of the study suggest that N-cadherin may play a significant role in human and experimental AKI. |
| doi_str_mv | 10.1007/s00418-010-0702-1 |
| format | Article |
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Decreased intercellular adhesion and alterations in adhesion molecules may contribute to the loss of renal function observed in AKI. In the present study, we evaluated the distribution of adhesion molecules in the human kidney and analyzed their expression in human and experimental AKI. Specimens of human kidneys obtained from patients with and without AKI were stained for the cell adhesion molecules E-cadherin, N-cadherin and β-catenin. Experimental AKI in rats was induced by renal artery clamping. Immunostaining and immunoblotting were carried out for E-cadherin, N-cadherin and β-catenin. Proximal tubule cells from opossum kidneys (OKs) were used to analyze the effect of chemical hypoxia (ATP depletion) in vitro. In the adult human kidney, N-cadherin was expressed in proximal tubules, while E-cadherin was expressed in other nephron segments. β-Catenin was expressed in both proximal and distal tubules. In human AKI and in ischemic rat kidneys, N-cadherin immunostaining was depleted from proximal tubules. There was no change in E-cadherin or β-catenin. In vitro, OK cells expressed N-cadherin only in the presence of collagen, and ATP depletion led to a depletion of N-cadherin. Collagen IV staining was reduced in ischemic rat kidneys compared to controls. The results of the study suggest that N-cadherin may play a significant role in human and experimental AKI.</description><identifier>ISSN: 0948-6143</identifier><identifier>EISSN: 1432-119X</identifier><identifier>DOI: 10.1007/s00418-010-0702-1</identifier><identifier>PMID: 20440507</identifier><language>eng</language><publisher>Berlin/Heidelberg: Berlin/Heidelberg : Springer-Verlag</publisher><subject>Acute kidney injury ; Acute Kidney Injury - physiopathology ; Adhesion junction ; Animals ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Cadherin ; Cadherins - chemistry ; Cadherins - classification ; Cadherins - metabolism ; Cell adhesion & migration ; Cell Biology ; Cells, Cultured ; Developmental Biology ; Disease Models, Animal ; Humans ; Immunohistochemistry ; Injuries ; Ischemia ; Kidney - injuries ; Kidney - metabolism ; Kidney - pathology ; Kidney Tubules, Proximal - metabolism ; Kidneys ; Male ; Membranes ; Opossums ; Original Paper ; Proteins ; Rats ; Rats, Sprague-Dawley</subject><ispartof>Histochemistry and cell biology, 2010-06, Vol.133 (6), p.641-649</ispartof><rights>Springer-Verlag 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c394t-6e72f00d2898ae5c48e90220ff3b56cb8064c7162286ea6c17e5d407bbfb1b0b3</citedby><cites>FETCH-LOGICAL-c394t-6e72f00d2898ae5c48e90220ff3b56cb8064c7162286ea6c17e5d407bbfb1b0b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00418-010-0702-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00418-010-0702-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20440507$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nürnberger, Jens</creatorcontrib><creatorcontrib>Feldkamp, Thorsten</creatorcontrib><creatorcontrib>Kavapurackal, Rosmaria</creatorcontrib><creatorcontrib>Opazo Saez, Anabelle</creatorcontrib><creatorcontrib>Becker, Jan</creatorcontrib><creatorcontrib>Hörbelt, Markus</creatorcontrib><creatorcontrib>Kribben, Andreas</creatorcontrib><title>N-cadherin is depleted from proximal tubules in experimental and human acute kidney injury</title><title>Histochemistry and cell biology</title><addtitle>Histochem Cell Biol</addtitle><addtitle>Histochem Cell Biol</addtitle><description>Ischemia remains the most common cause of acute kidney injury (AKI). Decreased intercellular adhesion and alterations in adhesion molecules may contribute to the loss of renal function observed in AKI. In the present study, we evaluated the distribution of adhesion molecules in the human kidney and analyzed their expression in human and experimental AKI. Specimens of human kidneys obtained from patients with and without AKI were stained for the cell adhesion molecules E-cadherin, N-cadherin and β-catenin. Experimental AKI in rats was induced by renal artery clamping. Immunostaining and immunoblotting were carried out for E-cadherin, N-cadherin and β-catenin. Proximal tubule cells from opossum kidneys (OKs) were used to analyze the effect of chemical hypoxia (ATP depletion) in vitro. In the adult human kidney, N-cadherin was expressed in proximal tubules, while E-cadherin was expressed in other nephron segments. β-Catenin was expressed in both proximal and distal tubules. In human AKI and in ischemic rat kidneys, N-cadherin immunostaining was depleted from proximal tubules. There was no change in E-cadherin or β-catenin. In vitro, OK cells expressed N-cadherin only in the presence of collagen, and ATP depletion led to a depletion of N-cadherin. Collagen IV staining was reduced in ischemic rat kidneys compared to controls. The results of the study suggest that N-cadherin may play a significant role in human and experimental AKI.</description><subject>Acute kidney injury</subject><subject>Acute Kidney Injury - physiopathology</subject><subject>Adhesion junction</subject><subject>Animals</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cadherin</subject><subject>Cadherins - chemistry</subject><subject>Cadherins - classification</subject><subject>Cadherins - metabolism</subject><subject>Cell adhesion & migration</subject><subject>Cell Biology</subject><subject>Cells, Cultured</subject><subject>Developmental Biology</subject><subject>Disease Models, Animal</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Injuries</subject><subject>Ischemia</subject><subject>Kidney - injuries</subject><subject>Kidney - metabolism</subject><subject>Kidney - pathology</subject><subject>Kidney Tubules, Proximal - metabolism</subject><subject>Kidneys</subject><subject>Male</subject><subject>Membranes</subject><subject>Opossums</subject><subject>Original Paper</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><issn>0948-6143</issn><issn>1432-119X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kEtv1TAQhS0EoreFH8AGLDZdBWb8SrJEFS-pggVUQmws25m0ueRxsWOp99_jKgUkFqxmNP7OmfFh7BnCKwSoXycAhU0FCBXUICp8wHaoZGmw_faQ7aBVTWXK5ISdprQHQN0K8ZidCFAKNNQ79v1TFVx3Q3GY-ZB4R4eRVup4H5eJH-JyO0xu5Gv2eaTEC0S3hwJPNK9l7uaO3-TJzdyFvBL_MXQzHQu2z_H4hD3q3Zjo6X09Y1fv3n69-FBdfn7_8eLNZRVkq9bKUC16gE40beNIB9VQC0JA30uvTfANGBVqNEI0hpwJWJPuFNTe9x49eHnGzjffcu7PTGm105ACjaObacnJ1lJqNBrrQr78h9wvOc7lOCtQo9bSmALhBoW4pBSpt4fyXxePFsHexW632G2J3d7FbrFont8bZz9R90fxO-cCiA1I5Wm-pvh38_9cX2yi3i3WXcch2asvAlACNgpbjfIXmpaV7g</recordid><startdate>20100601</startdate><enddate>20100601</enddate><creator>Nürnberger, Jens</creator><creator>Feldkamp, Thorsten</creator><creator>Kavapurackal, Rosmaria</creator><creator>Opazo Saez, Anabelle</creator><creator>Becker, Jan</creator><creator>Hörbelt, Markus</creator><creator>Kribben, Andreas</creator><general>Berlin/Heidelberg : Springer-Verlag</general><general>Springer-Verlag</general><general>Springer Nature B.V</general><scope>FBQ</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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20100601</creationdate><title>N-cadherin is depleted from proximal tubules in experimental and human acute kidney injury</title><author>Nürnberger, Jens ; Feldkamp, Thorsten ; Kavapurackal, Rosmaria ; Opazo Saez, Anabelle ; Becker, Jan ; Hörbelt, Markus ; Kribben, Andreas</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c394t-6e72f00d2898ae5c48e90220ff3b56cb8064c7162286ea6c17e5d407bbfb1b0b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Acute kidney injury</topic><topic>Acute Kidney Injury - physiopathology</topic><topic>Adhesion junction</topic><topic>Animals</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cadherin</topic><topic>Cadherins - chemistry</topic><topic>Cadherins - classification</topic><topic>Cadherins - metabolism</topic><topic>Cell adhesion & migration</topic><topic>Cell Biology</topic><topic>Cells, Cultured</topic><topic>Developmental Biology</topic><topic>Disease Models, Animal</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Injuries</topic><topic>Ischemia</topic><topic>Kidney - injuries</topic><topic>Kidney - metabolism</topic><topic>Kidney - pathology</topic><topic>Kidney Tubules, Proximal - metabolism</topic><topic>Kidneys</topic><topic>Male</topic><topic>Membranes</topic><topic>Opossums</topic><topic>Original Paper</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nürnberger, Jens</creatorcontrib><creatorcontrib>Feldkamp, Thorsten</creatorcontrib><creatorcontrib>Kavapurackal, Rosmaria</creatorcontrib><creatorcontrib>Opazo Saez, Anabelle</creatorcontrib><creatorcontrib>Becker, Jan</creatorcontrib><creatorcontrib>Hörbelt, Markus</creatorcontrib><creatorcontrib>Kribben, Andreas</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - 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Decreased intercellular adhesion and alterations in adhesion molecules may contribute to the loss of renal function observed in AKI. In the present study, we evaluated the distribution of adhesion molecules in the human kidney and analyzed their expression in human and experimental AKI. Specimens of human kidneys obtained from patients with and without AKI were stained for the cell adhesion molecules E-cadherin, N-cadherin and β-catenin. Experimental AKI in rats was induced by renal artery clamping. Immunostaining and immunoblotting were carried out for E-cadherin, N-cadherin and β-catenin. Proximal tubule cells from opossum kidneys (OKs) were used to analyze the effect of chemical hypoxia (ATP depletion) in vitro. In the adult human kidney, N-cadherin was expressed in proximal tubules, while E-cadherin was expressed in other nephron segments. β-Catenin was expressed in both proximal and distal tubules. In human AKI and in ischemic rat kidneys, N-cadherin immunostaining was depleted from proximal tubules. There was no change in E-cadherin or β-catenin. In vitro, OK cells expressed N-cadherin only in the presence of collagen, and ATP depletion led to a depletion of N-cadherin. Collagen IV staining was reduced in ischemic rat kidneys compared to controls. The results of the study suggest that N-cadherin may play a significant role in human and experimental AKI.</abstract><cop>Berlin/Heidelberg</cop><pub>Berlin/Heidelberg : Springer-Verlag</pub><pmid>20440507</pmid><doi>10.1007/s00418-010-0702-1</doi><tpages>9</tpages></addata></record> |
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| subjects | Acute kidney injury Acute Kidney Injury - physiopathology Adhesion junction Animals Biochemistry Biomedical and Life Sciences Biomedicine Cadherin Cadherins - chemistry Cadherins - classification Cadherins - metabolism Cell adhesion & migration Cell Biology Cells, Cultured Developmental Biology Disease Models, Animal Humans Immunohistochemistry Injuries Ischemia Kidney - injuries Kidney - metabolism Kidney - pathology Kidney Tubules, Proximal - metabolism Kidneys Male Membranes Opossums Original Paper Proteins Rats Rats, Sprague-Dawley |
| title | N-cadherin is depleted from proximal tubules in experimental and human acute kidney injury |
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