Evolution of renal function and Na+, K +-ATPase expression during ischaemia-reperfusion injury in rat kidney
The aim of the present work was to study the effects of an unilateral ischaemic-reperfusion injury on Na+, K+-ATPase activity, alpha1 and beta1 subunits protein and mRNA abundance and ATP content in cortical and medullary tissues from postischaemic and contralateral kidneys. Right renal artery was c...
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| Veröffentlicht in: | Molecular and cellular biochemistry 2006-07, Vol.287 (1-2), p.33-42 |
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| creator | Molinas, Sara M Trumper, Laura Serra, Esteban Elías, M Mónica |
| description | The aim of the present work was to study the effects of an unilateral ischaemic-reperfusion injury on Na+, K+-ATPase activity, alpha1 and beta1 subunits protein and mRNA abundance and ATP content in cortical and medullary tissues from postischaemic and contralateral kidneys. Right renal artery was clamped for 40 min followed by 24 and 48 h of reperfusion. Postischaemic and contralateral renal function was studied cannulating the ureter of each kidney. Postischaemic kidneys after 24 (IR24) and 48 (IR48) hours of reperfusion presented a significant dysfunction. Na+, K+-ATPase alpha1 subunit abundance increased in IR24 and IR48 cortical tissue and beta1 subunit decreased in IR48. In IR24 medullary tissue, alpha1 abundance increased and returned to control values in IR48 while beta1 abundance was decreased in both periods. Forty minutes of ischaemia without reperfusion (I40) promoted an increment in alpha1 mRNA in cortex and medulla that normalised after 24 h of reperfusion. beta1 mRNA was decreased in IR24 medullas. No changes were observed in contralateral kidneys. This work provides evidences that after an ischaemic insult alpha1 and beta1 protein subunit abundance and mRNA levels are independently regulated. After ischaemic-reperfusion injury, cortical and medullary tissue showed a different pattern of response. Although ATP and Na+, K+-ATPase activity returned to control values, postischemic kidney showed an abnormal function after 48 h of reflow. |
| doi_str_mv | 10.1007/s11010-005-9021-6 |
| format | Article |
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Right renal artery was clamped for 40 min followed by 24 and 48 h of reperfusion. Postischaemic and contralateral renal function was studied cannulating the ureter of each kidney. Postischaemic kidneys after 24 (IR24) and 48 (IR48) hours of reperfusion presented a significant dysfunction. Na+, K+-ATPase alpha1 subunit abundance increased in IR24 and IR48 cortical tissue and beta1 subunit decreased in IR48. In IR24 medullary tissue, alpha1 abundance increased and returned to control values in IR48 while beta1 abundance was decreased in both periods. Forty minutes of ischaemia without reperfusion (I40) promoted an increment in alpha1 mRNA in cortex and medulla that normalised after 24 h of reperfusion. beta1 mRNA was decreased in IR24 medullas. No changes were observed in contralateral kidneys. This work provides evidences that after an ischaemic insult alpha1 and beta1 protein subunit abundance and mRNA levels are independently regulated. After ischaemic-reperfusion injury, cortical and medullary tissue showed a different pattern of response. Although ATP and Na+, K+-ATPase activity returned to control values, postischemic kidney showed an abnormal function after 48 h of reflow.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-005-9021-6</identifier><identifier>PMID: 16708288</identifier><language>eng</language><publisher>Netherlands: Springer Nature B.V</publisher><subject>Adenosine Triphosphate - analysis ; Animals ; ATP ; Gene Expression Regulation ; Kidney Cortex - blood supply ; Kidney Cortex - metabolism ; Kidney Cortex - pathology ; Kidney Medulla - blood supply ; Kidneys ; Male ; Protein Subunits - analysis ; Protein Subunits - genetics ; Rats ; Rats, Wistar ; Renal Artery - pathology ; Renal function ; Reperfusion Injury - enzymology ; Reperfusion Injury - physiopathology ; RNA, Messenger - analysis ; Sodium-Potassium-Exchanging ATPase - analysis ; Sodium-Potassium-Exchanging ATPase - genetics</subject><ispartof>Molecular and cellular biochemistry, 2006-07, Vol.287 (1-2), p.33-42</ispartof><rights>Springer Science+Business Media, Inc. 2006</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c326t-27e3f94b4c05b8a69b16479344d5b1534febdb868f2ea3af44a717f2e80245f83</citedby><cites>FETCH-LOGICAL-c326t-27e3f94b4c05b8a69b16479344d5b1534febdb868f2ea3af44a717f2e80245f83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16708288$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Molinas, Sara M</creatorcontrib><creatorcontrib>Trumper, Laura</creatorcontrib><creatorcontrib>Serra, Esteban</creatorcontrib><creatorcontrib>Elías, M Mónica</creatorcontrib><title>Evolution of renal function and Na+, K +-ATPase expression during ischaemia-reperfusion injury in rat kidney</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><description>The aim of the present work was to study the effects of an unilateral ischaemic-reperfusion injury on Na+, K+-ATPase activity, alpha1 and beta1 subunits protein and mRNA abundance and ATP content in cortical and medullary tissues from postischaemic and contralateral kidneys. Right renal artery was clamped for 40 min followed by 24 and 48 h of reperfusion. Postischaemic and contralateral renal function was studied cannulating the ureter of each kidney. Postischaemic kidneys after 24 (IR24) and 48 (IR48) hours of reperfusion presented a significant dysfunction. Na+, K+-ATPase alpha1 subunit abundance increased in IR24 and IR48 cortical tissue and beta1 subunit decreased in IR48. In IR24 medullary tissue, alpha1 abundance increased and returned to control values in IR48 while beta1 abundance was decreased in both periods. Forty minutes of ischaemia without reperfusion (I40) promoted an increment in alpha1 mRNA in cortex and medulla that normalised after 24 h of reperfusion. beta1 mRNA was decreased in IR24 medullas. No changes were observed in contralateral kidneys. This work provides evidences that after an ischaemic insult alpha1 and beta1 protein subunit abundance and mRNA levels are independently regulated. After ischaemic-reperfusion injury, cortical and medullary tissue showed a different pattern of response. Although ATP and Na+, K+-ATPase activity returned to control values, postischemic kidney showed an abnormal function after 48 h of reflow.</description><subject>Adenosine Triphosphate - analysis</subject><subject>Animals</subject><subject>ATP</subject><subject>Gene Expression Regulation</subject><subject>Kidney Cortex - blood supply</subject><subject>Kidney Cortex - metabolism</subject><subject>Kidney Cortex - pathology</subject><subject>Kidney Medulla - blood supply</subject><subject>Kidneys</subject><subject>Male</subject><subject>Protein Subunits - analysis</subject><subject>Protein Subunits - genetics</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Renal Artery - pathology</subject><subject>Renal function</subject><subject>Reperfusion Injury - enzymology</subject><subject>Reperfusion Injury - physiopathology</subject><subject>RNA, Messenger - analysis</subject><subject>Sodium-Potassium-Exchanging ATPase - analysis</subject><subject>Sodium-Potassium-Exchanging ATPase - 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analysis</topic><topic>Animals</topic><topic>ATP</topic><topic>Gene Expression Regulation</topic><topic>Kidney Cortex - blood supply</topic><topic>Kidney Cortex - metabolism</topic><topic>Kidney Cortex - pathology</topic><topic>Kidney Medulla - blood supply</topic><topic>Kidneys</topic><topic>Male</topic><topic>Protein Subunits - analysis</topic><topic>Protein Subunits - genetics</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Renal Artery - pathology</topic><topic>Renal function</topic><topic>Reperfusion Injury - enzymology</topic><topic>Reperfusion Injury - physiopathology</topic><topic>RNA, Messenger - analysis</topic><topic>Sodium-Potassium-Exchanging ATPase - analysis</topic><topic>Sodium-Potassium-Exchanging ATPase - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Molinas, Sara M</creatorcontrib><creatorcontrib>Trumper, Laura</creatorcontrib><creatorcontrib>Serra, Esteban</creatorcontrib><creatorcontrib>Elías, M Mónica</creatorcontrib><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>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS 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>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research 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 One Sustainability</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>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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 Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Molinas, Sara M</au><au>Trumper, Laura</au><au>Serra, Esteban</au><au>Elías, M Mónica</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Evolution of renal function and Na+, K +-ATPase expression during ischaemia-reperfusion injury in rat kidney</atitle><jtitle>Molecular and cellular biochemistry</jtitle><addtitle>Mol Cell Biochem</addtitle><date>2006-07-01</date><risdate>2006</risdate><volume>287</volume><issue>1-2</issue><spage>33</spage><epage>42</epage><pages>33-42</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>The aim of the present work was to study the effects of an unilateral ischaemic-reperfusion injury on Na+, K+-ATPase activity, alpha1 and beta1 subunits protein and mRNA abundance and ATP content in cortical and medullary tissues from postischaemic and contralateral kidneys. Right renal artery was clamped for 40 min followed by 24 and 48 h of reperfusion. Postischaemic and contralateral renal function was studied cannulating the ureter of each kidney. Postischaemic kidneys after 24 (IR24) and 48 (IR48) hours of reperfusion presented a significant dysfunction. Na+, K+-ATPase alpha1 subunit abundance increased in IR24 and IR48 cortical tissue and beta1 subunit decreased in IR48. In IR24 medullary tissue, alpha1 abundance increased and returned to control values in IR48 while beta1 abundance was decreased in both periods. Forty minutes of ischaemia without reperfusion (I40) promoted an increment in alpha1 mRNA in cortex and medulla that normalised after 24 h of reperfusion. beta1 mRNA was decreased in IR24 medullas. No changes were observed in contralateral kidneys. This work provides evidences that after an ischaemic insult alpha1 and beta1 protein subunit abundance and mRNA levels are independently regulated. After ischaemic-reperfusion injury, cortical and medullary tissue showed a different pattern of response. Although ATP and Na+, K+-ATPase activity returned to control values, postischemic kidney showed an abnormal function after 48 h of reflow.</abstract><cop>Netherlands</cop><pub>Springer Nature B.V</pub><pmid>16708288</pmid><doi>10.1007/s11010-005-9021-6</doi><tpages>10</tpages></addata></record> |
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| ispartof | Molecular and cellular biochemistry, 2006-07, Vol.287 (1-2), p.33-42 |
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| subjects | Adenosine Triphosphate - analysis Animals ATP Gene Expression Regulation Kidney Cortex - blood supply Kidney Cortex - metabolism Kidney Cortex - pathology Kidney Medulla - blood supply Kidneys Male Protein Subunits - analysis Protein Subunits - genetics Rats Rats, Wistar Renal Artery - pathology Renal function Reperfusion Injury - enzymology Reperfusion Injury - physiopathology RNA, Messenger - analysis Sodium-Potassium-Exchanging ATPase - analysis Sodium-Potassium-Exchanging ATPase - genetics |
| title | Evolution of renal function and Na+, K +-ATPase expression during ischaemia-reperfusion injury in rat kidney |
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