RGD Reference Report - Mild hyperhomocysteinemia reduces the activity and immunocontent, but does not alter the gene expression, of catalytic a subunits of cerebral Na+,K+-ATPase. - Rat Genome Database

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Mild hyperhomocysteinemia reduces the activity and immunocontent, but does not alter the gene expression, of catalytic a subunits of cerebral Na+,K+-ATPase.

Authors: Scherer, Emilene B S  Loureiro, Samanta O  Vuaden, Fernanda C  Schmitz, Felipe  Kolling, Janaína  Siebert, Cassiana  Savio, Luiz Eduardo B  Schweinberger, Bruna M  Bogo, Maurício R  Bonan, Carla D  Wyse, Angela T S 
Citation: Scherer EB, etal., Mol Cell Biochem. 2013 Jun;378(1-2):91-7. doi: 10.1007/s11010-013-1598-6. Epub 2013 Mar 7.
RGD ID: 11576285
Pubmed: PMID:23467881   (View Abstract at PubMed)
DOI: DOI:10.1007/s11010-013-1598-6   (Journal Full-text)

Na(+),K(+)-ATPase is a membrane protein which plays a key role in the maintenance of ion homeostasis that is necessary to neuronal excitability, secondary transport and neurotransmitter uptake. Mild hyperhomocysteinemia leads to several clinical manifestations and particularly cerebral diseases; however, little is known about the mechanisms of homocysteine on cerebral Na(+),K(+)-ATPase. In the present study, we investigated the effect of mild hyperhomocysteinemia on the activity, the immunocontent of catalytic subunits (a1, a2, and a3) and the gene expression of this enzyme. We used the experimental model of mild hyperhomocysteinemia that was induced by homocysteine administration (0.03 µmol/g of body weight) twice a day, from the 30th to the 60th postpartum day. Controls received saline in the same volumes. Results showed that mild hyperhomocysteinemia significantly decreased the activity and the immunocontent of the a 1 and a 2 subunits of the Na(+),K(+)-ATPase in cerebral cortex and hippocampus of adult rats. On the other hand, we did not observe any change in levels of Na(+),K(+)-ATPase mRNA transcripts in such cerebral structures of rats after chronic exposure to homocysteine. The present findings support that the homocysteine modulates the Na(+),K(+)-ATPase and this could be associated, at least in part, with the risk to the development of cerebral diseases in individuals with mild hyperhomocysteinemia.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
ATP1A1Humanhyperhomocysteinemia  ISOAtp1a1 (Rattus norvegicus)protein:decreased expression:cerebral cortexRGD 
ATP1A2Humanhyperhomocysteinemia  ISOAtp1a2 (Rattus norvegicus)protein:decreased expression:cerebral cortexRGD 
Atp1a1Rathyperhomocysteinemia  IEP protein:decreased expression:cerebral cortexRGD 
Atp1a1Mousehyperhomocysteinemia  ISOAtp1a1 (Rattus norvegicus)protein:decreased expression:cerebral cortexRGD 
Atp1a2Rathyperhomocysteinemia  IEP protein:decreased expression:cerebral cortexRGD 
Atp1a2Mousehyperhomocysteinemia  ISOAtp1a2 (Rattus norvegicus)protein:decreased expression:cerebral cortexRGD 

Objects Annotated

Genes (Rattus norvegicus)
Atp1a1  (ATPase Na+/K+ transporting subunit alpha 1)
Atp1a2  (ATPase Na+/K+ transporting subunit alpha 2)

Genes (Mus musculus)
Atp1a1  (ATPase, Na+/K+ transporting, alpha 1 polypeptide)
Atp1a2  (ATPase, Na+/K+ transporting, alpha 2 polypeptide)

Genes (Homo sapiens)
ATP1A1  (ATPase Na+/K+ transporting subunit alpha 1)
ATP1A2  (ATPase Na+/K+ transporting subunit alpha 2)


Additional Information