RGD Reference Report - Loss of intracellular dystrophin: a potential mechanism for myocardial reperfusion injury. - Rat Genome Database

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Loss of intracellular dystrophin: a potential mechanism for myocardial reperfusion injury.

Authors: Kyoi, S  Otani, H  Sumida, T  Okada, T  Osako, M  Imamura, H  Kamihata, H  Matsubara, H  Iwasaka, T 
Citation: Kyoi S, etal., Circ J. 2003 Aug;67(8):725-7.
RGD ID: 1581347
Pubmed: PMID:12890920   (View Abstract at PubMed)

Because the absence of sarcolemmal dystrophin renders cardiomyocytes vulnerable to mechanical force, the present study investigated whether sarcolemmal membrane fragility upon reperfusion is associated with the loss of membrane dystrophin. Dystrophin was distributed exclusively in the sarcolemmal membrane of buffer-perfused rat cardiomyocytes, but was translocated to the myofibrils during 30 min of ischemia and then lost during reperfusion. Upon reperfusion, the membrane impermeable dye, Evans blue (EB), accumulated in cardiomyocytes depleted of dystrophin. Reperfusion with the contractile blocker 2,3-butanedione monoxime (BDM) resulted in no accumulation of EB in cardiomyocytes despite the loss of dystrophin. Upon withdrawal of BDM, however, EB accumulated in dystrophin-depleted cardiomyocytes. Loss of sarcolemmal dystrophin may be involved in the mechanism of contractile force-induced reperfusion injury.

Gene Ontology Annotations    Click to see Annotation Detail View

Cellular Component
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
myofibril  IDA 1581347 RGD 

Molecular Function

Objects Annotated

Genes (Rattus norvegicus)
Arr3  (arrestin 3)
Arrb2  (arrestin, beta 2)
Dmd  (dystrophin)
Drd2  (dopamine receptor D2)


Additional Information