RGD Reference Report - Changing pattern of gene expression is associated with ventricular myocyte dysfunction and altered mechanisms of Ca2+ signalling in young type 2 Zucker diabetic fatty rat heart. - Rat Genome Database

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Changing pattern of gene expression is associated with ventricular myocyte dysfunction and altered mechanisms of Ca2+ signalling in young type 2 Zucker diabetic fatty rat heart.

Authors: Howarth, FC  Qureshi, MA  Hassan, Z  Al Kury, LT  Isaev, D  Parekh, K  Yammahi, SR  Oz, M  Adrian, TE  Adeghate, E 
Citation: Howarth FC, etal., Exp Physiol. 2011 Mar;96(3):325-37. Epub 2011 Jan 7.
RGD ID: 6892953
Pubmed: PMID:21216827   (View Abstract at PubMed)
DOI: DOI:10.1113/expphysiol.2010.055574   (Journal Full-text)

The association between type 2 diabetes and obesity is very strong, and cardiovascular complications are the major cause of morbidity and mortality in diabetic patients. The aim of this study was to investigate early changes in the pattern of genes encoding cardiac muscle regulatory proteins and associated changes in ventricular myocyte contraction and Ca(2+) transport in young (9- to 13-week-old) type 2 Zucker diabetic fatty (ZDF) rats. The amplitude of myocyte shortening was unaltered; however, time-to-peak shortening and time to half-relaxation of shortening were prolonged in ZDF myocytes (163 +/- 5 and 127 +/- 7 ms, respectively) compared with age-matched control rats (136 +/- 5 and 103 +/- 4 ms, respectively). The amplitude of the Ca(2+) transient was unaltered; however, time-to-peak Ca(2+) transient was prolonged in ZDF myocytes (66.9 +/- 2.6 ms) compared with control myocytes (57.6 +/- 2.3 ms). The L-type Ca(2+) current was reduced, and inactivation was prolonged over a range of test potentials in ZDF myocytes. At 0 mV, the density of L-type Ca(2+) current was 1.19 +/- 0.28 pA pF(-1) in ZDF myocytes compared with 2.42 +/- 0.40 pA pF(-1) in control myocytes. Sarcoplasmic reticulum Ca(2+) content, release and uptake and myofilament sensitivity to Ca(2+) were unaltered in ZDF myocytes compared with control myocytes. Expression of genes encoding various L-type Ca(2+) channel proteins (Cacna1c, Cacna1g, Cacna1h and Cacna2d1) and cardiac muscle proteins (Myh7) were upregulated, and genes encoding intracellular Ca(2+) transport regulatory proteins (Atp2a2 and Calm1) and some cardiac muscle proteins (Myh6, Myl2, Actc1, Tnni3, Tnn2, and Tnnc1) were downregulated in ZDF heart compared with control heart. A change in the expression of genes encoding myosin heavy chain and L-type Ca(2+) channel proteins might partly underlie alterations in the time course of contraction and Ca(2+) transients in ventricular myocytes from ZDF rats.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
type 2 diabetes mellitus  ISOAtp2a2 (Rattus norvegicus)6892953; 6892953mRNA:decreased expression:heart left ventricleRGD 
type 2 diabetes mellitus  IEP 6892953mRNA:decreased expression:heart left ventricleRGD 
type 2 diabetes mellitus  ISOCalm1 (Rattus norvegicus)6892953; 6892953mRNA:decreased expression:heartRGD 
type 2 diabetes mellitus  IEP 6892953mRNA:decreased expression:heartRGD 

Objects Annotated

Genes (Rattus norvegicus)
Atp2a2  (ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 2)
Calm1  (calmodulin 1)

Genes (Mus musculus)
Atp2a2  (ATPase, Ca++ transporting, cardiac muscle, slow twitch 2)
Calm1  (calmodulin 1)

Genes (Homo sapiens)
ATP2A2  (ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 2)
CALM1  (calmodulin 1)


Additional Information