Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptome Alteration in the Diabetic Heart by Rosiglitazone: Implications for Cardiovascular Mortality


ABSTRACT: The type 2 diabetes medication, rosiglitazone, has come under scrutiny for possibly increasing the risk of cardiac disease and death. To investigate the effects of rosiglitazone on the diabetic heart, we performed cardiac transcriptional profiling of a murine model of type 2 diabetes, the C57BL/KLS-leprdb/leprdb (db/db) mouse. We compared cardiac gene expression profiles from three groups: untreated db/db mice (db-c), db/db mice after rosiglitazone treatment (db-t), and non-diabetic db/+ mice. Mice were divided into three groups: Non-diabetic controls (db/+), untreated diabetic controls (db-c), and rosiglitazone-treated diabetic mice (db-t). Whole-heart RNA from five mice from each of the three groups after four months with or without treatment was used for microarray analysis.Universal Reference RNAs for mouse (Stratagene, La Jolla, CA) were purchased as microarray reference controls.

ORGANISM(S): Mus musculus

SUBMITTER: Kitchener Wilson 

PROVIDER: E-GEOD-36875 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcriptome alteration in the diabetic heart by rosiglitazone: implications for cardiovascular mortality.

Wilson Kitchener D KD   Li Zongjin Z   Wagner Roger R   Yue Patrick P   Tsao Phillip P   Nestorova Gergana G   Huang Mei M   Hirschberg David L DL   Yock Paul G PG   Quertermous Thomas T   Wu Joseph C JC  

PloS one 20080709 7


<h4>Background</h4>Recently, the type 2 diabetes medication, rosiglitazone, has come under scrutiny for possibly increasing the risk of cardiac disease and death. To investigate the effects of rosiglitazone on the diabetic heart, we performed cardiac transcriptional profiling and imaging studies of a murine model of type 2 diabetes, the C57BL/KLS-lepr(db)/lepr(db) (db/db) mouse.<h4>Methods and findings</h4>We compared cardiac gene expression profiles from three groups: untreated db/db mice, db/d  ...[more]

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