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Series GSE7487 Query DataSets for GSE7487
Status Public on Mar 08, 2010
Title Gene profiling of pathological cardiac hypertrophy vs physiological hypertrophy
Organism Mus musculus
Experiment type Expression profiling by array
Summary Cardiac hypertrophy can lead to heart failure, and is induced either by physiological stimuli eg postnatal development, chronic exercise training or pathological stimuli eg pressure or volume overload. Majority of new therapies for heart failure has mixed outcomes. A combined mouse model and oligo-array approach are used to examine whether phosphoinositide 3-kinase (p110-alpha isoform) activity is critical for maintenance of cardiac function and long-term survival in a setting of heart failure. The significance and expected outcome are to recognise genes involved in models of heart failure ie pathological- vs physiology-hypertrophy, and examine the molecular mechanisms responsible for such activity.
Growth of the heart can be induced by physiological stimuli e.g., postnatal development, chronic exercise training, or pathological stimuli e.g., pressure or volume overload. Physiological hypertrophy (“good”) is characterised by a normal organisation of cardiac structure, and normal or enhanced cardiac function. In comparison, pathological hypertrophy (”bad”) is associated with fibrosis, cardiac dysfunction, and increased morbidity and mortality. The mechanistic process which allows the heart to enlarge in response to physiological stimuli while maintaining normal or enhanced function is of great clinical relevance because one potential therapeutic strategy is to inhibit the pathological growth process while augmenting the physiological growth process. One of the major process that regulate heart size is by phosphoinositide 3-kinase (PI3K). Thus the end goal of this project is to determine whether the p110 alpha isoform of PI3K could be a potential tool for augmenting physiological growth and improving cardiac function of the failing diseased heart, and to examine the underlying mechanisms responsible.
Keywords: Disease progression analysis
Overall design Ntg (nontransgenic), dnPI3K (cardiac-specific transgenic model with reduced PI3K activity) and caPI3K (transgenic mice with increased PI3K activity) mice were used. Mice were divided into MI (myocardial infarction) group and sham (control operation) groups, resulting in 6 experimental groups. 4 arrays were included in each group, each assigned an array number as follows:

Ntg sham: 415, 416, 1184. 1185

Ntg MI: 140, 1127, 1174, 1190

dnPI3K sham: 417, 418, 1191, 1181

dnPI3K MI: 228, 1117, 87, 927

caPI3K sham: 1416, 1413, 1417, 1410

caPI3K MI: 257, 261, 1123, 987

The following comparisons were studied:
-Ntg sham compared to Ntg MI
-caPI3K sham compared to caPI3K MI
-dnPI3K sham compared to dnPI3K MI
-(Ntg MI-Ntg sham) to (caPI3K MI-caPI3K sham) to (dnPI3K MI-dnPI3K sham)

Multiple comparison normalised to Ntg sham.
Contributor(s) McMullen JR, Lin RC
Citation(s) 20237330
Submission date Apr 10, 2007
Last update date Feb 11, 2019
Contact name Ruby CY Lin
Organization name The Westmead Institute for Medical Research
Street address 176 Hawkesbury Road, Westmead
City Sydney
State/province NSW
ZIP/Postal code 2145
Country Australia
Platforms (1)
GPL1261 [Mouse430_2] Affymetrix Mouse Genome 430 2.0 Array
Samples (24)
GSM181383 Ntg sham 415
GSM181386 Ntg sham 416
GSM181387 Ntg sham 1184
BioProject PRJNA100305

Download family Format
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Supplementary file Size Download File type/resource
GSE7487_RAW.tar 95.1 Mb (http)(custom) TAR (of CEL, CHP)
Raw data provided as supplementary file
Processed data provided as supplementary file

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