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Series GSE3383 Query DataSets for GSE3383
Status Public on Aug 25, 2006
Title Analysis of Akt1 activation in transgenic mouse hearts show expression profiles associated with hypertrophy and failure
Organism Mus musculus
Experiment type Expression profiling by array
Summary To investigate molecular mechanisms involved in the development of cardiac hypertrophy and heart failure, a tetracycline-regulated transgenic system to conditionally switch a constitutively-active form of the Akt1 protein kinase on or off in the adult heart was developed. Short-term activation (2 weeks) of Akt1 resulted in completely reversible hypertrophy with maintained contractility. In contrast, chronic Akt1 activation (6 weeks) induced extensive cardiac hypertrophy, severe contractile dysfunction, and massive interstitial fibrosis. The focus of this study was to create a transcript expression profile of the heart as it undergoes reversible Akt1-mediated hypertrophy and during the transition from compensated hypertrophy to heart failure. Heart tissue was analyzed before transgene induction, 2 weeks after transgene induction, 2 weeks of transgene induction followed by 2 days of repression, 6 weeks after transgene induction and 6 weeks of transgene induction followed by 2 weeks of repression. Acute over expression of Akt1 (2 weeks) leads to changes in the expression of 826 transcripts relative to non-induced hearts, whereas chronic induction (6 weeks) led to changes in the expression of 1611, of which 65% represented transcripts that were regulated during the pathological phase of heart growth. Another set of genes identified were uniquely regulated during heart regression but not growth, indicating that non-overlapping transcription programs participate in the processes of cardiac hypertrophy and atrophy. These data define the gene regulatory programs downstream of Akt that control heart size and contribute to the transition from compensatory hypertrophy to heart failure.
Keywords: transgenic mice, Akt1, time course, cardiac hypertrophy and contractile dysfunction, DNA microarrays
Overall design Gene expression data from DTG-positive mouse hearts were examined before the induction of the transgene Akt1 (time point 1), 2 weeks after the induction of the transgene Akt1(time point 2), 2 weeks after the induction of the transgene Akt1 and 2 days after the repression of the transgene Akt1 (time point 3), 6 weeks after the induction of the transgene Akt1(time point 4) and 6 weeks after the induction of the transgene Akt1 and 2 weeks after the repression of the transgene Akt1 (time point 5). N = 3 to 4 sets of independent hybridizations from individual mice were performed for each time point.
Contributor(s) Schiekofer S, Shiojima I, Sato K, Kraus BJ, Galasso G, Walsh K
Citation(s) 16882883
Submission date Sep 29, 2005
Last update date Jan 08, 2019
Contact name Stephan Schiekofer
Organization name Boston University School of Medicine
Department Molecular Cardiology
Lab Kenneth Walsh Lab
Street address 700 Albany Street, W611
City Boston
State/province MA
ZIP/Postal code 02118
Country USA
Platforms (2)
GPL339 [MOE430A] Affymetrix Mouse Expression 430A Array
GPL340 [MOE430B] Affymetrix Mouse Expression 430B Array
Samples (36)
GSM76311 DTG_heart_control_rep1_chip430A
GSM76312 DTG_heart_control_rep2_chip430A
GSM76313 DTG_heart_control_rep3_chip430A
BioProject PRJNA93517

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