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Physiol. Genomics 16: 90-98, 2003. First published October 21, 2003; doi:10.1152/physiolgenomics.00108.2003
1094-8341/03 $5.00
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Received 7 July 2003; accepted in final form 10 October 2003.
Physiological Genomics 16:90-98 (2003)
1094-8341/03 $5.00 © 2003 American Physiological Society

Serial analysis of gene expression in mouse kidney following angiotensin II administration

Faina Schwartz , Arvi Duka , Elena Triantafyllidi , Conrado Johns , Irena Duka , Jing Cui and Haralambos Gavras

Department of Medicine, Hypertension Section, Boston University School of Medicine, Boston, Massachusetts 02118

As a new line of inquiry into the molecular mechanisms underlying pathophysiological processes associated with angiotensin (ANG II)-dependent hypertension, we applied the method of serial analysis of gene expression (SAGE) to examine genome-wide transcription changes in the kidneys of mice that developed hypertension in response to chronic ANG II administration. Mice were infused subcutaneously via osmotic minipumps with ANG II for 7 days, and systolic blood pressure was measured by tail-cuff plethysmography. Subsequently, mice were euthanized, and the total RNA isolated from the kidneys was used to construct SAGE libraries. Comparison of 11,447 SAGE tags from the hypertensive kidneys, representing 5,740 unique transcripts, and 11,273 tags from the control kidneys, corresponding to 5,619 different transcripts, identified genes that are significantly (P < 0.05) down- or upregulated in the hypertensive kidney. Our assessment of the genome-wide influence of ANG II resulted in the detection of several novel genes and in a recognition of potential new roles for the previously characterized genes, thus providing new probes with which to further explore the ANG II effects in normal and disease states.

hypertension; mouse kidney transcriptome; angiotensin excess; tissue kallikrein; cathepsin D




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