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Differential Gene Expression Found in Normal and Hypertensive Kidneys

By LabMedica International staff writers
Posted on 22 Nov 2011
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In a comparison of gene expression in kidney tissues isolated from patients with hypertension and controls with normal blood pressure researchers found 14 genes and 11 miRNAs (microRNAs) that were differentially expressed in the medulla.

Investigators at the University of Leicester (United Kingdom) and colleagues from Poland and Australia analyzed tissue samples selected from 15 patients known to have high blood pressure, along with seven patients with normal blood pressure who were used as the control group for the study. The samples of human kidneys were stored in the Silesian Renal Tissue Bank (SRTB), and came from Polish males, individuals of white European ancestry.

Results of microarray analysis published in the October 31, 2011, online edition of the journal Hypertension revealed 14 genes and 11 miRNAs that were differentially expressed in the kidney medulla. Two of the miRNAs, which had lower levels of expression in the tissues from the hypertension patients, were linked to renin expression. Inhibition of miRNAs that reduce renin synthesis causes increased expression of renin activity. An overactive renin-angiotension system leads to vasoconstriction and retention of sodium and water. These effects lead to hypertension.

“I am very excited about this publication,” said contributing author Dr. Maciej Tomaszewski, senior clinical lecturer in cardiovascular medicine at the University of Leicester. “Renin is one of the most important contributors to blood pressure regulation. The novel insights into its expression within the human kidney from this study open up new avenues for the development of new antihypertensive medications. The collection of hypertensive and normotensive kidneys is available for our studies in Leicester thanks to a long-term international collaboration. We will continue using this unique research resource in our further studies to decipher the genetic background of human hypertension.”

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University of Leicester



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