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Identification of a common molecular pathway in hypertensive renal damage: comparison of rat and human gene expression profiles
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2015 (English)In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 33, no 3, 584-596 p.Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: There is a common structural progression in hypertensive renal damage with early arterial damage and fibrosis in the juxtamedullary cortex.

METHOD: The present investigation identifies a common pathway using three-gene expression profiles from hypertensive rat models: 60-week-old spontaneously hypertensive rat (SHR), salt-loaded stroke-prone SHR (SHRSP), and the non-clipped kidney after 24 weeks of two-kidney, one-clip hypertension (2K1C). Kidney damage was scored using a specialized system. Gene-expression profiles were determined using microarrays and validated using a panel of 47 genes by quantitative real-time PCR.

RESULTS: All groups showed kidney damage (SHRs: 0.32 ± 0.09 vs. Wistar-Kyoto rats: 0.06 ± 0.03; 2K1C: 0.27 ± 0.13 vs. pooled controls: 0.01 ± 0.01; SHRSP: 1.13 ± 0.14 vs. WKY: 0.04 ± 0.03; all P < 0.05). A total of 1614 genes were changed in the SHR experiment, 1323 in the SHRSP, and 576 in the 2K1C. Eighty-eight genes were similarly regulated in all three models. Gene ontology enrichment analysis identified 59 ontologies that were enriched in all three datasets. These included over-representation to extracellular matrix, response to oxidative stress, and immune system processes. Out of the 88 in-common genes, 40 could be connected in a common pathway that was compared to two gene-expression profiles from human kidneys with histologically verified fibrosis to identify a highly significant number of in-common genes that were also represented in the common genetic pathway.

CONCLUSION: There is a common pathway during the development of hypertensive kidney damage in rats irrespective of model. Interestingly, large parts of this common pathway are conserved in human kidney damage, which may indicate a broader importance in the development of chronic kidney disease.

Place, publisher, year, edition, pages
2015. Vol. 33, no 3, 584-596 p.
National Category
Physiology
Identifiers
URN: urn:nbn:se:uu:diva-235818DOI: 10.1097/HJH.0000000000000395ISI: 000349003300021PubMedID: 25380151OAI: oai:DiVA.org:uu-235818DiVA: diva2:762311
Funder
Swedish Society for Medical Research (SSMF)Swedish Heart Lung Foundation
Available from: 2014-11-11 Created: 2014-11-11 Last updated: 2017-12-05Bibliographically approved

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Hultström, Michael

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