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Novel candidate genes for impaired nephron development in a rat model with inherited nephron deficit and albuminuria
Author(s) -
Herlan Laura,
Schulz Angela,
Schulte Leonard,
Schulz Herbert,
Hübner Norbert,
Kreutz Reinhold
Publication year - 2015
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12462
Subject(s) - nephron , albuminuria , endocrinology , gene , medicine , biology , kidney , genetics
Summary Defects in nephrogenesis can have detrimental effects on cardiovascular and renal health in adult life. This is confirmed by observations in the Munich Wistar Frömter ( MWF ) rat that exhibits a congenital nephron deficit and renal failure with age. Here, we performed genome‐wide transcriptome analysis in embryonic kidneys to identify candidate genes for the reduced nephron number in MWF . We compared MWF rats at embryonic day (E)15.5 with stage‐matched spontaneously hypertensive rats ( SHR ) at E16. Microarray analysis revealed 311 transcripts representing 253 known genes with differential expression between MWF and SHR (fold change > +1.5 or < −1.5, respectively). Genes located on rat chromosome ( RNO ) 6 were of special interest because RNO 6 carries genetic loci previously linked to the nephron deficit and renal damage in MWF . Differentially expressed genes located on RNO 6 were further investigated by Real‐time PCR including the late‐stage of fetal kidney development, i.e. E19.0/E19.5, and week 4 of postnatal life when nephrogenesis is completed. Seven genes including Abcg5, Ab1‐233, Efcab11, Fntb, Gpx2, Lrrn3 , and Rtn1 were assigned on RNO 6 and their differential expression was confirmed. Thus, we identified several genes that may act as crucial players in nephron development and are responsible for the nephron deficit in the MWF model.