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2015 ; 10
(8
): e0136441
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Kidney-Specific Reduction of Oxidative Phosphorylation Genes Derived from
Spontaneously Hypertensive Rat
#MMPMID26308211
Collett JA
; Paulose JK
; Cassone VM
; Osborn JL
PLoS One
2015[]; 10
(8
): e0136441
PMID26308211
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Mitochondrial (Mt) dysfunction contributes to the pathophysiology of renal
function and promotes cardiovascular disease such as hypertension. We hypothesize
that renal Mt-genes derived from female spontaneously hypertensive rats (SHR)
that exhibit hypertension have reduced expression specific to kidney cortex.
After breeding a female Okamoto-Aoki SHR (SAP = 188mmHg) with Brown Norway (BN)
males (SAP = 100 and 104 mmHg), hypertensive female progeny were backcrossed with
founder BN for 5 consecutive generations in order to maintain the SHR
mitochondrial genome in offspring that contain over increasing BN nuclear genome.
Mt-protein coding genes (13 total) and nuclear transcription factors mediating
Mt-gene transcription were evaluated in kidney, heart and liver of normotensive
(NT: n = 20) vs. hypertensive (HT: n = 20) BN/SHR-mtSHR using quantitative
real-time PCR. Kidney cortex, but not liver or heart Mt-gene expression was
decreased ~2-5 fold in 12 of 13 protein encoding genes of HT BN/SHR-mtSHR. Kidney
cortex but not liver mRNA expression of the nuclear transcription factors Tfam,
NRF1, NRF2 and Pgc1? were also decreased in HT BN/SHR-mtSHR. Kidney cortical
tissue of HT BN/SHR-mtSHR exhibited lower cytochrome oxidase histochemical
staining, indicating a reduction in renal oxidative phosphorylation but not in
liver or heart. These results support the hypothesis that renal cortex of rats
with SHR mitochondrial genome has specifically altered renal expression of genes
encoding mitochondrial proteins. This kidney-specific coordinated reduction of
mitochondrial and nuclear oxidative metabolism genes may be associated with
heritable hypertension in SHR.
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