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Maternally derived mitochondria in SHR exhibit significant reduction in oxidative phosphorylation gene expression
Author(s) -
Collett Jason A,
Paulose Jiffin K.,
Cassone Vincent M.,
Osborn Jeffrey L.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.955.4
Subject(s) - tfam , endocrinology , medicine , biology , nrf1 , offspring , gene expression , blood pressure , kidney , gene , oxidative stress , transcription factor , genetics , pregnancy
Mitochondrial (Mt) dysfunction contributes to the pathophysiology of renal function and promotes cardiovascular disease including hypertension. We hypothesize that renal Mt‐genes derived from female SHR are linked to high blood pressure in offspring of SHR and normotensive (NT) Brown Norway (BN) rat crosses. After breeding a female Okamoto‐Aoki SHR (MAP=160mmHg) with a BN male (MAP=91mmHg), hypertensive female progeny were backcrossed with the founder BN for 5 consecutive generations. Mt‐protein coding genes (13 total) and nuclear transcription factors mediating Mt‐transcription were evaluated in kidney, heart and liver of NT(n=20) vs. HT(n=20) SHR/BN using quantitative real‐time PCR. GAPDH was used as reference. Renal but not liver or heart Mt‐gene expression was decreased ~2–5 fold in 12 of 13 protein coding genes of HT SHR/BN. Renal but not liver mRNA expression of nuclear transcription factors for Tfam, NRF1, NRF2 and Pgc1α were decreased in HT SHR/BN. This renal specific reduction of nuclear and Mt‐gene expression may down‐regulate oxidative metabolism and increase renal reactive oxygen species production in SHR leading to hypertension and cardiovascular disease.