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Alterations to the Liver RAS in Antenatal Induced MLPD Systemic Hypertension
Author(s) -
Stewart John Michael,
Goyal Ravi,
Longo Lawrence
Publication year - 2010
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.24.1_supplement.786.8
Subject(s) - offspring , fetus , medicine , endocrinology , gestation , messenger rna , biology , low protein diet , kidney , dot blot , blood pressure , pregnancy , pancreas , gene , biochemistry , genetics
Objective It has been well established that systemic hypertension can be result of fetal programming by antenatal maternal low protein diet (MLPD). Furthermore, as apposed to the ‘classical’ systemic renin‐angiotensinogen system (RAS) several studies have suggested that many tissues including lungs, pancreas, kidney, brain, and liver have their own ‘alternative’ RAS. In mice, we tested the hypothesis that hypertensive mice resulting from antenatal MLPD show changes in the liver specific RAS pathway. Methods Mice dams were fed a specified isocaloric low protein diet from 7 days precoitus maintained thoughout gestation. We isolated DNA, mRNA, and protein from livers of offspring female and male mice exposed to 50% MLPD and 33% MLPD at 3 weeks and 33 weeks of age. We examined eight RAS genes with qPCR and dot blot analysis at the transcript and protein level. Results AGT transcript levels were altered in MLPD mice while there was no significant change in protein. Female AGT transcripts were increased at 3 weeks of age but not 33 weeks and protein levels were not significantly different from control. Conclusions In response to an antenatal maternal low protein diet AGT transcript levels change while protein levels do not. These changes in liver RAS, may help elucidate mechanisms responsible for fetal programming of disease, especially increased blood pressure.