Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Interaction between diabetes and hypertension in a rat model of diabetic nephropathy

ABSTRACT: Fisher male Cyp1a1mRen2 rats were allocated into four groups of four biological replicates each: control; streptozotocin-induced diabetes alone; indole-3-carbinol induced hypertension alone; combined induced diabetes and hypertension.
Kidneys were harvested for microarray analysis.analysis.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Donald Dunbar

PROVIDER: E-MEXP-3165 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Hyperglycemia and renin-dependent hypertension synergize to model diabetic nephropathy.

Conway Bryan R BR Rennie Jillian J Bailey Matthew A MA Dunbar Donald R DR Manning Jonathan R JR Bellamy Christopher O CO Hughes Jeremy J Mullins John J JJ

Journal of the American Society of Nephrology : JASN 20111222 3

Rodent models exhibit only the earliest features of human diabetic nephropathy, which limits our ability to investigate new therapies. Hypertension is a prerequisite for advanced diabetic nephropathy in humans, so its rarity in typical rodent models may partly explain their resistance to nephropathy. Here, we used the Cyp1a1mRen2 rat, in which the murine renin-2 gene is incorporated under the Cytochrome P4501a1 promoter. In this transgenic strain, administration of low-dose dietary indole-3-carb ...[more]

PMID: 22193383

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Project description:AIMS/HYPOTHESIS: Pregnancies complicated by diabetes have a higher risk of adverse outcomes for mothers and children, including predisposition to disease later in life, such as metabolic syndrome and hypertension. We hypothesized that adverse outcomes from diabetic pregnancies may be linked to compromised placental function. Our goal in this study was to identify cellular and molecular abnormalities in diabetic placenta. METHODS: Using a mouse model of diabetic pregnancy, placental gene expression was assayed at midgestation and cellular composition was analyzed at various stages. Genome-wide expression profiling was validated by quantitative PCR, and tissue localization studies were performed to identify cellular correlates of altered gene expression in diabetic placenta. RESULTS: We detected significantly altered gene expression in diabetic placenta for genes expressed in the maternal as well as those in the embryonic compartments. We also found altered cellular composition of the decidual compartment. Furthermore, the junctional and labyrinth layers were reduced in diabetic placenta, accompanied by aberrant differentiation of spongiotrophoblast cells. CONCLUSIONS/INTERPRETATION: Diabetes during pregnancy alters transcriptional profiles in the murine placenta, affecting cells of both embryonic and maternal origin, and involving several genes not previously implicated in diabetic pregnancies. The molecular changes and abnormal differentiation of multiple cell types precede impaired growth of junctional zone and labyrinth, and placenta overall. Whether these changes represent direct responses to hyperglycaemia or physiological adaptations, they are likely to play a role in pregnancy complications and outcomes, and have implications for developmental origins of adult disease. The STZ diabetic mouse model was used to investigate gene expression changes in diabetic placentae at E10.5. Placentae were dissected from 5 different FVB dams at embryonic day 10.5 under diabetic conditions and from 5 control dams. Gene expression profiles from five individual placentae from independent pregnancies per group were compared.

Dataset Information

Interaction between diabetes and hypertension in a rat model of diabetic nephropathy

Publications

Hyperglycemia and renin-dependent hypertension synergize to model diabetic nephropathy.

Similar Datasets

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