Cell death by ischemia may occur by apoptosis as well as necrosis in experimental models of renal injury [7, 8].
In animal models of renal, intestinal, liver, cardiac, and cerebral ischemia, alcohol exposure is shown to reduce ischemia-reperfusion injury.
Bone morphogenetic protein (BMP -7 exhiBMP -7nti-fibrotic exhibitsin animal models of renal fibrosis and reffects EMT in renanimalular cells in vitro[100, 196].
The loss of interstitial capillaries is a feature of several experimental models of renal disease and this contributes to secondary kidney injury.
Most animal models of renal failure are not highly reproducible and poorly represent clinical manifestations of this condition [19], [20].
Multiple studies have also revealed that meprin expression is down-regulated in models of renal injury leading to acute renal failure.
Heme-oxygenase-1 (HO-1) is a cytoprotective molecule that has been shown to be beneficial in various models of renal injury.
This is in contrast to findings in alternative models of renal insufficiency, i.e. the renal artery ligation model where bp is markedly increased [29].
To address these issues we performed whole genome scale expression studies in healthy and diseased human kidney samples and mouse models of renal disease.
Following these results in the UUO model, we set out to investigate whether the effects on NF-κB regulation by Ang-(1 7) and Mas are restricted to the UUO model or also act in other models of renal inflammation.
We used MDCK and Caco-2 cells stably transfected with meprinα and or meprinβ to establish models of renal and intestinal epithelial cells expressing this protease at physiological levels.
