Researchers at Massachusetts General Hospital in Boston have made functioning rat kidneys in the laboratory, a bioengineering achievement that may one day lead to the ability to create replacement organs for people with kidney disease.
Recently, it was reported that decellularization of intact rat kidneys in a manner that preserved the intricate architecture allowed seeded ES cells to populate and proliferate within the glomerular, vascular, and tubular structures [ 119].
Such a phenomenon has been demonstrated, for example, in mesangial cells of rat kidneys, in which transfection with the COX-2 gene was followed by an increase in MDR1/P-gp expression [ 14], and in cells of the gastric mucosa during infection with Helicobacter pylori [ 30].
We examined angiotensinogen gene expression in rat kidney by in situ hybridization histochemistry.
These findings indicate that chronic fluorosis can lead to the abnormal mitochondrial dynamics and changed morphology in the rat kidney, which in mechanism might be induced by a high level of oxidative stress in the disease.
For this purpose, we focused on meprinβ expression in healthy rat kidney and in two models of rat glomerular disease: passive Heymann nephritis (PHN), a rat model of human membranous nephropathy, and anti-Thy 1.1 mesangial proliferative nephritis [3], [40] [42].
As shown in Table 2, proteins identified from rat kidney tissue in the ERLIC04 method are involved in various biological processes such as protein metabolism, RNA metabolism, cellular component organization, transport and developmental processes.
In summary, the current studies demonstrate the expression of occludin and ZO-1 in the normal rat kidney and in response to ischemia reperfusion injury.
