1. The prorenin/renin receptor ((P)RR) is a multifunctional protein that is widely distributed in various organs.
2. To investigate the role of tubular (P)RR in blood pressure regulation, transgenic mice overexpressing (P)RR in tubular epithelial cells were generated using the Ksp-Cadherin promoter.
3. The (P)RR transgene was predominantly expressed in the medulla and caused hypertension, lower osmolality and Na+ excretion, and lethal renal tubular damage when mated with alternative renin transgenic mice.
The article “Blood Pressure Elevation of Tubular Specific (P)RR Transgenic Mice and Lethal Tubular Degeneration due to Possible Intracellular Interactions between (P)RR and Alternative Renin Products” by Sae Saigo et al., published in PMC8745386, provides an overview of the roles of the prorenin/renin receptor ((P)RR), a multifunctional protein found in various organs, on blood pressure regulation. The authors generated transgenic mice overexpressing (P)RR in tubular epithelial cells using the Ksp-Cadherin promoter to investigate its role in BP regulation.
The article is generally reliable and trustworthy as it provides detailed information on the methods used for generating transgenic mice, as well as results from experiments conducted on these mice. Furthermore, it presents evidence for its claims through quantitative RT-PCR results and histopathological findings which support its conclusions. However, there are some potential biases present in this article which should be noted. Firstly, there is a lack of discussion regarding possible risks associated with overexpression of (P)RR or mating with alternative renin transgenic mice which could have been explored further. Additionally, while the authors provide evidence for their claims through quantitative RT-PCR results and histopathological findings, they do not provide any evidence for their claim that intracellular renin may be involved in (P)RR signaling other than stating that lethal renal tubular damage was observed when mated with alternative renin transgenic mice; this could have been further explored by providing more evidence such as gene expression data or biochemical assays to support this claim.
In conclusion, while this article provides detailed information on its methods and results from experiments conducted on these mice to