The root of Parkinson’s disease (PD) points to a poorly regulated electron transport chain leading to mitochondrial damage, where many proteins need to work cohesively to ensure proper function. The two key players of this pathway are PINK1, also known as PTEN or PARK6, and Parkin, also known as PARK2 - where PINK1 acts as an upstream effector of Parkin to regulate mitochondrial dynamics. Mitochondria must maintain a healthy equilibrium and do so by undergoing a series of fission and fusion events. The proteins Drp-1 and OPA-1, respectively, govern these events. While PINK1 and Parkin are directly involved in the progression of PD, their role in maintaining mitochondrial health has associated them with autophagy and mitophagy events in other models such as the loss of retinal pigment epithelial cell (RPE) viability. Using a Parkin antibody is a great way to monitor the behavior of this protein in RPE research.
Parkin Antibody [NB100-91921] - Analysis of Parkin in mouse liver and hypatocytes using Parkin antibody. Image from verified customer review.
The first use of a Parkin antibody in RPE research is from Lee et al, to study the connection between mitotic catastrophe and autophagy in RPE cells where cell death leads to a wide range of ocular pathological outcomes. To begin, it has been established that mitochondrial DNA damage leads to decreased function of RPE cells. After a study specifically pointed to the mitochondrial complex I involvement, an assessment of PINK1 and Parkin behavior during different treatments were carried out. For starters, a Beclin-1 antibody was used in western blot on ARPE-19 cells to show that the mitochondrial complex I chemical “Rotenone” lead to increased autophagy. Next, an up-regulation of Parkin in RPE-MC (mitotic catastrophic) cells was noted with the use of a Parkin antibody in western blot. Likewise, knockdown of Parkin and subsequent testing with a Parkin antibody in western blot showed a significant aggravation to RPE-MC cells. Overall, their research illustrated how PINK-1 mediated Parkin translocation is responsible for the cytoprotection of RPE-MC cells.
Next, a Parkin antibody was used by Chen et al to study the role of autophagy in the protection of RPE cells from light-induced degeneration. While it had been pre-determined that autophagy occurs at a basal level in RPE cells in order to maintain cellular homeostasis, exposure to light has been proven to up-regulate the autophagic process and lead to damage. Due to the high level of mitochondria present in photoreceptor and RPE cells, the role of mitophagy was closely examined. Using a Parkin antibody in immunohistochemistry, they demonstrated that Parkin is indeed expressed in the retina of albino WT mice and upregulated in the presence of light-induced retinopathy. Interestingly, a Parkin deficiency also results in light-induced retinopathy, strengthening its role in the mechanism. In the end, Parkin related mitochondrial quality control could be the root cause of RPE degeneration with exposure to light.
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