AI Article Synopsis
- Pericyte loss is an early sign of diabetic retinopathy, and this study focuses on the role of SENP1 in this process.
- High glucose levels were found to inhibit SENP1 expression, leading to increased DBC1 sumoylation and subsequent apoptosis in retinal pericytes.
- The findings suggest that manipulating SENP1 activity could provide insights into potential treatments for diabetic retinopathy by preventing pericyte loss.
Article Abstract
Pericyte loss is an early characteristic change in diabetic retinopathy, but its precise molecular mechanisms have not been elucidated. This study investigated the role of SENP1 in pericyte loss in diabetic retinopathy. We demonstrated that a high concentration of glucose inhibited the expression of the Sentrin/SUMO-specific protease 1 (SENP1), which resulted in an increase in DBC1 sumoylation in bovine retinal pericytes (BRPCs). Furthermore, SENP1 overexpression attenuated hyperemia-induced apoptosis of BPRCs, and SENP1 knockdown aggravated this effect. We also provide evidence that DBC1 sumoylation/desumoylation is involved in the SENP1-regulated apoptosis of BRPCs under high glucose conditions. Understanding the role of SENP1 in the pathogenesis of high glucose induced pericyte loss could help elucidate important targets for future pharmacological interventions.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4826714 | PMC |
| http://dx.doi.org/10.1155/2016/6392658 | DOI Listing |
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