Asset Details
Do you wish to reserve the book?
Polycomb Repressive Complex 2 Regulates MiR-200b in Retinal Endothelial Cells: Potential Relevance in Diabetic Retinopathy
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Polycomb Repressive Complex 2 Regulates MiR-200b in Retinal Endothelial Cells: Potential Relevance in Diabetic Retinopathy
Do you wish to request the book?
Polycomb Repressive Complex 2 Regulates MiR-200b in Retinal Endothelial Cells: Potential Relevance in Diabetic Retinopathy
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Polycomb Repressive Complex 2 Regulates MiR-200b in Retinal Endothelial Cells: Potential Relevance in Diabetic Retinopathy
2015
Overview
Glucose-induced augmented vascular endothelial growth factor (VEGF) production is a key event in diabetic retinopathy. We have previously demonstrated that downregulation of miR-200b increases VEGF, mediating structural and functional changes in the retina in diabetes. However, mechanisms regulating miR-200b in diabetes are not known. Histone methyltransferase complex, Polycomb Repressive Complex 2 (PRC2), has been shown to repress miRNAs in neoplastic process. We hypothesized that, in diabetes, PRC2 represses miR-200b through its histone H3 lysine-27 trimethylation mark. We show that human retinal microvascular endothelial cells exposed to high levels of glucose regulate miR-200b repression through histone methylation and that inhibition of PRC2 increases miR-200b while reducing VEGF. Furthermore, retinal tissue from animal models of diabetes showed increased expression of major PRC2 components, demonstrating in vivo relevance. This research established a repressive relationship between PRC2 and miR-200b, providing evidence of a novel mechanism of miRNA regulation through histone methylation.
Publisher
Public Library of Science,Public Library of Science (PLoS)
Subject
/ Animals
/ Diabetes
/ Diabetes Mellitus - metabolism
/ Diabetes Mellitus - pathology
/ Diabetic Retinopathy - metabolism
/ Diabetic Retinopathy - pathology
/ Endothelial Cells - drug effects
/ Endothelial Cells - metabolism
/ Endothelial Cells - pathology
/ Endothelium, Vascular - drug effects
/ Endothelium, Vascular - metabolism
/ Endothelium, Vascular - pathology
/ Glucose
/ Histones
/ Humans
/ Lysine
/ Male
/ MicroRNA
/ miRNA
/ Polycomb Repressive Complex 2 - genetics
/ Polycomb Repressive Complex 2 - metabolism
/ Retina
/ Structure-function relationships
