Amyloidogenic Medin Impairs Endothelial Cell Autophagy and Viability that is Reversed by Monosialoganglioside Nanoliposomes
Abstract
Medin peptides form the most common human amyloid proteins that accumulate in the vasculature with aging and are thus implicated as potential etiologic agents in the phenotypic changes associated with vascular aging. We previously showed that med in impairs endothelium‐mediated dilator response in human microvessels and induces pro‐inflammatory signaling. Impaired autophagy has been implicated in cellular aging and endothelial dysfunction and could be a mechanism by which med in links aging and vascular dysfunction. We also previously showed that monosialoganglioside nanoliposomes (NLGM1), phospholipids containing 5% monosialoganglioside, 70% phosphatidylcholine and 25% cholesterol, protect against endothelial dysfunction induced by amyloidogenic light chain proteins.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Apr 01, 2018
- Source ID
- 10.1096/fasebj.2018.32.1_supplement.846.16
Entities
People
- Diana Guzman‐villanueva
- Hannah Davies
- Jillian Madine
- Nina Karamanova
- Raymond Migrino
- Seth Truran
- Volkmar Weissig
Organizations
- British Heart Foundation
- Midwestern University
- National Institutes of Health
- United States Department of Defense
- University of Arizona
- University of Liverpool