Abstract 352: Adventitial Stem Cell Progenitors Express Neural Stem Cell Markers
Many forms of cardiovascular disease (CVD) are charaterised by intimal medial thickening (IMT) due to the formation of a neointimal layer as a result of the accumulation of vascular smooth muscle cells (vSMC) within the vessel wall. There is strong evidence, albeit controversial, that indicates a putative role for both adventitial (Sca1+, CD34+ and Lin-) and medial multipotent vascular progenitor stem cell-derived [Sox10, Sox17 and S100β] vSMC in contributing to IMT.
The objective of this study was to characterise adventitial progenitor stem cells (APCs) from aortic explants and compare them to medial MVSCs. APC and MVSC phenotype was determined by immunocytochemistry using antisera specific for adventitial stem cell marker Sca1 and stem cell markers Sox10, Sox 17 and S100β respectively. Differentiated vSMC markers, α-actin, calponin 1 and smooth muscle myosin hevy chain II (Myh11) were used to detect SMCs. Discrete APC populations were positive for neural stem cell markers [Sox 10, Sox17 and S100β] as well as marker α-actin. Notably a significant number of intial cells migrating from the adventitial explant were Sox 10, Sox 17 and S100β positive respectively. Similarly, MVSC from medial explants were positive for neural stem cell markers [Sox 10, Sox17 and S100β] and Sca1 (when grown in maintenance media). There was a distinct absence of smooth muscle myosin heavy chain II filaments (differentiated vSMC markers) in both the APC and MVSC cell populations.
We conclude that APCs and MVSCs may be derived from a similar source.
Author Disclosures: E. Fitzpatrick: None. E. Kennedy: None. R. Hakimjavadi: None. P.A. Cahill: None.
This research has received full or partial funding support from the American Heart Association.
- © 2015 by American Heart Association, Inc.