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ORIGINAL ARTICLE

Multidistrict human mesenchymal vascular cells: pluripotency and stemness characteristics

, , , , , , , , , , , & show all
Pages 275-287 | Received 07 Oct 2009, Accepted 04 Jan 2010, Published online: 15 Mar 2010
 

Abstract

Background aims. The presence of ectopic tissues in the pathologic artery wall raises the issue of whether multipotent stem cells may reside in the vasculature itself. Recently mesenchymal stromal cells (MSC) have been isolated from different human vascular segments (VW MSC), belying the previous view that the vessel wall is a relatively quiescent tissue. Methods. Resident multipotent cells were recovered from fresh arterial segments (aortic arches, thoracic and femoral arteries) collected in a tissue-banking facility and used to establish an in situ and in vitro study of the stemness features and multipotency of these multidistrict MSC populations. Results. Notch-1+, Stro-1+, Sca-1+ and Oct-4+ cells were distributed along an arterial wall vasculogenic niche. Multidistrict VW MSC homogeneously expressed markers of stemness (Stro-1, Notch-1 and Oct-4) and MSC lineages (CD44, CD90, CD105, CD73, CD29 and CD166) whilst they were negative for hematopoietic and endothelial markers (CD34, CD45, CD31 and vWF). Each VW MSC population had characteristics of stem cells, i.e. a high efflux capability for Hoechst 33342 dye and the ability to form spheroids when grown in suspension and generate colonies when seeded at low density. Again, VW MSC cultured in induction media exhibited adipogenic, chondrogenic and leiomyogenic potential but less propensity to osteogenic differentiation, as documented by histochemical, immunohistochemical, molecular and electron microscopy analysis. Conclusions. Overall, these findings may enlighten the physiopathologic mechanisms of vascular wall diseases as well as having potential implications for cellular, genetic and tissue engineering approaches to treating vascular pathologies when these are unresponsive to medical and surgical therapies.

Acknowledgement

This work was supported by Fondazione Fanti Melloni and Fondazione del Monte (AS, GP) and Programma di Ricerca Regione Emilia-Romagna-Università di Bologna, Area 1-b ‘Cell Therapy of Heart Failure’ (GP). We gratefully acknowledge Annamaria Ricciardi for her technical assistance and Ralph Nisbet for his editing support.

Disclosures

None.

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