Endothelial Cell–Dependent Regulation of Arteriogenesis

Now if we can just get our researchers to figure out how to put arteriogenesis together with angiogenesis or vasculogenesis and new stem cells for the brain to fill in those dead areas. Sounds pretty damn simple to me. A great stroke association would tackle and solve something like that. Nothing ventured, nothing gained.
Maybe leptin administration;

Delayed leptin administration after stroke induces neurogenesis and angiogenesis

http://circres.ahajournals.org/content/113/9/1076.abstract.html?etoc

1. Filipa Moraes,
2. Julie Paye,
3. Feilim Mac Gabhann,
4. Zhen W. Zhuang,
5. Jiasheng Zhang,
6. Anthony A. Lanahan,
7. Michael Simons

+ Author Affiliations

1. From the Department of Internal Medicine, Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, New Haven, CT (F.M., Z.W.Z., J.Z., A.A.L., M.S.); Dartmouth College, Hanover, NH (J.P.); Institute for Computational Medicine and Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD (F.M.G.); and Department of Cell Biology, Yale University School of Medicine, New Haven, CT (M.S.). The online-only Data Supplement is available with this article at http://circres.ahajournals.org/lookup/suppl/doi:10.1161/CIRCRESAHA.113.301340/-/DC1.

1. Correspondence to Michael Simons, MD, Cardiovascular Medicine, Yale University School of Medicine, PO Box 802017, 333 Cedar St, New Haven, CT 06520-2017. E-mail michael.simons@yale.edu

Abstract

Rationale: Arteriogenesis is the process of formation of arterial conduits. Its promotion is an attractive therapeutic strategy in occlusive atherosclerotic diseases. Despite the functional and clinical importance of arteriogenesis, the biology of the process is poorly understood. Synectin, a gene previously implicated in the regulation of vascular endothelial cell growth factor signaling, offers a unique opportunity to determine relative contributions of various cell types to arteriogenesis.

Objective: We investigated the cell-autonomous effects of a synectin knockout in arterial morphogenesis.

Methods and Results: A floxed synectin knockin mouse line was crossbred with endothelial-specific (Tie2, Cdh5, Pdgfb) and smooth muscle myosin heavy chain–specific Cre driver mouse lines to produce cell type–specific deletions. Ablation of synectin expression in endothelial, but not smooth muscle cells resulted in the presence of developmental arterial morphogenetic defects (smaller size of the arterial tree, reduced number of arterial branches and collaterals) and impaired arteriogenesis in adult mice.

Conclusions: Synectin modulates developmental and adult arteriogenesis in an endothelial cell–autonomous fashion. These findings show for the first time that endothelial cells are central to both developmental and adult arteriogenesis and provide a model for future studies of factors involved in this process.