Maybe leptin administration;
http://circres.ahajournals.org/content/113/9/1076.abstract.html?etoc
- Filipa Moraes,
- Julie Paye,
- Feilim Mac Gabhann,
- Zhen W. Zhuang,
- Jiasheng Zhang,
- Anthony A. Lanahan,
- Michael Simons
+ Author Affiliations
- 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.
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