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2017 ; 37
(6
): 1115-1126
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Endoglin Mediates Vascular Maturation by Promoting Vascular Smooth Muscle Cell
Migration and Spreading
#MMPMID28450296
Tian H
; Ketova T
; Hardy D
; Xu X
; Gao X
; Zijlstra A
; Blobe GC
Arterioscler Thromb Vasc Biol
2017[Jun]; 37
(6
): 1115-1126
PMID28450296
show ga
OBJECTIVE: Endoglin, a transforming growth factor-? superfamily coreceptor, is
predominantly expressed in endothelial cells and has essential roles in vascular
development. However, whether endoglin is also expressed in vascular smooth
muscle cells (VSMCs), especially in vivo, remains controversial. Furthermore, the
roles of endoglin in VSMC biology remain largely unknown. Our objective was to
examine the expression and determine the function of endoglin in VSMCs during
angiogenesis. APPROACH AND RESULTS: Here, we determine that endoglin is robustly
expressed in VSMCs. Using CRISPR/CAS9 knockout and short hairpin RNA knockdown in
the VSMC/endothelial coculture model system, we determine that endoglin in VSMCs,
but not in endothelial cells, promotes VSMCs recruitment by the endothelial cells
both in vitro and in vivo. Using an unbiased bioinformatics analysis of RNA
sequencing data and further study, we determine that, mechanistically, endoglin
mediates VSMC recruitment by promoting VSMC migration and spreading on
endothelial cells via increasing integrin/FAK pathway signaling, whereas endoglin
has minimal effects on VSMC adhesion to endothelial cells. In addition, we
further determine that loss of endoglin in VSMCs inhibits VSMC recruitment in
vivo. CONCLUSIONS: These studies demonstrate that endoglin has an important role
in VSMC recruitment and blood vessel maturation during angiogenesis and also
provide novel insights into how discordant endoglin function in endothelial and
VSMCs may regulate vascular maturation and angiogenesis.