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Defective pericyte recruitment of villous stromal vessels as the possible
etiologic cause of hydropic change in complete hydatidiform mole
#MMPMID25849742
Kim KR
; Sung CO
; Kwon TJ
; Lee J
; Robboy SJ
PLoS One
2015[]; 10
(4
): e0122266
PMID25849742
show ga
The pathogenetic mechanism underlying the hydropic change in complete
hydatidiform moles (CHMs) is poorly understood. A growing body of data suggests
that pericytes play a role in vascular maturation. Since maturation of villous
stromal vessels in CHMs is markedly impaired at early stages, we postulated that
a defect in pericytes around stromal vessels in chorionic villi might cause
vascular immaturity and subsequent hydropic change. To investigate this, we
examined several markers of pericytes, namely, ?-smooth muscle actin (?-SMA),
platelet-derived growth factor receptor-? (PDGFR-?), and desmin, in 61 normally
developing placentas and 41 CHMs with gestational ages of 4-12 weeks. The
ultrastructure of villous stromal vessels was also examined. Mature blood vessels
from normal placentas show patent vascular lumens and formed hematopoietic
components in the villous stroma. ?-SMA and PDGFR-? expression in the villous
stroma gradually increased and extended from the chorionic plate to peripheral
villous branches. The labeled cells formed a reticular network in the villous
stroma and, after week 7, encircled villous stromal vessels. In comparison, ?-SMA
and PDGFR-? expression in the villous stroma and stromal vessels of CHMs was
significantly lower (p<0.05). Ultrastructurally, endothelial cells in villous
stromal vessels in normal placentas were consistently attached by pericytes after
week 7 when the vessels formed distinct lumen, whereas the villous stromal
vessels in CHMs consisted of linear chains of endothelial cells, often disclosing
primitive clefts without hematopoietic cells inside, and neither pericytes nor
basal lamina surrounded the endothelial cells at any gestational age studied.
This suggests that pericytes recruitment around villous stromal vessels is
defective in CHMs and links to the persistent vascular immaturity of the villous
stroma in CHMs, which in turns leads to hydropic villi.
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