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Fig. 8 Injection of VEGF-A
164
, but not VEGFR1-specific ligand PlGF, accelerates the
regeneration of liver mass (a), associated with an incremental increase in VEGFR
+
CD34
-
liver
SEC number (b)(n= 4). c Regenerative liver section of Id1
VenusYFP
mouse. Id1 is selectively
upregulated by partial hepatectomy in VE-cadherin
+
vessels. d VEGFR2 deletion diminishes Id1
upregulation in the regenerative liver d (n = 5).; *P \ 0.05, **P \ 0.01. Scale bars, 50 lm
placental growth factor (PlGF), as the latter selectively activates VEGFR1 [
69
].
After partial PH, VEGF
164
, but not PlGF, accelerated the regeneration of both liver
mass and the number of VEGFR3
+
CD34
-
LSECs, which were sustained for at
least 28 days (Fig.
8
a, b). Therefore, after partial hepatectomy, the activation of
VEGF-A/VEGFR2, but not PlGF/VEGFR1, is crucial for priming LSECs to ini-
tiate and maintain hepatic proliferation.
5.2 Microarray Analysis
To identify the angiocrine signals that stimulate liver regeneration, we used
microarray analysis (Fig.
9
). Among the endothelial-specific genes, the tran-
scription factor Id1 was specifically upregulated in the endothelial cells activated
by PH [
70
]. Using Id1
venusYFP
reporter mice in which the venus YFP expression is
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