Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28710479
&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
Endothelial cells by inactivation of VHL gene direct angiogenesis, not
vasculogenesis via Twist1 accumulation associated with hemangioblastoma
neovascularization
#MMPMID28710479
Wang Y
; Chen DQ
; Chen MY
; Ji KY
; Ma DX
; Zhou LF
Sci Rep
2017[Jul]; 7
(1
): 5463
PMID28710479
show ga
Inactivation of the VHL tumour suppressor gene is a highly frequent genetic event
in the carcinogenesis of central nervous system-(CNS) hemangioblastomas (HBs).
The patterning of the similar embryonic vasculogenesis is an increasing concern
in HB-neovascularization, and the classic vascular endothelial growth factor
(VEGF)-mediated angiogenesis driven by VHL loss-of-function from human
endothelium have been questioned. With this regard, we identify a distinct, VHL
silencing-driven mechanism in which human vascular endothelial cells by means of
increasing cell proliferation and decreasing cell apoptosis, is concomitant with
facilitating accumulation of Twist1 protein in vascular endothelial cells in
vitro. Importantly, this molecular mechanism is also pinpointed in CNS-HBs, and
associated with the process of HB-neovascularization. In contrast with recent
studies of HB-neovascularization, these modified cells did not endow with the
typical features of vasculogenesis, indicating that this is a common angiogenesis
implementing the formation of the vascular network. Taken together, these
findings suggest that vasculogenesis and angiogenesis may constitute
complementary mechanisms for HB-neovascularization, and could provide a rational
recognition of single anti-angiogenic intervention including targeting to the
Twist1 signalling for HBs.
free
free
free
