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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Curr+Opin+Hematol
2018 ; 25
(3
): 212-218
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NOTCH regulation of the endothelial cell phenotype
#MMPMID29547401
Mack JJ
; Iruela-Arispe ML
Curr Opin Hematol
2018[May]; 25
(3
): 212-218
PMID29547401
show ga
PURPOSE OF REVIEW: The formation of a hierarchical vascular network is a complex
process that requires precise temporal and spatial integration of several
signaling pathways. Amongst those, Notch has emerged as a key regulator of
multiple steps that expand from endothelial sprouting to arterial specification
and remains relevant in the adult. This review aims to summarize major concepts
and rising hypotheses on the role of Notch signaling in the endothelium. RECENT
FINDINGS: A wealth of new information has helped to clarify how Notch signaling
cooperates with other pathways to orchestrate vascular morphogenesis, branching,
and function. Endothelial vascular endothelial growth factor, C-X-C chemokine
receptor type 4, and nicotinamide adenine dinucleotide phosphate oxidase 2 have
been highlighted as key regulators of the pathway. Furthermore, blood flow forces
during vascular development induce Notch1 signaling to suppress endothelial cell
proliferation, enhance barrier function, and promote arterial specification.
Importantly, Notch1 has been recently recognized as an endothelial mechanosensor
that is highly responsive to the level of shear stress to enable differential
Notch activation in distinct regions of the vessel wall and suppress
inflammation. SUMMARY: Although it is well accepted that the Notch signaling
pathway is essential for vascular morphogenesis, its contributions to the
homeostasis of adult endothelium were uncovered only recently. Furthermore, its
exquisite regulation by flow and impressive interface with multiple signaling
pathways indicates that Notch is at the center of a highly interactive web that
integrates both physical and chemical signals to ensure vascular stability.
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