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2017 ; 37
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Homocysteine inhibits angiogenesis through cytoskeleton remodeling
#MMPMID28864781
Pan L
; Yu G
; Huang J
; Zheng X
; Xu Y
Biosci Rep
2017[Oct]; 37
(5
): ä PMID28864781
show ga
Homocysteine (Hcy) is an intermediate non-diet amino acid connecting methionine
and folate cycles. Elevated total Hcy level in blood, denoted as
hyperhomocysteinemia, has emerged as a prevalent and strong risk factor for
multiple diseases including atherosclerotic vascular disease in coronary,
cerebral, and peripheral vessels. Its detrimental effect on vascular system
implies the potential application as an inhibitor of angiogenesis. However, the
detailed mechanism is unveiled. Inhibitory effect of Hcy was assessed on vascular
endothelial growth factor (VEGF) induced cell proliferation and migration with
endothelial cell (EC) culture system. Its effect on angiogenesis was further
examined in vitro and in vivo After Hcy treatment, key angiogenic factors were
measured by RT-qPCR. Cellular skeletal structure was also evaluated by actin
stress fiber staining. VEGF-induced human umbilical vein EC (HUVEC) proliferation
and migration were dramatically down-regulated by Hcy in a dose-responsive
manner. Hcy treatment significantly inhibited the VEGF-induced angiogenesis in
vitro by tube formation assay and chick chorioallantoic membrane (CAM) vessel
formation in vivo Key angiogenic factors like VEGFR1/2 and angiopoietin (Ang)1/2
were substantially reduced by Hcy in HUVEC- and VEGF-induced actin stress fiber
cytoskeletal structure was abolished. We demonstrated that Hcy could inhibit
angiogenesis by targetting key angiogenic factor and disruption of actin
cytoskeleton which is crucial for cell migration.
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