In vivo modulation of angiogenesis by beta 2 glycoprotein I

Passam, Freda; Qi, Jun; Tanaka, Kumiko; Matthaei, Klaus I.; Krilis, Steven A.

doi:10.1016/j.jaut.2010.06.013

Cited by 28 publications

(24 citation statements)

References 34 publications

(41 reference statements)

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“…Our previous study identified that DI-IV inhibits human umbilical vein cell angiogenesis through the VEGF pathway (8). To determine whether DI-IV inhibited AGE-induced RF/6A angiogenesis through a similar mechanism, the transcript levels of VEGF and its receptors were measured.…”

Section: Di-iv Inhibits the Age-induced Mrna Expression Of Vegfr-2mentioning

confidence: 99%

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Domain I-IV of β2-glycoprotein I inhibits advanced glycation end product-induced angiogenesis by down-regulating vascular endothelial growth factor 2 signaling

Wang

Zhou

Meng

et al. 2014

Molecular Medicine Reports

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Section: Di-iv Inhibits the Age-induced Mrna Expression Of Vegfr-2mentioning

confidence: 99%

“…β2-GPI is the major autoantigen in patients with antiphospholipid syndrome (7). β2-GPI has anti-angiogenetic properties (8) and one of its mutants, in which domain V of domains I-IV is absent (DI-IV), has the potential to produce more marked effects (9).…”

Section: Introductionmentioning

confidence: 99%

Domain I-IV of β2-glycoprotein I inhibits advanced glycation end product-induced angiogenesis by down-regulating vascular endothelial growth factor 2 signaling

Wang

Zhou

Meng

et al. 2014

Molecular Medicine Reports

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“…It has been shown that angiogenesis can be regulated by β 2 -GPI which inhibits neovascularization of endothelial cells [14,16,17]. Recently, the inhibitory effect of β 2 -GPI on angiogenesis was also demonstrated in vivo by using β 2 -GPI-deficient mice [15]. Nakagawa et al [45] found that a dual effect of β 2 -GPI on angiogenesis is dependent on its interaction with or without angiostatin.…”

Section: Enos Mediates the Inhibitory Effect Of β 2 -Gpi On Haec Migrmentioning

confidence: 99%

“…Uncontrolled angiogenesis promotes various diseases, including retinopathies and cancer [10]. β 2 -GPI may exert its anti-angiogenic property in some tumours, such as melanoma, bladder and prostate cancer, suggesting that β 2 -GPI is a potential factor in angiogenesis-targeted therapy [14][15][16]. Nevertheless, whether β 2 -GPI plays a role in cell migration and what molecular mechanism it may use still remain unknown.…”

Section: Enos Mediates the Inhibitory Effect Of β 2 -Gpi On Haec Migrmentioning

confidence: 99%

“…Several factors generated by the vasculature or in the circulation can regulate migration or proliferation of endothelial cells [12,13]. β 2 -GPI has been recently defined as a vasoactive substance with anti-angiogenic properties [14][15][16][17]; however, the molecular basis of the action of β 2 -GPI on endothelial cell migration remains unknown.…”

Section: Introductionmentioning

confidence: 99%

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β2-Glycoprotein I inhibits endothelial cell migration through the nuclear factor κB signalling pathway and endothelial nitric oxide synthase activation

Chiu¹,

Chiou

Chiang³

2012

Biochemical Journal

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β₂-GPI (β₂-glycoprotein I) is a plasma glycoprotein ascribed with an anti-angiogenic function; however, the biological role and molecular basis of its action in cell migration remain unknown. The aim of the present study was to assess the contribution of β₂-GPI to HAEC (human aortic endothelial cell) migration and the details of its underlying mechanism. Using wound healing and Boyden chamber assays, we found that β₂-GPI inhibited endothelial cell migration, which was restored by its neutralizing antibody. NF-κB (nuclear factor κB) inhibitors and lentiviral siRNA (small interfering RNA) silencing of NF-κB significantly attenuated the inhibitory effect of β₂-GPI on cell migration. Moreover, β₂-GPI was found to induce IκBα (inhibitor of NF-κB) phosphorylation and translocation of p65 and p50. We further demonstrated that mRNA and protein levels of eNOS [endothelial NO (nitric oxide) synthase] and NO production were all increased by β₂-GPI and these effects were remarkably inhibited by NF-κB inhibitors and siRNAs of p65 and p50. Furthermore, β₂-GPI-mediated inhibition of cell migration was reversed by eNOS inhibitors and eNOS siRNAs. The findings of the present study provide novel insight into the ability of β₂-GPI to inhibit endothelial cell migration predominantly through the NF-κB/eNOS/NO signalling pathway, which indicates a potential direction for clinical therapy in vascular diseases.

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