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VEGF/VEGFR2 interaction down-regulates matrix metalloproteinase–9 via STAT1 activation and inhibits B chronic lymphocytic leukemia cell migration

AuthorsUgarte-Berzal, Estefanía ; Redondo-Muñoz, Javier ; Eroles, Pilar; Hernández del Cerro, Mercedes ; García-Marco, José A.; Terol, María José; García-Pardo, Angeles
Lymphocytic leukemia
Issue Date28-Jan-2010
PublisherAmerican Society of Hematology
CitationBlood, 115:846-849 (2010 )
AbstractB-cell chronic lymphocytic leukemia (B-CLL) migration involves several molecules, including matrix metalloproteinase–9 (MMP-9) and vascular endothelial growth factor (VEGF). We have studied whether VEGF regulates MMP-9. VEGF significantly reduced MMP-9 protein expression in a dose-dependent manner, measured by gelatin zymography. Blocking the VEGFR2 receptor restored MMP-9 levels, implicating this receptor in the observed effect. Down-regulation of MMP-9 by VEGF resulted in significant inhibition of B-CLL cell migration through Matrigel or human umbilical vein endothelial cells, confirming the crucial role of MMP-9 in these processes. Reverse-transcription polymerase chain reaction analyses revealed that VEGF regulated MMP-9 at the transcriptional level. Indeed, VEGF induced STAT1 tyrosine phosphorylation, and this was blocked by inhibiting VEGFR2. STAT1 was responsible for MMP-9 down-regulation, as STAT1 gene silencing restored MMP-9 production and B-CLL cell migration in the presence of VEGF. Thus, the levels of VEGF and MMP-9 influence B-CLL cell expansion and both molecules could constitute therapeutic targets for this disease.
DescriptionBrief Report. Artículo breve.
Publisher version (URL)http://bloodjournal.hematologylibrary.org/content/115/4/846.full.pdf
Appears in Collections:(CIB) Artículos
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