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NF-kappaB contributes to transcription of placenta growth factor and interacts with metal responsive transcription factor-1 in hypoxic human cells


Cramer, Mirjam; Nagy, Ivana; Murphy, Brian J; Gassmann, Max; Hottiger, Michael O; Georgiev, Oleg; Schaffner, Walter (2005). NF-kappaB contributes to transcription of placenta growth factor and interacts with metal responsive transcription factor-1 in hypoxic human cells. Biological Chemistry, 386(9):865-872.

Abstract

Placenta growth factor (PlGF) is a member of the vascular endothelial growth factor family of cytokines that control vascular and lymphatic endothelium development. It has been implicated in promoting angiogenesis in pathological conditions via signaling to vascular endothelial growth factor receptor-1. PlGF expression is induced by hypoxia and proinflammatory stimuli. Metal responsive transcription factor 1 (MTF-1) was shown to take part in the hypoxic induction of PlGF in Ras-transformed mouse embryonic fibroblasts. Here we report that PlGF expression is also controlled by NF-kappaB. We identified several putative binding sites for NF-kappaB in the PlGF promoter/enhancer region by sequence analyses, and show binding and transcriptional activity of NF-kappaB p65 at these sites. Expression of NF-kappaB p65 from a plasmid vector in HEK293 cells caused a substantial increase of PlGF transcript levels. Furthermore, we found that hypoxic conditions induce nuclear translocation and interaction of MTF-1 and NF-kappaB p65 proteins, suggesting a role for this complex in hypoxia-induced transcription of PlGF.

Abstract

Placenta growth factor (PlGF) is a member of the vascular endothelial growth factor family of cytokines that control vascular and lymphatic endothelium development. It has been implicated in promoting angiogenesis in pathological conditions via signaling to vascular endothelial growth factor receptor-1. PlGF expression is induced by hypoxia and proinflammatory stimuli. Metal responsive transcription factor 1 (MTF-1) was shown to take part in the hypoxic induction of PlGF in Ras-transformed mouse embryonic fibroblasts. Here we report that PlGF expression is also controlled by NF-kappaB. We identified several putative binding sites for NF-kappaB in the PlGF promoter/enhancer region by sequence analyses, and show binding and transcriptional activity of NF-kappaB p65 at these sites. Expression of NF-kappaB p65 from a plasmid vector in HEK293 cells caused a substantial increase of PlGF transcript levels. Furthermore, we found that hypoxic conditions induce nuclear translocation and interaction of MTF-1 and NF-kappaB p65 proteins, suggesting a role for this complex in hypoxia-induced transcription of PlGF.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Center for Integrative Human Physiology
05 Vetsuisse Faculty > Institute of Veterinary Physiology
05 Vetsuisse Faculty > Department of Molecular Mechanisms of Disease
07 Faculty of Science > Department of Molecular Mechanisms of Disease
Dewey Decimal Classification:570 Life sciences; biology
Language:English
Date:September 2005
Deposited On:15 Apr 2015 13:17
Last Modified:08 Dec 2017 12:49
Publisher:De Gruyter
ISSN:1431-6730
Publisher DOI:https://doi.org/10.1515/BC.2005.101
PubMed ID:16164411

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