RGD Reference Report - Lipocalin-2 enhances angiogenesis in rat brain endothelial cells via reactive oxygen species and iron-dependent mechanisms. - Rat Genome Database

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Lipocalin-2 enhances angiogenesis in rat brain endothelial cells via reactive oxygen species and iron-dependent mechanisms.

Authors: Wu, Limin  Du, Yang  Lok, Josephine  Lo, Eng H  Xing, Changhong 
Citation: Wu L, etal., J Neurochem. 2015 Mar;132(6):622-8. doi: 10.1111/jnc.13023. Epub 2015 Jan 29.
RGD ID: 126790477
Pubmed: PMID:25557118   (View Abstract at PubMed)
PMCID: PMC4359653   (View Article at PubMed Central)
DOI: DOI:10.1111/jnc.13023   (Journal Full-text)

Inflammation is a key part of central nervous system pathophysiology. However, inflammatory factors are now thought to have both beneficial and deleterious effects. Here, we examine the hypothesis that lipocalin-2 (LCN2), an inflammatory molecule that can be up-regulated in the distressed central nervous system, may enhance angiogenesis in brain endothelial cells. Adding LCN2 (0.5-2.0 μg/mL) to RBE (Rat brain endothelial cells). 4 rat brain endothelial cells significantly increased matrigel tube formation and scratch migration, and also elevated levels of iron and reactive oxygen species. Co-treatment with a radical scavenger (U83836E), a Nox inhibitor (apocynin) and an iron chelating agent (deferiprone) significantly dampened the ability of LCN2 to enhance tube formation and scratch migration in brain endothelial cells. These findings provide in vitro proof of the concept that LCN2 can promote angiogenesis via iron- and reactive oxygen species-related pathways, and support the idea that LCN2 may contribute to the neurovascular recovery aspects of inflammation. Angiogenesis is an important part of stroke recovery. In the present study, we examined the hypothesis that lipocalin-2 (LCN2) may enhance angiogenesis in brain endothelial cells. LCN2 promoted tube formation and migration via iron and ROS-related pathways in rat brain endothelial cells. ROS scavengers, Nox inhibitors and iron chelators all dampened the ability of LCN2 to enhance in vitro angiogenesis. These findings support the idea that LCN2 that is released by damaged neurons may act as a 'help me' signal that promotes neurovascular recovery after stroke and brain injury.



Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  

Objects Annotated

Genes (Rattus norvegicus)
Lcn2  (lipocalin 2)


Additional Information