Tubular morphogenesis by genotoxic therapeutic agents that induce NF-κB activation in humanvascular endothelial cells View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1998-12

AUTHORS

Daisuke Goto, Hiroto Izumi, Mayumi Ono, Takeshi Okamoto, Kimitoshi Kohno, Michihiko Kuwano

ABSTRACT

Angiogenic stimuli induce tubular morphogenesis and angiogenesis in vascular endothelial cells, but these cells are highly vulnerable to cytokines, oxidative stress, and genotoxic anticancer agents. A transcription factor, NF-κB, is involved in the protection against apoptosis and in angiogenesis in response to stimuli that could induce cell death. NF-κB was specifically activated by the genotoxic anticancer therapeutic agents etoposide and doxorubicin, but not by bleomycin, mitomycin C and cisplatin, in human vascular endothelial cells in three independent assay systems: nuclear translocation of NF-κB, binding of NF-κB to its consensus sequence, and NF-κB -dependent transcription. Exposure to etoposide and doxorubicin induced tubular morphogenesis by vascular endothelial cells in type I collagen gel at rates comparable to tumor necrosis factor-α. Co-administration of NF-κB antisense oligonucleotides inhibited the angiogenesis by doxorubicin and etoposide. In contrast, bleomycin, mitomycin C, and cisplatin did not induce angiogenesis. An angiogenic factor, interleukin 8, was dramatically induced in vascular endothelial cells treated with doxorubicin, but not in cells treated with cisplatin. Co-administration of anti-interleukin 8 antibody almost completely blocked the doxorubicin-induced angiogenesis in vitro, suggesting a paracrine/autocrine control through drug-induced angiogenic factor(s). The presence or absence of NF-κB activation may have an essential role in tubular morphogenesis by vascular endothelial cells during chemotherapeutic treatment, possibly through interleukin 8. More... »

PAGES

345-356

Identifiers

URI

http://scigraph.springernature.com/pub.10.1023/a:1009252811114

DOI

http://dx.doi.org/10.1023/a:1009252811114

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1051493338

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/14517454


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