Fullerene nanoparticles selectively enter oxidation-damaged cerebral microvessel endothelial cells inhibit JNK-related apoptosis

Fang Lao, Long Chen, Wei Li, Cuicui Ge, Ying Qu, Quanmei Sun, Yuliang Zhao, Dong Han, Chunying Chen

Research output: Contribution to journalArticle

111 Scopus citations

Abstract

There is a dearth in fundamental cellular-level understanding of how nanoparticles interact with the cells of the blood brain barrier (BBB), particularly under the oxidative environment. The apoptosis of cerebral microvessel endothelial cells (CMECs) induced by oxidative stress injury plays a key role in the dysfunction of BBB. By use of CMECs as an in vitro BBB model, we show for the first time that C60(C(COOH)2)2 nanoparticles can selectively enter oxidized CMECs rather than normal cells, and maintain CMECs integrity by attenuating H2O2-induced F-actin depolymerization via the observation of several state-of-the art microscopic techniques. Additionally, we have found that C60(C(COOH) 2)2 nanoparticles greatly inhibit the apoptosis of CMECs induced by H2O2, which is related to their modulation of the JNK pathway. C60(C(COOH)2)2 nanoparticles can regulate several downstream signaling events related to the JNK pathway, including reduction of JNK phosphorylation, activation of activator protein 1 (AP-1) and caspase-3, and inhibition of polyADP-ribose polymerase (PARP) cleavage and mitochondrial cytochrome c release. Our results indicate that C60(C(COOH)2)2 nanoparticles possess a novel ability of selectively entering oxidation-damaged cerebral endothelial cells rather than normal endothelial cells and then protecting them from apoptosis.

Original languageEnglish (US)
Pages (from-to)3358-3368
Number of pages11
JournalACS Nano
Volume3
Issue number11
DOIs
StatePublished - Nov 24 2009

Keywords

  • Apoptosis
  • C(C(COOH))
  • JNK pathway
  • Microvessel endothelial cells
  • Oxidative injury

ASJC Scopus subject areas

  • Engineering(all)
  • Materials Science(all)
  • Physics and Astronomy(all)

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