PMID- 22129238
OWN - NLM
STAT- MEDLINE
DCOM- 20120126
LR  - 20220410
IS  - 1528-7394 (Print)
IS  - 0098-4108 (Linking)
VI  - 75
IP  - 2
DP  - 2012
TI  - Cell permeability, migration, and reactive oxygen species induced by multiwalled 
      carbon nanotubes in human microvascular endothelial cells.
PG  - 112-28
LID - 10.1080/15287394.2011.615110 [doi]
AB  - Multiwalled carbon nanotubes (MWCNT) have elicited great interest in biomedical 
      applications due to their extraordinary physical, chemical, and optical 
      properties. Intravenous administration of MWCNT-based medical imaging agents and 
      drugs in animal models was utilized. However, the potential harmful health 
      effects of MWCNT administration in humans have not yet been elucidated. 
      Furthermore, to date, there are no apparent reports regarding the precise 
      mechanisms of translocation of MWCNT into target tissues and organs from blood 
      circulation. This study demonstrates that exposure to MWCNT leads to an increase 
      in cell permeability in human microvascular endothelial cells (HMVEC). The 
      results obtained from this study also showed that the MWCNT-induced rise in 
      endothelial permeability is mediated by reactive oxygen species (ROS) production 
      and actin filament remodeling. In addition, it was found that MWCNT promoted cell 
      migration in HMVEC. Mechanistically, MWCNT exposure elevated the levels of 
      monocyte chemoattractant protein-1 (MCP-1) and intercellular adhesion molecule 1 
      (ICAM-1) in HMVEC. Taken together, these results provide new insights into the 
      bioreactivity of MWCNT, which may have implications in the biomedical application 
      of MWCNT in vascular targeting, imaging, and drug delivery. The results generated 
      from this study also elucidate the potential adverse effects of MWCNT exposure on 
      humans at the cellular level.
FAU - Pacurari, M
AU  - Pacurari M
AD  - Mary Babb Randolph Cancer Center, West Virginia University, Morgantown, West 
      Virginia 26506-9300, USA.
FAU - Qian, Y
AU  - Qian Y
FAU - Fu, W
AU  - Fu W
FAU - Schwegler-Berry, D
AU  - Schwegler-Berry D
FAU - Ding, M
AU  - Ding M
FAU - Castranova, V
AU  - Castranova V
FAU - Guo, N L
AU  - Guo NL
LA  - eng
GR  - R01 LM009500-03/LM/NLM NIH HHS/United States
GR  - P20 RR016440/RR/NCRR NIH HHS/United States
GR  - R01 LM009500/LM/NLM NIH HHS/United States
GR  - P20 RR016440-09S1/RR/NCRR NIH HHS/United States
GR  - P20RR16440/RR/NCRR NIH HHS/United States
GR  - R01LM009500/LM/NLM NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - England
TA  - J Toxicol Environ Health A
JT  - Journal of toxicology and environmental health. Part A
JID - 100960995
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Drug Carriers)
RN  - 0 (Environmental Pollutants)
RN  - 0 (Nanotubes, Carbon)
RN  - 0 (Reactive Oxygen Species)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
SB  - IM
MH  - Actin Cytoskeleton/drug effects
MH  - Cell Line
MH  - Cell Membrane Permeability/*drug effects
MH  - Cell Movement/*drug effects
MH  - Chemokine CCL2/metabolism
MH  - Drug Carriers/adverse effects/*metabolism
MH  - Electric Impedance
MH  - Endothelium, Vascular/*drug effects/metabolism/ultrastructure
MH  - Environmental Pollutants/adverse effects/metabolism
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/metabolism
MH  - Kinetics
MH  - Microscopy, Electron, Transmission
MH  - Microvessels/*drug effects/metabolism/ultrastructure
MH  - Nanotubes, Carbon/adverse effects/*chemistry/ultrastructure
MH  - Phagocytosis/drug effects
MH  - Reactive Oxygen Species/*metabolism
PMC - PMC3230883
MID - NIHMS318463
EDAT- 2011/12/02 06:00
MHDA- 2012/01/27 06:00
PMCR- 2013/01/15
CRDT- 2011/12/02 06:00
PHST- 2011/12/02 06:00 [entrez]
PHST- 2011/12/02 06:00 [pubmed]
PHST- 2012/01/27 06:00 [medline]
PHST- 2013/01/15 00:00 [pmc-release]
AID - 10.1080/15287394.2011.615110 [doi]
PST - ppublish
SO  - J Toxicol Environ Health A. 2012;75(2):112-28. doi: 10.1080/15287394.2011.615110.