Induction of Apoptosis in Rat Lung Epithelial Cells by Multiwalled Carbon Nanotubes

2013 ◽  
Vol 27 (5) ◽  
pp. 286-286 ◽  
Author(s):  
Prabakaran Ravichandran ◽  
Adaikkappan Periyakaruppan ◽  
Bindu Sadanandan ◽  
Vani Ramesh ◽  
Joseph C. Hall ◽  
...  
2009 ◽  
Vol 23 (5) ◽  
pp. 333-344 ◽  
Author(s):  
Prabakaran Ravichandran ◽  
Adaikkappan Periyakaruppan ◽  
Bindu Sadanandan ◽  
Vani Ramesh ◽  
Joseph C. Hall ◽  
...  

APOPTOSIS ◽  
2010 ◽  
Vol 15 (12) ◽  
pp. 1507-1516 ◽  
Author(s):  
Prabakaran Ravichandran ◽  
Sudhakar Baluchamy ◽  
Bindhu Sadanandan ◽  
Ramya Gopikrishnan ◽  
Santosh Biradar ◽  
...  

2012 ◽  
Vol 26 (6) ◽  
pp. 831-840 ◽  
Author(s):  
Cinzia Lucia Ursini ◽  
Delia Cavallo ◽  
Anna Maria Fresegna ◽  
Aureliano Ciervo ◽  
Raffaele Maiello ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Anurag Mishra ◽  
Yon Rojanasakul ◽  
Bean T. Chen ◽  
Vincent Castranova ◽  
Robert R. Mercer ◽  
...  

Multiwalled carbon nanotubes have been shown to possess unusual fibrogenic activityin vivoand are currently the focus of intense toxicological investigations. This study further determines the fibrogenic potential of well-dispersed MWCNT in human lung cell culture models and to develop a novel platform for understanding the cellular mechanisms of MWCNT-induced lung fibrosis. Survanta, a natural lung surfactant, showed effectiveness in dispersing agglomerates of MWCNT to fine structures similar in size to aerosolized one. At relevant low doses (0.002–0.2 μg/cm2), MWCNT exhibited a dose-dependent bio-effect on the human lung epithelial cells which is more pronounced in dispersed-MWCNT compared to non-dispersed form. Significantly elevated levels of fibrogenic mediators, such as transforming growth factor-β1 and matrix metalloprotienases-9 were observed in the dispersed-MWCNT treated lung epithelial cells. Based on previousin vivostudies showing that dispersed-MWCNT penetrated the interstitium and caused rapid interstitial fibrosis, we evaluated the potential direct interaction between lung fibroblasts and MWCNT. Direct stimulation of human lung fibroblast cell proliferation, collagen expression and fibroblast growth factor-2 were observed which suggests novel mechanisms of MWCNT-induced lung fibrosis. Our results indicate that the dispersion status of MWCNT determines their fibrogenic activity which is consistent within vivofindings.


2001 ◽  
Vol 171 (2) ◽  
pp. 94-106 ◽  
Author(s):  
Bogdan A. Stoica ◽  
A.Hamid Boulares ◽  
Dean S. Rosenthal ◽  
Sudha Iyer ◽  
Ivan D.G. Hamilton ◽  
...  

2006 ◽  
Vol 291 (4) ◽  
pp. L725-L733 ◽  
Author(s):  
Ulrich Sydlik ◽  
Katrin Bierhals ◽  
Maria Soufi ◽  
Josef Abel ◽  
Roel P. F. Schins ◽  
...  

Apoptosis and proliferation are important causes of adverse health effects induced by inhaled ultrafine particles. The molecular mechanisms of particle cell interactions mediating these end points are therefore a major topic of current particle toxicology and molecular preventive medicine. Initial studies revealed that ultrafine particles induce apoptosis and proliferation in parallel in rat lung epithelial cells, dependent on time and dosage. With these end points, two antagonistic reactions seem to be induced by the same extracellular stimulus. It was therefore investigated whether proliferation is induced directly by the particles or as a compensation of particle-caused cell death. Experimental conditions excluding compensatory proliferation demonstrated that both end points are induced independently by specific signaling pathways. Events eliciting signaling cascades leading to apoptosis and proliferation were studied with specific inhibitors of membrane receptors. Epidermal growth factor receptor (EGF-R) kinase activity was identified as essential for apoptosis as well as for proliferation. As ultrafine particle-induced proliferation alone was dependent on the activation of β1-integrins, these membrane receptors are suggested to mediate the specificity of EGF-R signaling concerning the decision as to whether apoptosis or proliferation is triggered. Accordingly, MAP kinase signaling downstream of EGF-R showed comparable specificity with regard to receptor-dependent induction of apoptosis and proliferation. As key mediators of signaling cascades, the activation of extracellular signal-regulated kinases 1 and 2 proved to be specific for proliferation in a β1-integrin-dependent manner, whereas phosphorylation of c-Jun NH2-terminal kinases 1 and 2 was correlated with the induction of apoptosis.


Toxicology ◽  
2008 ◽  
Vol 253 (1-3) ◽  
pp. 131-136 ◽  
Author(s):  
D. Elgrabli ◽  
S. Abella-Gallart ◽  
F. Robidel ◽  
F. Rogerieux ◽  
J. Boczkowski ◽  
...  

2007 ◽  
Vol 7 (7) ◽  
pp. 2466-2472 ◽  
Author(s):  
Chidananda S. Sharma ◽  
Shubhashish Sarkar ◽  
Adaikkappan Periyakaruppan ◽  
Johnny Barr ◽  
Kimberly Wise ◽  
...  

Toxicology ◽  
1999 ◽  
Vol 133 (1) ◽  
pp. 43-58 ◽  
Author(s):  
B.A. Hart ◽  
C.H. Lee ◽  
G.S. Shukla ◽  
A. Shukla ◽  
M. Osier ◽  
...  

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