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Changes in cell function and protein expression of mouse renal principal cells, mpkCCD, after carbon nanoparticle (CNP) exposure
Author(s) -
Amos Adam David,
Witzmann Frank A.,
Chernoff Ellen A.,
Hong David,
Lai Xianyn,
Ringham Heather N.,
BlazerYost Bonnie L.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.942.2
Subject(s) - chemistry , microbiology and biotechnology , cell culture , biophysics , cytochalasin d , cell , cytoskeleton , biochemistry , biology , genetics
To assess effects of CNP exposure on renal epithelial cells, 3 types of CNP, single‐wall carbon nanotubes (SWCNT), multi‐wall carbon nanotubes (MWCNT), and fullerenes (4–200 μg/cm 2 , 48 hrs) were applied to mpkCCD cells, a renal barrier epithelial line, and functional changes determined via electrophysiology. CNP‐treated cells showed significant decreases in transepithelial resistance compared to control. To determine CNP‐induced structural changes, confluent cells were incubated with CNP (21.1 μg/cm 2 , 48 hrs). Actin filaments and nuclei were visualized in fixed cells. Cultures treated with SWCNT and MWCNT showed an increase in large, multinucleated cells. CNP agglomerates were surrounded by actin filaments. Differential protein expression analysis by LC‐MS/MS revealed changes in several proteins, including intra‐ and extra‐cellular membrane‐associated proteins stathmin‐like 2 and enolase (increased) and myotubularin related protein 9, gap junction alpha‐8 protein coiled‐coil domain‐containing protein 44, zona pellucida glycoprotein 4, olfactory receptor 586, phosphomannomutase 2, RAN binding protein 1, and actin (decreased). These results indicate a profound impact of CNPs on renal epithelial cell structure and function and merit further study of effects of CNPs on barrier epithelial cells. Funding: IUPUI Undergraduate Research Opportunities Program & AFOSR Grant FA9550‐06‐1‐0083.