Time filter

Source Type

Ren X.,Southern Medical University | Ren X.,Medical Key Laboratory of Shenzhen Center for Disease Control and Prevention | Li J.,Southern Medical University | Xia B.,Southern Medical University | And 10 more authors.
Toxicology Mechanisms and Methods | Year: 2015

Trichloroethylene (TCE) is an environmental and occupational toxicant that has been shown to cause serious hepatotoxicity. However, the mechanisms underlying the hepatotoxicity of TCE remain unclear. Previously, we identified several apoptosis-related proteins in TCE-induced hepatic cytotoxicity. This study is aimed to analyze the changes in phosphoproteins in L-02 liver cells exposed to TCE using iTRAQ labeling, IMAC enrichment and LC-MS/MS. We identified 1878 phosphorylation sites in 107 proteins and found that 20 sites in 16 phosphoproteins were differentially phosphorylated in L-02 cells after TCE treatment. Among these phosphoproteins, 20% were protein localization and formation processes-related proteins, 38% were metabolism-related proteins and 42% were cellular process-related proteins, including transcriptional regulation and biogenesis. Moreover, two phosphoproteins, 4E-BP1 (37T) and MCM2 (139S), were validated as TCE-induced alteration of phosphorylation at specific sites by Western-blot analysis. Taken together, our study demonstrated that TCE exposure changed the levels of multiple phosphoproteins in L-02 liver cells, and the functional analysis suggested that these differentially expressed phosphoproteins might be involved in TCE-induced hepatic cytotoxicity. © 2015 Informa Healthcare USA, Inc.


PubMed | Medical Key Laboratory of Shenzhen Center for Disease Control and Prevention, Shenzhen University and Southern Medical University
Type: Journal Article | Journal: Toxicology mechanisms and methods | Year: 2015

Trichloroethylene (TCE) is an environmental and occupational toxicant that has been shown to cause serious hepatotoxicity. However, the mechanisms underlying the hepatotoxicity of TCE remain unclear. Previously, we identified several apoptosis-related proteins in TCE-induced hepatic cytotoxicity. This study is aimed to analyze the changes in phosphoproteins in L-02 liver cells exposed to TCE using iTRAQ labeling, IMAC enrichment and LC-MS/MS. We identified 1878 phosphorylation sites in 107 proteins and found that 20 sites in 16 phosphoproteins were differentially phosphorylated in L-02 cells after TCE treatment. Among these phosphoproteins, 20% were protein localization and formation processes-related proteins, 38% were metabolism-related proteins and 42% were cellular process-related proteins, including transcriptional regulation and biogenesis. Moreover, two phosphoproteins, 4E-BP1 (37T) and MCM2 (139S), were validated as TCE-induced alteration of phosphorylation at specific sites by Western-blot analysis. Taken together, our study demonstrated that TCE exposure changed the levels of multiple phosphoproteins in L-02 liver cells, and the functional analysis suggested that these differentially expressed phosphoproteins might be involved in TCE-induced hepatic cytotoxicity.

Loading Medical Key Laboratory of Shenzhen Center for Disease Control and Prevention collaborators
Loading Medical Key Laboratory of Shenzhen Center for Disease Control and Prevention collaborators