Mink epithelial cell killing by pathogenic murine leukemia viruses involves endoplasmic reticulum stress
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Published on: August 24, 2015
Suparna Nanua1, Fayth K Yoshimura
1Department of Immunology and Microbiology, Karmanos Cancer Institute, Wayne State University, 540 E. Canfield Ave., Detroit, MI 48201, USA.
Abstract:
We previously demonstrated that mink cells undergo apoptosis after MCF13 murine leukemia virus (MLV) infection. In this study, we observed that virus-infected mink epithelial cells had significantly larger amounts of steady-state levels of MCF13 MLV envelope precursor protein (gPr80(env)) than did Mus dunni fibroblasts, which are resistant to virus-induced cytopathicity. Infection of mink cells with the noncytopathic NZB-9 MLV did not result in the accumulation of gPr80(env). MCF13 MLV infection of mink cells produced low cell surface expression of envelope glycoprotein and less efficient spread of infectious virus. Western blot analysis of mink epithelial cells infected with MCF13 MLV showed an increase in GRP78/BiP, which was not observed for either mink cells infected with NZB-9 MLV or M. dunni fibroblasts infected with MCF13 MLV. MCF13 MLV infection of mink cells also resulted in a significant upregulation of CHOP/GADD153. These results indicate that the accumulation of MCF13 MLV gPr80(env) triggers endoplasmic reticulum stress, which may mediate apoptosis in mink epithelial cells.
Insights
Murine leukemia virus (MLV) envelope precursor protein accumulation in mink cells triggers endoplasmic reticulum stress, leading to apoptosis. This explains MLV-induced cell death in mink epithelial cells.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Mink cells undergo apoptosis following MCF13 murine leukemia virus (MLV) infection.
- MCF13 MLV infection leads to significant accumulation of the envelope precursor protein (gPr80(env)) in mink cells.
Purpose of the Study:
- To investigate the mechanism by which MCF13 MLV infection induces apoptosis in mink cells.
- To determine the role of MCF13 MLV envelope precursor protein accumulation in endoplasmic reticulum stress and subsequent cell death.
Main Methods:
- Comparing gPr80(env) levels in MCF13 MLV-infected mink cells versus resistant Mus dunni fibroblasts.
- Analyzing cell surface glycoprotein expression and viral spread post-infection.
- Utilizing Western blot to detect GRP78/BiP and CHOP/GADD153 expression in infected cells.
Main Results:
- Mink cells showed higher steady-state levels of gPr80(env) compared to Mus dunni fibroblasts.
- MCF13 MLV infection resulted in low cell surface envelope glycoprotein expression and reduced viral spread.
- Increased GRP78/BiP and CHOP/GADD153 upregulation was observed in MCF13 MLV-infected mink cells, but not in cells infected with noncytopathic MLV or in M. dunni fibroblasts.
Conclusions:
- Accumulation of MCF13 MLV gPr80(env) is linked to endoplasmic reticulum (ER) stress in mink epithelial cells.
- ER stress, induced by gPr80(env) accumulation, is a likely mediator of apoptosis in MCF13 MLV-infected mink cells.
