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Dual-specificity phosphatases in the hypo-osmotic stress response of keratin-defective epithelial cell lines
Mirjana Liovic1, Brian Lee, Marjana Tomic-Canic
1National Institute of Chemistry, Ljubljana, Slovenia; CRUK Cell Structure Research Group, University of Dundee College of Life Sciences, MSI/WTB Complex, Dundee, UK. mirjana.liovic@ki.si
Abstract:
Although mutations in intermediate filament proteins cause many human disorders, the detailed pathogenic mechanisms and the way these mutations affect cell metabolism are unclear. In this study, selected keratin mutations were analysed for their effect on the epidermal stress response. Expression profiles of two keratin-mutant cell lines from epidermolysis bullosa simplex patients (one severe and one mild) were compared to a control keratinocyte line before and after challenge with hypo-osmotic shock, a common physiological stress that transiently distorts cell shape. Fewer changes in gene expression were found in cells with the severely disruptive mutation (55 genes altered) than with the mild mutation (174 genes) or the wild type cells (261 genes) possibly due to stress response pre-activation in these cells. We identified 16 immediate-early genes contributing to a general cell response to hypo-osmotic shock, and 20 genes with an altered expression pattern in the mutant keratin lines only. A number of dual-specificity phosphatases (MKP-1, MKP-2, MKP-3, MKP-5 and hVH3) are differentially regulated in these cells, and their downstream targets p-ERK and p-p38 are significantly up-regulated in the mutant keratin lines. Our findings strengthen the case for the expression of mutant keratin proteins inducing physiological stress, and this intrinsic stress may affect the cell responses to secondary stresses in patients' skin.
Insights
Mutant keratin proteins in epidermolysis bullosa simplex cause intrinsic cellular stress. This stress impacts how skin cells respond to environmental challenges, affecting disease severity.
Area of Science:
- Cell Biology
- Genetics
- Dermatology
Background:
- Mutations in intermediate filament proteins, like keratins, are linked to human disorders.
- The precise pathogenic mechanisms and metabolic effects of these mutations remain largely unknown.
Purpose of the Study:
- To investigate the impact of specific keratin mutations on epidermal stress response.
- To compare gene expression profiles in keratin-mutant keratinocytes under hypo-osmotic stress.
Main Methods:
- Analysis of gene expression profiles in two keratin-mutant cell lines (severe and mild epidermolysis bullosa simplex) and a control keratinocyte line.
- Exposure of cells to hypo-osmotic shock to simulate physiological stress.
- Identification of differentially regulated genes and signaling pathways.
Main Results:
- Cells with severe keratin mutations exhibited fewer gene expression changes post-stress compared to mild or wild-type cells, suggesting pre-activation of stress responses.
- 16 immediate-early genes were identified as key responders to hypo-osmotic shock.
- Mutant keratin lines showed altered expression of dual-specificity phosphatases (e.g., MKP-1, MKP-3) and up-regulation of downstream targets p-ERK and p-p38.
Conclusions:
- Expression of mutant keratin proteins induces a state of intrinsic physiological stress within epidermal cells.
- This intrinsic stress potentially alters cellular responses to secondary environmental stresses in the skin of patients with these mutations.
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