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P8 deficiency increases cellular ROS and induces HO-1
Sebastian Weis1, Tobias Bielow2, Ines Sommerer2
1Division of Gastroenterology and Rheumatology, Department of Internal Medicine, Neurology and Dermatology, University Hospital Leipzig, Germany; Center for Sepsis Control & Care, Jena University Hospital, Jena, Germany; Center for Infectious Diseases and Infection Control, Jena University Hospital, Jena, Germany.
Archives of Biochemistry and Biophysics
|December 6, 2014
Summary
The p8 protein deficiency increases reactive oxygen species (ROS) and heme oxygenase 1 (HO-1) expression. This suggests p8 plays a role in cellular antioxidant defense mechanisms.
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- The gene p8 encodes a cytoprotective protein involved in cellular responses.
- p8 expression increases during inflammation.
- p8 suppression in astrocytes induces heme oxygenase 1 (HO-1).
Purpose of the Study:
- To investigate the relationship between p8 and HO-1 in mouse embryonic fibroblasts (MEFs).
- To determine the role of p8 in reactive oxygen species (ROS) generation and antioxidant defense.
Main Methods:
- Assessed HO-1 expression in p8-deficient (p8(-/-)) MEFs.
- Measured ROS levels in p8(-/-) MEFs and MiaPaCa-2 cells with suppressed p8.
- Investigated the source of ROS and the involvement of the NADPH oxidase complex.
Main Results:
- p8 deficiency led to increased HO-1 expression in MEFs, independent of the cell cycle.
- p8(-/-) MEFs exhibited higher ROS generation, not originating from mitochondria or NADPH oxidases.
- Increased intracellular ROS was also observed in MiaPaCa-2 cells with suppressed p8.
- p8 deficiency did not impact the Rac1-dependent NADPH oxidase complex.
Conclusions:
- p8 deficiency increases ROS and subsequently upregulates antioxidant enzymes like HO-1.
- p8 appears to be involved in cellular antioxidant defense.
- Impaired pancreatic antioxidant capacity due to increased ROS in p8(-/-) mice may contribute to pancreatitis severity.
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