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Abstract
Cellular senescence is a phenotype characterized by cessation of cell division, which can be caused by exhaustive replication or environmental stress. It is involved in age-related pathophysiological conditions and affects both the cellular cytoskeleton and the prime cellular mechanosensors, focal adhesion complexes. While the size of focal adhesions increases during senescence, it is unknown if and how this is accompanied by a remodeling of the internal focal adhesion structure. Our study uses metal-induced energy transfer to study the axial dimension of focal adhesion proteins from oxidative-stress-induced senescent cells with nanometer precision, and compares these to unstressed cells. We influenced cytoskeletal tension and the functioning of mechanosensitive ion channels using drugs and studied the combined effect of senescence and drug intervention on the focal adhesion structure. We found that H2O2-induced restructuring of the focal adhesion complex indicates a loss of tension and altered talin complexation. Mass spectroscopy-based proteomics confirmed the differential regulation of several cytoskeletal proteins induced by H2O2 treatment.
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1 Ulm University, Institute of Experimental Physics, Ulm, Germany (GRID:grid.6582.9) (ISNI:0000 0004 1936 9748)
2 The Hebrew University of Jerusalem, Edmond J. Safra Campus-Givat Ram, Alexander Silberman Institute of Life Science, Jerusalem, Israel (GRID:grid.9619.7) (ISNI:0000 0004 1937 0538)
3 Ulm University, Department of Dermatology and Allergic Diseases, Ulm,, Germany (GRID:grid.6582.9) (ISNI:0000 0004 1936 9748)