Cellular biomechanics impairment in keratinocytes is associated with a C-terminal truncated desmoplakin: An atomic force microscopy investigation.

In a tissue continuously challenged by mechanical stresses, such as the skin or the heart, cells perceive information about their microenvironment through several adhesive protein complexes and activate cell-signaling events to maintain tissue cohesion. Consequently, alteration of cell adhesion components leads to aberrant assembly of the associated cytoplasmic scaffolding and signaling pathways, which may reflect changes to the tissue physiology and mechanical resistance. Desmoplakin is an essential component of the cell-cell junction, anchoring the desmosomal protein complex to the intermediate filaments (IFs). Inherited mutations in desmoplakin are associated with both heart and skin disease (cardiocutaneous syndrome). In this study, we investigated the mechanical properties of human keratinocytes harboring a cardiocutaneous-associated homozygous C-terminal truncation in desmoplakin (JD-1) compared to a control keratinocyte line (K1). Using Single Cell Force Spectroscopy (SCFS) AFM-based measurements, JD-1 keratinocytes displayed an overall alteration in morphology, elasticity, adhesion capabilities and viscoelastic properties, highlighting the profound interconnection between the adhesome pathways and the IF scaffold.Fondation Leducq, Transatlantic Network of Excellence (14-CVD 03)

Origin of Hysteresis Observed During Fatigue of Ceramic-Matrix Composites

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66076/1/j.1151-2916.1990.tb05239.x.pd

Thermomechanical Fatigue Behavior of a Silicon Carbide Fiber-Reinforced Calcium Aluminosilicate Composite

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65874/1/j.1151-2916.1993.tb04022.x.pd

Tensile creep behaviour of a fibre-reinforced SiC-Si 3 N 4 composite

The tensile creep behaviour of a SiC-fibre-Si 3 N 4 -matrix composite was investigated in air at 1350 ‡C. The unidirectional composite, containing 30 vol % SCS-6 SiC fibres, was prepared by hot pressing at 1700 ‡C. Creep testing was conducted at stress levels of 70, 110, 150 and 190 MPa. An apparent steady-state creep rate was observed at stress levels between 70 and 150 MPa; at 190 MPa, only tertiary creep was observed. For an applied stress of 70 MPa, the steady-state creep rate was approximately 2.5×10 −10 s −1 with failure times in excess of 790 h. At 150 MPa, the steady-state creep rate increased to an average of 5.6×10 −8 s −1 with failure times under 40 h. The creep rate of the composite is compared with published data for the steady-state creep rate of monolithic Si 3 N 4 .Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44708/1/10853_2004_Article_BF00543607.pd

Current understanding of the role of cytoskeletal cross-linkers in the onset and development of cardiomyopathies

Cardiomyopathies affect individuals worldwide, without regard to age, sex and ethnicity and are associated with significant morbidity and mortality. Inherited cardiomyopathies account for a relevant part of these conditions. Although progresses have been made over the years, early diagnosis and curative therapies are still challenging. Understanding the events occurring in normal and diseased cardiac cells is crucial, as they are important determinants of overall heart function. Besides chemical and molecular events, there are also structural and mechanical phenomena that require to be investigated. Cell structure and mechanics largely depend from the cytoskeleton, which is composed by filamentous proteins that can be cross-linked via accessory proteins. Alpha-actinin 2 (ACTN2), filamin C (FLNC) and dystrophin are three major actin cross-linkers that extensively contribute to the regulation of cell structure and mechanics. Hereby, we review the current understanding of the roles played by ACTN2, FLNC and dystrophin in the onset and progress of inherited cardiomyopathies. With our work, we aim to set the stage for new approaches to study the cardiomyopathies, which might reveal new therapeutic targets and broaden the panel of genes to be screened