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Queen Mary University of LondonQueen Mary University of London
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School of Engineering and Materials Science
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PhD Thesis: Modulation of the effect of tensile strain on fibroblasts by extracellular matrix molecules and serum

Author: BARIA, Katherine

Year: 2006

Supervisor(s): David Lee, Martin Knight

This thesis investigates the roles of adhesions in combination with serum derived soluble factors in the response of human dermal fibroblasts to uniaxial tensile strain.

Initial chapters in this thesis established that while functionalisation of a polyorganosiloxane membrane with either collagen I or ProNectin F, and incubation with media with different serum contents, did alter the its surface chemistry and topology, these effects were less important to cell behaviour than the specific proteins. In later chapters two cell straining systems were used to investigate the effects of these functionalised surfaces and media on the response of dermal fibroblasts to tensile strain. An incubated cell straining system was used to investigate proliferation, morphology and protein synthesis and a microscope based cell straining system was used to examine cell morphology during tensile strain. The results demonstrated that fibroblasts displayed a similar synthetic phenotype in response to strain on both coatings, characterised by decreased proliferation and increased protein production. However surface modification modulated the rate or extent of the response. In addition, the data illustrate that the reorientation, morphological and biochemical responses to tensile strain was enhanced by medium serum content.

This latter cell straining system was also used to monitor change in actin cytoskeleton during tensile strain. These studies revealed that while cellular reorientation in response to tensile strain is dependent on ECM coating, reorientation of the actin cytoskeleton is not. However it is influenced by the initial cell orientation with respect to the direction of the applied. In addition, it was possible to image reorientation of the actin cytoskeleton occurring via fragmentation and reorientation of the fragments.