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Lauko, J.

Publications and source records attributed to Lauko, J..

2 recordsLinked to original sources

Tuning non-linear mechanics in collagen hydrogels modulates three dimensional cellular morphotypes

Collagen networks contribute to tissue architecture and modulate cellular responses in crowded three-dimensional environments. Therefore, it is the most widely used biological polymer in three-dimensional studies of cellular interactions with the extracellular matrix. In vivo, collagen exists embedded within additional matrix components. Studies have shown that the combination of matrices induces synergistic mechanical interactions, influencing the non-linear mechanical behaviour of collagen networks. However, how cells respond to changes in collagen non-linear elasticity remains largely unknown. By precisely controlling the mechanical behaviour of collagen networks with the biologically inert and semiflexible polymer polyisocyanopeptides, we demonstrate that changes in the non-linear elasticity of collagen induces morphological cell responses that influence how cells migrate, proliferate, and interact with collagen. We found that when collagen rigidifies in the presence of a second component, this induces morphological changes in cell-matrix interactions, resulting in a decrease in migration and the ability of cells to deform collagen matrices. Our results demonstrate that the onset of collagen stiffening is key to inducing intracellular tension which dictates morphological cell responses in three-dimensional collagen networks. We anticipate our findings will prove useful in understanding how cells respond to changes in collagen mechanics when combined in double network systems which better recapitulates tissues in vivo.

biophysics↗

Cerebral Cavernous Malformation severity is impacted by distinct forms of Hyaluronic acid in the vascular microenvironment

Cerebral Cavernous Malformations (CCMs) are vascular lesions that predominantly form in blood vessels of the central nervous system (CNS) upon loss of the CCM multimeric protein complex. The endothelial cells (ECs) within CCM lesions are characterised by overactive MEKK3 kinase and KLF2/4 transcription factor signalling, leading to pathological changes such as increased EC spreading and reduced junctional integrity. Concomitant to aberrant EC signalling, non-autonomous signals from the extracellular matrix (ECM) have also been implicated in CCM lesion growth and these factors might explain why CCM lesions mainly develop in the CNS. Here, we adapted a three dimensional (3D) microfluidic system to examine CCM1 deficient human micro-vessels in distinctive ECMs. We validate that EC pathological hallmarks are maintained in this 3D model. We further show that key genes responsible for homeostasis of Hyaluronic Acid (HA), a major ECM component of the CNS, are dysregulated in CCM. Supplementing the ECM in our model with forms of HA that are predicted to be reduced, inhibits CCM cellular phenotypes, independent of KLF2/4. This study thereby provides a proof-of-principle that ECM embedded 3D microfluidic models are ideally suited to identify how changes in ECM structure and signalling impact vascular malformations.

cell biology↗