Cell adhesion

Summary

Cell adhesion is the process by which cells interact and attach to neighbouring cells through specialised molecules of the cell surface. This process can occur either through direct contact between cell surfaces such as cell junctions or indirect interaction, where cells attach to surrounding extracellular matrix, a gel-like structure containing molecules released by cells into spaces between them. Cells adhesion occurs from the interactions between cell-adhesion molecules (CAMs), transmembrane proteins located on the cell surface. Cell adhesion links cells in different ways and can be involved in signal transduction for cells to detect and respond to changes in the surroundings. Other cellular processes regulated by cell adhesion include cell migration and tissue development in multicellular organisms. Alterations in cell adhesion can disrupt important cellular processes and lead to a variety of diseases, including cancer and arthritis. Cell adhesion is als

Official source

https://en.wikipedia.org/wiki/Cell_adhesion

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Study of Cell Adhesion and Tracking Methods for in Vivo Cell Localisation in a Tissue-Engineering Scaffold

Thaïs Cléa Laura Séverine Clouet, Tanja Cloé Hausherr

Bone fracture healing problems, because of the loss of tissue regeneration, can affect many old or multi-pathologic patients around the world. Among the therapeutic strategies, bone substitutes, such as poly-(L-lactitve acid) with 5% wt. % ß-tricalcium phosphate (PLA/5%ß-TCP) scaffolds, are promising as a clinical solution. One strategy to tune their osteoinductive properties is the addition of bone progenitor cells. Therefore, cell- free and cell-seeded PLA/5% ß-TCP scaffolds were implanted into femoral condyles of rats to promote bone regeneration. The in vivo study showed that the bone growth inside a cell-seeded scaffold with human bone progenitor cells was delayed compared to cell-free scaffold. What happened to the cells? Did they trigger an immune response, migrate or die? Therefore, the goals of this project are to evaluate the cell adhesion in vitro to the scaffold and to propose a reliable cell labeling method to track them in future in vivo studies. In the first aim, the adhesion of the cells was qualitatively assessed by the cell morphology and the presence of fibronectin using fluorescence imaging. To quantify their adherence, seeded scaffolds were washed up to 3 times with a 0.9 % NaCl solution. The luminescence of the scaffolds and the washing solutions was measured using a cell viability assay. These experiments demonstrated that after 72h of culture, the measured adherent bone progenitor cells on the scaffolds decreased after 3 washes down to 50 % while it stayed stable after 14 days of culture. In the second aim, we focused on methods to label the cells either once implanted or prior to implantation. The first method was to translate the in situ hybridization protocol with the human specific Alu sequence from paraffin embedded samples to resin embedded ones. The obtained results were so far inconclusive. Concerning the labeling of the cells before implantation, the transmembrane label PKH26 was investigated. Its staining efficacy was high just after labeling, while it decreased drastically over time due to cell division.

2015

Proprotein Convertases (PCs) constitute a family of serine proteases that activate various hormones, growth factors and cell adhesion molecules by mediating endoproteolytic cleavage of their secreted inactive precursors during their transit in the secretory pathway. Their physiological roles in most tissues, in cancer and other diseases have remained nowadays poorly defined, partly because of technical hurdles in clearly distinguishing functionally overlapping PC activities from each other. Related to this, a major unsolved question is where, among the different subcellular compartments of the secretory pathway, substrate cleavage takes place. To address these questions, we mapped intracellular PC activities of two unrelated cell lines (HEK293T and B16F1 melanoma) by ratiometric and Förster Resonance Energy Transfer (FRET)-based imaging of the PC-specific biosensors, called cell-linked indicator of proteolysis (CLIP)v3 and CLIPv4 respectively, which are sorted to different subcellular compartments by specific trafficking signals. Until now, PCs have been thought to cleave the majority of the substrates in the trans-Golgi network (TGN). By contrast, our analysis of compartment-specific CLIPv3 and CLIPv4 variants in cultured cells suggested that PC activities are much higher in post-exocytic compartments. Furthermore, imaging in B16F1 Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)-edited clones for endogenously expressed Furin or PC7, revealed an enrichment of Furin activity in endosomes compared to TGN, whereas PC7 activity was confined to a distinct compartment resistant to the pan-PC inhibitor CMK, demonstrating that endogenous Furin and PC7 are biologically active in distinct compartments. In addition, we also demonstrated that substrate and protease localization are rate-limiting of how efficiently a given substrate is processed. PC inhibition represses human primary melanoma cells motility and migration in vitro and proliferation in other skin cancer cells both in vitro and in vivo. To elucidate the roles of PC activities in melanoma progression and differentiation, we evaluated relative contribution of Furin and PC7 in B16F1 tumor grafts. Both proteins were required for tumor pigmentation, whereas Furin deletion reduced tumor growth, but its loss may be rescued by PC7 deletion. Altogether, these findings will be important to inform future therapeutic approaches and strategies for targeting PCs to preferentially block oncogenic activities.

EPFL2018

Group Decisions Influence Emergence and Regulation of Leaders during Collective Migration of Epithelial Cells

Medhavi Vishwakarma

Collective migration is a central event involving coordinated movement of several individuals. One of the critical events during collective migration is the emergence of leading individuals, who provide directional guidance for the group movement. While on the move, animals select their leaders by a collective decision making process, which require active participation of the followers. On the contrary, the prevalent view on collective cell migration, especially in the context of epithelial cells during wound healing, assumes a hierarchical leader-follower organization and belittles the contribution of follower cells in choosing or regulating the leaders. Furthermore, how the dynamics of cells located at the wound margin evolve as the wound heals, remains illusive. Here, we report and analyse distinct phases of collective migration during wound closure and demonstrate how cellular-level shared decision-making process and collective mechanical dynamics influence selection, regulation and kinematics of leader cells in these phases. We found that in the preparatory phase, before the initiation of migration (Phase 0), the selection of leader cells at the epithelial wound margin depends on the pre-migratory dynamics of the follower cells situated immediately behind the future leaders. Long before the prospective leaders actually start displaying their phenotypic peculiarities, cells behind them manifest stochastic augmentations in the traction forces and monolayer stresses, and display large perimeter-to-area ratio indicating a local unjamming in the followers much before the leaders are selected. Further, introducing an unjammed or fluidic follower at the back stimulates leader cell formation at the margin thereby indicating the role of collective bulk dynamics in leader cell selection. Interestingly, the length upto which cells cooperatively join forces, corresponds very well with the distance between the two emerging leaders and this mechano-biological control remains preserved even in the presence of geometric bias or physiological levels of chemical cue at the interface. Immediately after the initiation of migration (Phase 1), leaders show their distinct phenotypes and drive the cellular outgrowths. In this phase, pluricellular actin belt at the margin regulates the fraction of marginal leaders, which therefore remains unchanged, while the number of followers per leader increases with time. As the migration progresses, fraction of leader cells increases while the latter settles to a steady level set again by the length scale of cell-cell force transmission (Phase 2). Any perturbations in mechanical forces that modifies the force correlation lengths, invariably enforces a change in the number of followers per leader thereby modifying the time required to transit from one phase to the other. Furthermore, orientation of focal adhesions and persistence of cellular motions also display this phase specific behaviour. Together, these findings provide a novel system insight into collective cell migration and indicate integrative leader-follower interactions during wound closure. Given the physiological and pathological importance of leader cell formation in epithelial wound healing, in organogenesis and in metastatic migration of cancer cells, the system-view that the results offer here is anticipated to have to a long-standing impact on the design and discovery of avant-garde therapeutic strategies in future.

EPFL2017