Goldoni, Giacomo (2016) Role of CXCL12 in the regulation of neutrophil nuclear stiffness. [Laurea specialistica biennale]
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Neutrophil migration rapresent a critcal step for the establishment of immune responses. actually, when an onflammatory process occurs, netrophils leave the bone marrow following chemotactic gradients, extravasate and migrate towards inflamed tissue. To do this, neutrophilis have to interact with the endothelium and reorganize their shape in order to penetrate the endothelial barrier and navigate the basement membrane. Indeed, although the cytoplasm can quickly chenge consistence and form, the deformation of nucleus is mor challengin and the represents an interesting issue to be invesigated. Neutrophil migration in induced by chemokines, which are a familu of small soluble mediators regulating important pathophysiologu processes. Among chemokines, CXCL12 play a crucial role in the traffcking of immune cells by specifically binding the chemokine receptors, CXCR4 and CXCR7, which are both expressed in netrophils. Indeed an interesting possibility is tha signals controlling neutrophil migration, as chemokines, may modulate nuclear deformability. In order to acces the effect of CXCL12 on the nuclear deformability we took advantage of biocompatible micro-pillared surface fabricated by the departement of Industrial Engeneering. Using the microtechnology, we observed the the chemokine CXCL12 increases the nuclear deformability of netrophilis. Interestingly, we found the the signaling pathway connectin CXCL12 to the nuclear deformability does not involve Gai protein activation or calcium influx, Importantly, our experiments suggest the the effects of CXCL12 on the nuclear deformability is mediated by CXCR7, rather tan CXCR 4. Therefore, our study highlights an unexpected role of chemokines in the control of migration by affecting nuclear deformability on neutrophils.
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