Diego et al 2014a - Revision history

Cinmemj: Cinmemj moved page Draft Samper 617655499 to Diego et al 2014a

2017-10-25T08:50:22Z

Cinmemj moved page Draft Samper 617655499 to Diego et al 2014a

Cinmemj at 08:50, 25 October 2017

2017-10-25T08:50:00Z

Cinmemj at 13:49, 17 October 2017

2017-10-17T13:49:59Z

Cinmemj: Replaced content with "==Abstract== M144.pdf ==References== See pdf document"

2017-10-17T13:49:23Z

Replaced content with "==Abstract== M144.pdf ==References== See pdf document"

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Cinmemj: Created page with "==1 Title, abstract and keywords== Your document should start with a concise and informative title. Titles are often used in information-retrieval systems. Avoid abbreviation..."

2017-10-17T13:48:18Z

Created page with "==1 Title, abstract and keywords== Your document should start with a concise and informative title. Titles are often used in information-retrieval systems. Avoid abbreviation..."

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| style="text-align: center;"|Thickness
| style="text-align: center;"|3.175 mm
|-
| style="text-align: center;"|Young Modulus
| style="text-align: center;"|12.74 MPa
|-
| style="text-align: center;"|Poisson coefficient
| style="text-align: center;"|0.25
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| style="text-align: center;"|Density
| style="text-align: center;"|1107 kg/m<sup>3</sup>
|}
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@@ Line 15: / Line 15: @@
 polarization, setting the direction of migration, regulating the formation of adhesion
 sites and the generation of the forces that drive motion.
 Theoretical models based on an independent description of these processes
 have a limited capacity to predict cellular behavior observed in vitro, since their
@@ Line 40: / Line 41: @@
 challenges a long held view on the mechanisms of RhoGTPase crosstalk and
 suggests that the role of GDIs, GEFs and GAPs has to be revised. Recent
-experimental evidence supports this idea[6]. In addition, the model allows
+experimental evidence supports this idea[6].
 to recapitulate a continuous transition between the tear-like shape adopted
 by neutrophiles and the fan-like shape of keratocytes during migration [7] by
@@ Line 67: / Line 70: @@
+<pdf>Media:Draft_Samper_617655499_7553_M144.pdf</pdf>
-[[Media:Draft_Samper_617655499_8288_M144.pdf|M144.pdf]]
 ==References==
 See pdf document

← Older revision		Revision as of 13:49, 17 October 2017
Line 1:		Line 1:
	==Abstract==		==Abstract==
		+
		+	Cell migration is a fundamental element in a variety of physiological and
		+	pathological processes. Alteration of its regulatory mechanisms leads to loss of
		+	cellular adhesion and increased motility, which are critical steps in the initial
		+	stages of metastasis, before a malignant cell colonizes a distant tissue or organ.
		+	Consequently, cell migration has become the focus of intensive experimental
		+	and theoretical studies; however the understanding of many of its mechanism
		+	remains elusive. Cell migration is the result of a periodic sequence of
		+	protrusion, adhesion remodeling and contraction stages that leads to directed
		+	movement of cells towards external stimuli. The spatio-temporal coordination
		+	of these processes depends on the di erential activation of the signaling networks
		+	that regulate them at specific subcellular locations. Particularly, proteins
		+	from the family of small RhoGTPases play a central role in establishing cell
		+	polarization, setting the direction of migration, regulating the formation of adhesion
		+	sites and the generation of the forces that drive motion.
		+	Theoretical models based on an independent description of these processes
		+	have a limited capacity to predict cellular behavior observed in vitro, since their
		+	functionality depends intrinsically on the cross-regulation between their signaling
		+	pathways. This thesis presents a model of cell migration that integrates
		+	a description of force generation and cell deformation, adhesion site dynamics
		+	and RhoGTPases activation. The cell is modeled as a viscoelastic body capable
		+	of developing active traction and protrusion forces. The magnitude of stresses
		+	is determined by the activation level of the RhoGTPases, whose distribution
		+	in the cell body is described by a set of reaction-di usion equations. Adhesion
		+	sites are modeled as punctual clusters of transmembrane receptors that
		+	dynamically bind and unbind the extracellular matrix depending on the force
		+	transmitted to them and the distance with ligands on the substrate.
		+
		+	Onthe theoretical level, the major findings concern the relationship between
		+	the topology of a crosstalk scheme and the properties, as defined in [1], inherited by the associated reaction network as a gradient sensing and regulatory
		+	system: persistent and transient polarization triggered by external gradients,
		+	adaptation to uniform stimulus, reversible polarization, multi-stimuli response
		+	and amplification. This leads to models that remain functional against the biological
		+	diversity associated to di erent cell types and matches the observed cell
		+	behaviour in Chemotaxis essays [2, 3, 4, 5]: the capacity of cells to amplify gradients,
		+	polarize without featuring Turing patterns of activation, and switch the
		+	polarization axis and the direction of migration after the source of the external
		+	stimulus is changed. The RhoGTPase model, derived on theoretical premises,
		+	challenges a long held view on the mechanisms of RhoGTPase crosstalk and
		+	suggests that the role of GDIs, GEFs and GAPs has to be revised. Recent
		+	experimental evidence supports this idea[6]. In addition, the model allows
		+	to recapitulate a continuous transition between the tear-like shape adopted
		+	by neutrophiles and the fan-like shape of keratocytes during migration [7] by
		+	varying the relative magnitudes of protrusion and contraction forces or, alternatively,
		+	the strength of RhoGTPase Crosstalk. The second mechanism represents
		+	a novel explanation of the di erent morphologies observed in migrating cells.
		+	Di erences in RhoGTPase crosstalk strength could be mediated by di erences
		+	between the activity or concentration of GEFs, GAPs and GDIs in di erent cell
		+	types; an idea that can be explored experimentally.
		+
		+
		+	On cell mechanosensing, a new hypothesis based on a simple physical principle
		+	is proposed as the mechanism that might explain the universal preference
		+	of cells (bar neurons) to migrate along sti ness gradients. The theory provides
		+	a simple unifying explanation to a number of recent observations on force development
		+	and growth in real time at cell Focal adhesions [8, 9, 10, 11]. The
		+	apparently conflicting results have been attributed to the di erences in experimental
		+	set-ups and cell types used, and have fueled a longstanding controversy
		+	on how cells prove the mechanical properties of the extra-cellular matrix. The
		+	predictions of the theory recapitulate these experimental observations, and its
		+	founding hypothesis can be tested experimentally. This hypothesis directly
		+	suggests the mechanism that could explain the preference of cells to migrate
		+	along sti ness gradients, and for the first time, a plausible biological function
		+	for its existence. This phenomenon is known as Durotaxis, and its abnormal
		+	regulation has been associated to the malignant behaviour of cancer cells.
		+
		+

	[[Media:Draft_Samper_617655499_8288_M144.pdf\|M144.pdf]]		[[Media:Draft_Samper_617655499_8288_M144.pdf\|M144.pdf]]

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