Hybrid CPM (Angiogenesis and sprouting) Flashcards
What is the driving force of cell network formation during angiogenesis?
Cell shape (length) constraints which leads to steric hindrance.
While chemotaxis is vital and increases the speed of network formation it is not completely necessary.
Describe the mathematical model for the secretion and spread of chemical signal!
*epsilon is degradation rate
What is the mathematical formulation describing chemotactical movement of CPM cells?
where chi is
How is the diffusion PDE modified to align with the CPM?
It is discretized using the Euler method
What is most likely missing in the model of following simulation of a cell network?
A length constraint of the cells
How to estimate cell length?
How cell length estimation modified to be computationall managable?
Why solely adding length constraint to the CPM is not enough for a cell network simulation?
The combination of length and area constraint lead to disjoint cells as reaching a long optimal length clashes with reaching optimal area. Thus an additional connectivity constraint is neceassary to ensure cells do not get disjoint.
How can you ensure that no rupture of elongating cells can occur?
Connectivity constraint
What is orientational order parameter?
What kind of cell network is expected to have a global orientational order of ~0?
you cant be sure as globally almost any cell network will have no orientation
A lower local orientation order is expexted to be reached for a cell network without chemotaxis.
True or False
False
After enough time they more or less reach the same orientation. However what is significantly different is the speed at which the steady state orientation is reached.
What does the following graph show about cell network formation?
The graph shows that the rotational diffusion gets lower with increasing size of cell cluster size. Consequentially this leads to much more restricted movement and thus a steady state will be reached even if the most energetically favourable state is not such as long as the initial conditions are not close enough to the equilibrium: Contact inhibited motility. Contact inhibited motility can allow for network formation of cells which are not elongated.
How does Anti-VE cadherin treatment affect tissue configuration state?
network -> blobs
What is one mechanism behind contact inhibited motility cell network formation?
cells stop being chemotactic when in contact with other cells.
Describe how contact inhibition can give rise to sprouting.
Can sprouting occur without freefloating cells in the medium?
Yes. Extension-only chemotaxis (without refraction) can actuall allow for it.
Random motility of cells in a clump will create distrubances in the surface which wil result in pseudopod like formations. As the chemotaxis force is stronger in the concave regions of the clump and weaked in the convex ones which further drives the sprouting behaviour.
y
Write down the legend of the mechanisms of sprouting on this graph and explain your reasoning
Extension-only chemotaxis at high enough cell motility is in fact an “endothermic” process as it allows for storing energy in the tissue clump. Allowing for refraction/pushing of cells back in the clump on the other hand releases energy back in the medium and with higher cell motility energy is in fact more quickly being lost.
What is the mechanism of those two chemotactical sprouting processes?
Describe mathematically why at high cell motility it is possible to have extension only chemotaxis sprouting.
for deltaH > 0, P(deltaH) = e^(H0-deltaH)/T
thus high T => greater probablity of cells to move against the gradient and start sprouting due to the convex/concave cheomatactical force difference.
