Archive for January, 2012

The Dunn Lab’s Newest Paper!!

I’m excited to announce that our lab’s newest paper, “Strain Tunes Proteolytic Degradation and Diffusive Transport in Fibrin Networks,” has been accepted by the ACS journal Biomacromolecules.  We’re quite pleased with this study, because we believe it highlights the biophysical mechanisms that govern fibrin degradation.  Here’s the LINK!! Look for the final version in the next journal issue.

Fibrin clots are proteinaceous gels that polymerize in the blood at sites of vascular injury.  They provide the structural scaffolding for cells to remodel and repair the tissue at wound sites, and therefore must be resistant to degradation.  However, improper or incomplete degradation of fibrin could lead to the formation of thrombi that block blood vessels, leading to myocardial infarction (heart attack) and other cardiovascular diseases.

In this study, we found that strain on fibrin clots due to platelet contraction, fluid shear, or mechanical stress causes up to a 10-fold reduction in the rate of fibrin degradation.  The most likely cause for this is the hindered diffusion of the fibrinolytic enzyme into the clot as strain is applied.  To this end, we also revealed that anisotropic diffusion of dextran molecules accompanies the application of strain, possibly due to fiber alignment.

 

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January 6, 2012 at 8:17 am Leave a comment

(Cell) Death Most Beautiful

Now here’s quite an interesting Cell Picture Show.  The highlight of this one is “cell death.”

There are various forms of cell death.

Apoptosis refers to programmed cell death; the inability of cells to undergo apoptosis leads to numerous diseases, such as various cancers, autoimmune diseases, inflammatory diseases, and viral infections.  One common example of misprogrammed cell death is cancer, which is characterized by excessive cellular proliferation.  Necrosis on the other hand refers to the premature death of cells.  This can be caused by factors that are not programmed in the cells lifecycle and can be detrimental to the survival of an organism.  Because cells that die by necrosis do not send the same chemical signals as those that die by apoptosis, they are left unnoticed and can build up as dead tissue.

The picture (or actually movie) that is most interesting to me is the one titled “Mitochondria Let Loose.”  This is fascinating, because one can visualize (with colors) the activation of the caspase protease that aids in the apoptosis of the cell.  Using a FRET reporter is quite clever in this case, but I am wondering how they’ve arranged the donor and acceptor to report activation.  If anyone knows the details of this and wants to enlighten me, feel free to email at dunnlabstanford@gmail.com.

I also quite like the one titled “Cytoskeleton Gives up the Ghost.”  It’s curious that the actin cytoskeleton is the first casualty in the necroptotic process.  One might naively suspect that there are some geometrical constraints in the way the cytoskeleton collapses, but considering this is not programmed by the cell, it could be a stochastic destruction of the structural components.  Feel free to email me regarding this as well.

Death Most Beautiful

By Thomas Deerinck and Mark Ellisman, NCMIR, UCSD

Programmed cell death ensures that our bodies contain just the right number of cells. This tightly regulated process removes damaged cells, shapes our organs and digits, and refines our immune systems. Here, multiphoton fluorescence imaging reveals an apoptotic HeLa cell (middle) amongst non-dying neighbors.

Image: HeLa cells expressing GFP targeted to the Golgi apparatus (yellow) are stained to reveal the distribution of microtubules (red) and cell nuclei (blue).

[from the Cell Press Website]

January 6, 2012 at 7:21 am Leave a comment


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