Endothelial permeability

22 important questions on Endothelial permeability

What do venules (collect blood after capillary bed) regulate?

- Plasma leakage
- Leukocyte trafficking (important in immune response)

What two things regulate the transcapillary leak (Net Driving Force)?

- Transcapillary hydrostatic pressure difference (P)
- Effective osmotic pressure difference (π)

How is the Net Driving Force on the arterial and the venous side of the capillary?

- Arterial: the hydrostatic capillary pressure is higher than the osmotic pressure difference → filtration (flow out of capillary)
- Venous: hydrostatic capillary pressure has dropped → reabsorption
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What is the basal membrane of a vessel?

Sticky tissue around the endothelial cells, to keep them in place.

What are the three types of capillaries?

- Continuous capillary
- Fenestrated capillary (small holes: fenestra)
- Sinusoidal (discontinuous) capillary: large gaps between cells.

Where can those different types of capillaries be found in the body?

- Continuous: most common
- Fenestrated: glomerulus, endocrine glands
- Discontinuous: liver sinusoids

What happens in the case of an inflammatory reaction to the glycocalyx?

It's cleaved off.

What aspect of bulk flow is different in the brain, which creates the blood-brain barrier?

- The 2 endothelial cells express proteins that bind to each other, which creates a zipper,
- which is more pronounced in the brain, thereby creating a firm barrier.

What happens in inflammation with the vascular permeability?

The vessels become more leaky to allow infiltration of immune cells.

What happens to the vascular permeability and leakage in chronic inflammation?

Both stay high (so it lasts longer than a short while)

What are three types of cell-cell contacts, and what are their properties?

Tight junctions: control paracellular permeability, are really tight, only present in specific organs like the brain.
Gap junctions: form channels between 2 cells, so if something happens in a cell, other cells 'know'
Adherens junctions: only in endothelial cells, consist of VE-cadherin

What makes vascular permeability and leakage go up in inflammation?

The disassembly of cell junctions.

By what two things are the (dynamic) cell-cell contacts regulated?

1. Mechanical force (contraction)
2. Signaling through phosphorylation

What molecule controls the cell shape and adhesion?

Actin (forms a cytoskeleton)

At what place in the cell is the highest amount of actin?

At the sides of the cell (to regulate VE-cadherin).

How are the VE-cadherin interactions be regulated by actin?

By mechanical force/contraction (which works on actin).

What is the difference between the adherens junctions of healthy cells and other cells, and what causes this difference??

Linear adherens junctions: healthy cells (because actin is parallel to the gap)
disturbance or shear stress causes:
Focal adherens junctions: force causes larger gaps (because actin is perpendicular to the gap)

What is the problem with focal adherens junctions?

When force is exerted on the gap, the junction between the cells breaks.

How is the force on the cell regulated?

By phosphorylation (and de-phosphorylation) of myosin.

What is needed for optimal cell adhesion?

Some force.

What factor increases vascular permeability?

VEGF (because induces VVO formation)

What can disrupt the cell-to-cell contact by disassembly of cell junctions?

Cytokines and inflammatory mediators.

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