Liver Sinusoidal endothelial cells (LSECs) are specialized fenestrated endothelial cells in the liver and contain pores which size range from 50-150 nm. It has been shown that LSECs defenestration (loss of pores) is associated with inflammation and oxidative stress. Nevertheless, the importance of large pores (gaps: pore size >300 nm) following inflammation and oxidative stress remains unknown.
To what extent do we need to consider these gaps as an indicator of the Liver Sieve damage?
Hi Ravinder,LSEC pore sizes vary in relationship to animal species (NZwhite rabbits have small pores smaller than rats, but there is overlap. On TEM (Wisse) the pores appear bigger than on SEM due to preparation artefact. The pressure of perfusion fixation is also important & volume perfusion is more likely to lead to abnormally large artificial gaps. Hypoxia also. So really one is not sure what gaps are artefact, pathological, oxidative stress, from poisons or related to drugs,(paracetamol). Similar discussions involve defenestration, which may pre-date capillarization of sinusoids and basement membrane formation. In my opinion in comparing one factor with another, the fixative, pressure ,tem or sem or afm must be identical ,and if possible other methods also be used such as differential filtration of labelled particles. The best demonstration so far of sieving has been Akin Akink et al demonstration of siRNA inhibition of hepatocyte protein using different sized transport vesicles!
On the other hand, If the gaps are for real they will alter the LSEC porosity which mayl have profound effects on many liver metabolic functions. Good luck. Robin Fraser.
- Badges
- Science method