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Review
. 2013 Aug 24:8:e201308003.
doi: 10.5936/csbj.201308003. eCollection 2013.

A Sieve-Raft Hypothesis for the regulation of endothelial fenestrations

Affiliations
Review

A Sieve-Raft Hypothesis for the regulation of endothelial fenestrations

Victoria C Cogger et al. Comput Struct Biotechnol J. .
No abstract available

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Figures

Figure 1
Figure 1
Microscopy of LSEC fenestrations and the LSEC membrane. Figure 1A is a scanning electron micrograph of an isolated LSEC in culture. The micrograph clearly displays fenestrations, examples are denoted by an asterix (*), arranged in groups (sieve plates) or individually. The fenestrations are located in the thin cytoplasmic extensions of the cell, distal to the nucleus (N) Scale bar = 5 µm. Figure 1B is a transmission electron micrograph of perfusion fixed liver, the unique architecture of the sinusoid can be seen. The very thin endothelium (E) is perforated with fenestrations (#), allowing passage of substrates into the hepatocytes (H) for metabolism, storage and detoxification Scale bar = 2 µm. Figure 1C is a micrograph prepared by 3D structured illumination microscopy. The LSECs have been stained with Bodipy FL C5 ganglioside GM1, a marker for rafts (green) and Cell-Mask Orange, a cell membrane marker (orange). There is an inverse distribution between liver sieve plates and membrane rafts. Some sieve plates are identified by an arrow (→) and fenestrations can be resolved within the sieve plates. Scale bar = 1 µm.
Figure 2
Figure 2
The Sieve-Raft hypothesis: the composition and arrangement of lipids in the cell membrane is paramount in determining fenestration formation and cell function. We propose that fenestrations form in non-raft microdomains of the lipid bilayer and that rafts and actin engender membrane stability, while limiting fenestration formation.

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