Liver sinusoidal endothelial cell

Source: Wikipedia, the free encyclopedia.
Liver sinusoidal endothelial cell
Details
SystemCirculatory system
Locationblood vessels of liver
Anatomical terms of microanatomy

Liver sinusoidal endothelial cells (LSECs) form the lining of the smallest blood vessels in the liver, also called the

hepatic sinusoids. LSECs are highly specialized endothelial cells with characteristic morphology and function. They constitute an important part of the reticuloendothelial system
(RES).

Structure

Although the LSECs make up only about 3% of the total liver cell volume, their surface in a normal adult human liver is about 210 m2, or nearly the size of a tennis court.[1]

The LSEC structure differs from other

space of Disse, the fenestrae are crucial for lipoprotein traffic between the hepatocytes and the sinusoidal lumen.[3] The LSECs lack an organized basal lamina.[4] The LSECs contain 45% and 17% of the liver's total mass of pinocytic vesicles and lysosomes, and contain twice as many clathrin-coated pits per membrane unit, compared with two other major liver cells, Kupffer cells and hepatocytes,[5]
reflecting the high capacity clathrin-mediated endocytic activity of LSECs.

Physiological functions

LSECs play a central role in the clearance of blood borne waste. The cells express endocytosis receptors that mediate extremely rapid internalization of waste molecules. In rat it has been shown that LSECs express scavenger receptors (SR) class A, B, E and H.

hyaluronan receptor‐1),[11] and LRP‐1 (low‐density lipoprotein receptor‐related protein‐1).[12]

The capacity of LSECs as scavengers of blood borne waste assigns an important role of these cells in

toll like receptors (TLRs), MMR and SRs, as well as the high expression of inflammasome molecules NLRP-1, NLRP-3, and AIM2[13] point to innate immune functions of LSECs. In addition, LSECs display features of adaptive immunity, contributing to hepatic immune tolerance.[14]

Pathobiology

Liver fibrosis

LSECs have been reported to play a role in the development of

liver fibrosis. Liver fibrosis is associated with decreased LSEC fenestration, and appearance of an organized basal lamina in the space of Disse, a process called capillarization, which precedes the onset of liver fibrosis.[15] Normally differentiated LSECs prevent hepatic stellate cell activation and promote reversion to quiescence, whereas capillarized LSECs do not.[16]

Atherosclerosis

diabetes mellitus or old age may lead to prolonged postprandial lipoproteinemia and increased circulatory cholesterol levels, with increased risk for development of atherosclerosis.[18]

Autoimmunity

It has been suggested that reduced Fc receptor function in humans, causing increased circulating levels of soluble immune complexes is important in the etiology of autoimmune diseases such as

Sjögren's syndrome.[19] Moreover, the observation that small soluble IgG-antigen immune complexes are cleared in the mouse mainly via the LSEC FcγRIIb2 (8), along with the observation that deletion of same receptor causes spontaneous auto-immunity and SLE-like disease in mice,[20] point to a pivotal role of LSEC FcγRIIb2 in the disease mechanism of SLE. Furthermore, the finding that scavenging of blood borne DNAs is chiefly by SR-mediated uptake in LSECs,[21]
along with the fact that SLE is associated with generation of anti-DNA antibody, lend additional support to the hypothesis that LSECs participate in the onset of SLE.

Liver toxicology

LSECs may sometimes be the initial target of injury in a condition referred to as

acetaminophen.[22] Moreover, since LSECs are geared to (generally unwanted) active blood clearance of large molecule compounds and nano formulations (7) these cells may be easily intoxicated by off-target mechanisms, causing subsequent hepatotoxicity.[23]

Origin and renewal

Normal LSEC turnover is maintained by the liver resident population of LSEC progenitor cells; in addition, recruitment of bone marrow derived cells contributes to replenish the LSEC population when needed.[24]

History

By the end of the 19th and beginning of the 20th centuries researchers observed avid accumulation of intravenously administered colloidal vital dyes in cells lining the sinusoids of some tissues, with the highest uptake in the littoral cells of the hepatic sinusoids. These very active blood clearance cells were collectively named "The reticuloendothelial system", or RES.

nanoparticles roughly <200 nm by clathrin-mediated endocytosis whereas Kupffer cells clear larger particles >200 nm by phagocytosis
.

In a comparative context

All

jawless fishes, these endothelial cells constitute the lining of the gill capillaries. The name scavenger endothelial cells (SECs) has been coined to denote the endothelial cells in vertebrates that are geared to blood clearance.[28]
Thus, LSECs in mammals and other land-based vertebrates are a member of the vertebrate SEC family.

See also

References

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External links
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