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Hepatic Sinusoidal Endothelial Cells 5 CHAPTER 5 Hepatic Sinusoidal Endothelial Cells 5 Roman E. Perri, Vijay Shah 5.1 Development and Structure Hepatic sinusoidal endothelial cells (HSEC) are a morphologically distinct population of cells that form the lining of liver sinusoids. Features that dis- tinguish HSEC from endothelial cells in other or- gans and in larger liver vessels are the presence of multiple fenestrae throughout the cells and the lack of an underlying basement membrane [3, 7, 60, 72]. The sinusoids are positioned between hepato- cyte plates and initiate at the portal tract and termi- nate at the central vein. Sinusoids carry blood that converges in the liver from the portal venous sup- ply, as well as from the hepatic artery [76] (Fig. 5.1). Sinusoids are separated from adjacent hepatocytes by the perisinusoidal space, also known as the space of Disse. Due to their position, HSEC are the first cells in contact with blood flow into the sinusoids and serve to compartmentalize the vascular sinu- soidal channels from the hepatic parenchyma [60, 72]. The hepatic sinusoids range in diameter from Fig. 5.1. Vasculature architecture of the liver. Blood flow enters 4 µm near the portal triad to 5.5 µm near the cen- the liver via the portal vein (PVb) as well as the hepatic artery tral vein [30]. Because they are smaller than both (HAb). While portal blood enters directly into the sinusoids (S), red and white blood cells, there is distortion of both hepatic arterial blood perfuses into distinct anatomic locations cells and the sinusoids during passage of blood cells prior to re-entering the sinusoids. Sinusoidal blood leaves the [30, 78]. This process has been referred to as an “en- liver via the central veins (CV). Sinusoidal endothelial cells (En) dothelial massage,” which allows efficient exchange form the fenestrated sinusoidal wall. Kupffer cells (K) are lo- of compounds from the blood through sinusoidal cated within the sinusoids, whereas hepatic stellate cells, also fenestrae into the space of Disse [30, 76]. Also resid- termed fat-storing cells (FSC), lie within the space of Disse (DS), ing in the sinusoidal space are hepatic macrophages, adjacent to the single layer of hepatocytes (liver plate, LP). Bile or Kupffer cells, and hepatic natural killer cells, also canaliculi (BC) drain bile into the interlobular bile ducts (BDL) via called pit cells, each of which are covered in other the caniliculoductar junction (CD) in the opposite direction to chapters. flow in the vascular channels. (From Motta P, Muto M, Fujita T. During organogenesis, the primordial liver is The liver. An atlas of scanning electron microscopy. Igaku-Shoin vascularized by capillaries that are continuous and Medical Publishers, Inc., 1978:129) have a basement membrane. Differentiation of these capillaries occurs from precursors located in the septum transversum, a mesenchymal structure lo- septum transversum. Intrahepatic capillaries at this cated between the pericardium and the hepatic di- early stage of gestation have the phenotype of typi- verticulum [17, 28]. At 5 weeks of gestation, grow- cal fetal capillaries, containing cell–cell junctions ing cords of hepatoblasts derived from the hepatic and a basement membrane. Between 5 and 12 weeks diverticulum surround the precursor vessels of the of gestation, the vessels adjacent to hepatocytes de- 54 PART I: Cell Types and Matrix velop their mature phenotype, marked by the devel- sinusoids [41]. Adhesion molecules on the surface opment of fenestrae, the lack of a basement mem- of typical endothelial cells capture leukocytes in brane, and the loss of cell–cell junctions [17, 18, 79]. the passing blood flow, permitting recruitment of Interestingly, in some hepatic disease states, HSEC inflammatory cells to areas of invasion by foreign dedifferentiate from their specialized phenotype pathogens [34]. HSEC have been shown rarely to ex- back to the more typical endothelial cell phenotype press selectins, a class of adhesion molecules com- [38, 73, 78, 79]. monly expressed in various other tissues [67]. How- ever, other adhesion molecules, such as vascular adhesion protein (VAP-1), are expressed in HSEC, and are responsible for capture of rolling leukocytes 5.2 through the sinusoids, thus recruiting them to areas Cellular Functions of HSEC of inflammation [41, 47]. In addition, other leuko- cyte adhesion molecules, such as vascular cell adhe- sion molecule 1 (VCAM-1), are induced on HSEC in 5.2.1 states of liver inflammation [1, 41, 67, 68]. VCAM-1 Fenestration/Filtration also mediates, in part, the adhesion of melanoma cells to hepatic endothelium, thereby playing a key The most prominent feature of sinusoidal en- role in the development of hepatic metastatic lesions dothelial cells is the presence of multiple fenestrae in this disease [41]. Neutrophil attraction to HSEC throughout the cell. Fenestrae have diameters of is mediated by intercellular adhesion molecule 1 about 100 nm, and while the number of fenestrae (ICAM-1), which is constitutively expressed on increases as the sinusoids reach the central vein, HSEC and is upregulated in response to liver injury their diameter decreases [3, 30, 77]. An intracellu- [1, 56, 67]. lar cytoskeleton composed of microfilaments, in- Chemokines produced by inflamed tissues bind termediate filaments, and microtubules supports to receptors on leukocytes and prompt the subse- the dynamic fenestrae [7], which can reorganize to quent firm adhesion of leukocytes to endothelium. form additional fenestrae when stimulated [9]. The This process allows migration of leukocytes into in- fenestrae of the HSEC serve as a mechanical sieve, flamed tissues. The expression of multiple chemok- which facilitates the transfer of nutrients and mole- ines is upregulated in the inflamed liver [1]. T cells cules from the sinusoidal space to the hepatic paren- that infiltrate the liver have been demonstrated to chyma [11, 77]. As HSEC lack a basement membrane, express receptors for these chemokines [67]. After the presence of fenestrae allow for steric selection of adhesion molecules expressed by tissue endothelial compounds that permeate the endothelial cell bar- cells have captured a leukocyte, the leukocyte must rier and gain access to the space of Disse and the transit through the endothelium to reach inflamed hepatic parenchymal cells [7, 77]. For example, the tissue [6]. Many tissues have inter-endothelial-cell presence of fenestrae allows the passage of chylomi- tight junctions that present a barrier to migration cron remnants into the space of Disse to be recog- of leukocytes. However, HSEC form a discontinuous nized and affected by hepatocyte metabolism [7, 30]. barrier without tight junctions, which likely allows Chylomicrons themselves, too large to pass through for unique means of leukocyte migration through the HSEC fenestrae, remain in the sinusoidal space the endothelium barrier and into the inflamed pa- eventually to pass from the liver. The effect of vari- renchyma [41]. ous disease states on HSEC fenestrae is felt to have major implications on the clinical manifestations of each disease state [10, 73]. 5.2.3 Signaling: Nitric Oxide Production 5.2.2 Specific signaling pathways including those in HSEC Expression of Adhesion Molecules are covered in other chapters of this book. However, as nitric oxide (NO) is a key signaling pathway in Leukocytes are attracted and localized to sites of HSEC, some discussion of NO production in HSEC inflammation throughout the body. This occurs is provided. HSEC produce NO via endothelial nitric by attachment to adhesion molecules expressed on oxide synthase (eNOS) as well as inducible nitric ox- the surface of endothelial cells [1, 41]. The liver is ide synthase (iNOS). Production of NO via eNOS is exposed to numerous foreign antigens that traverse a characteristic that is exclusive to endothelial cells the bowel mucosa and enter the portal circulation, among hepatic cell types [41]. NO produced by the thereby gaining access to the liver via the hepatic HSEC may serve to regulate sinusoidal blood flow CHAPTER 5: Hepatic Sinusoidal Endothelial Cells 55 through a paracrine action on perisinusoidal con- heparin, albumin, lipoproteins, and hyaluronate has tractile cells [59]. Increase in NO production via been well described. For some substances such as eNOS is seen in HSEC subjected to shear stress, a heparin, the endocytotic capacity of HSEC exceeds characteristic that may serve to autoregulate blood that of Kupffer cells [3]. The ability of HSEC to take flow through the liver [62]. By this mechanism, if up hyaluronate via endocytosis has been used as a blood flow through the hepatic sinusoid is high, functional marker of sinusoidal endothelial cells eNOS-mediated production of NO may serve locally [64]. Rising serum hyaluronate levels have been to dilate the vascular bed, thus decreasing the re- demonstrated to correlate with decreased endocy- sistance of the vascular bed [62]. In cirrhotic states, totic capabilities of sinusoidal endothelial cells. production of NO via eNOS is diminished [53]. Other A typical endocytosis pathway has been de- important agonists that promote eNOS-derived NO scribed in HSEC. The mannose receptor functions generation include endothelin (via the ET-B recep- by binding and internalizing compounds or anti- tor), VEGF, estrogen and others [5, 31, 56, 59]. Every gens that contain terminal glycoproteins. The man- cell type within the liver has the capacity to gener- nose receptor exists on the cell wall, in coated pits, ate NO via iNOS upon stimulation by liver injury and there is a large intracellular pool of additional or cytokine induction, though this does not occur receptors. When the receptor binds to ligand, rapid during normal conditions [54, 63]. HSEC have been internalization occurs and the ligand is delivered to demonstrated to produce NO via induction of iNOS endosomes and lysosomes for degradation. New re- in response to cytokines such as interferon (IFN)-γ ceptors, either from intracellular stores or recycled and lipopolysaccharides (LPS), agents that do not by receptors, return to the cell surface to bind addi- themselves stimulate iNOS induction in hepatocytes tional ligand [45].
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