Pandey Ekta, Nour Aiah S, Harris Edward N
Department of Biochemistry, Universityof Nebraska, Lincoln, NE, United States.
Front Physiol. 2020 Jul 21;11:873. doi: 10.3389/fphys.2020.00873. eCollection 2020.
Liver sinusoidal endothelial cells (LSECs) are the most abundant non-parenchymal cells lining the sinusoidal capillaries of the hepatic system. LSECs are characterized with numerous fenestrae and lack basement membrane as well as a diaphragm. These unique morphological characteristics of LSECs makes them the most permeable endothelial cells of the mammalian vasculature and aid in regulating flow of macromolecules and small lipid-based structures between sinusoidal blood and parenchymal cells. LSECs have a very high endocytic capacity aided by scavenger receptors (SR), such as SR-A, SR-B (SR-B1 and CD-36), SR-E (Lox-1 and mannose receptors), and SR-H (Stabilins). Other high-affinity receptors for mediating endocytosis include the FcγRIIb, which assist in the antibody-mediated removal of immune complexes. Complemented with intense lysosomal activity, LSECs play a vital role in the uptake and degradation of many blood borne waste macromolecules and small (<280 nm) colloids. Currently, seven Toll-like receptors have been investigated in LSECs, which are involved in the recognition and clearance of pathogen-associated molecular pattern (PAMPs) as well as damage associated molecular pattern (DAMP). Along with other SRs, LSECs play an essential role in maintaining lipid homeostasis with the low-density lipoprotein receptor-related protein-1 (LRP-1), in juxtaposition with hepatocytes. LSECs co-express two surface lectins called L-Specific Intercellular adhesion molecule-3 Grabbing Non-integrin Receptor (L-SIGN) and liver sinusoidal endothelial cell lectin (LSECtin). LSECs also express several adhesion molecules which are involved in the recruitment of leukocytes at the site of inflammation. Here, we review these cell surface receptors as well as other components expressed by LSECs and their functions in the maintenance of liver homeostasis. We further discuss receptor expression and activity and dysregulation associated with the initiation and progression of many liver diseases, such as hepatocellular carcinoma, liver fibrosis, and cirrhosis, alcoholic and non-alcoholic fatty liver diseases and pseudocapillarization with aging.
肝窦内皮细胞(LSECs)是肝系统窦状毛细血管中最丰富的非实质细胞。LSECs的特征是有许多窗孔,缺乏基底膜和隔膜。LSECs这些独特的形态特征使其成为哺乳动物脉管系统中渗透性最强的内皮细胞,有助于调节大分子和小的脂质结构在窦状血液与实质细胞之间的流动。LSECs具有很高的内吞能力,这得益于清道夫受体(SR),如SR-A、SR-B(SR-B1和CD-36)、SR-E(Lox-1和甘露糖受体)以及SR-H(稳定素)。其他介导内吞作用的高亲和力受体包括FcγRIIb,它有助于抗体介导清除免疫复合物。LSECs具有强烈的溶酶体活性,在摄取和降解许多血源性废弃大分子和小(<280nm)胶体方面发挥着至关重要的作用。目前,已在LSECs中研究了七种Toll样受体,它们参与病原体相关分子模式(PAMPs)以及损伤相关分子模式(DAMP)的识别和清除。与其他SRs一起,LSECs与肝细胞并列,在通过低密度脂蛋白受体相关蛋白-1(LRP-1)维持脂质稳态方面发挥着重要作用。LSECs共表达两种表面凝集素,称为L-特异性细胞间粘附分子-3抓取非整合素受体(L-SIGN)和肝窦内皮细胞凝集素(LSECtin)。LSECs还表达几种粘附分子,它们参与炎症部位白细胞的募集。在此,我们综述这些细胞表面受体以及LSECs表达的其他成分及其在维持肝脏稳态中的功能。我们还进一步讨论了受体表达、活性以及与许多肝脏疾病(如肝细胞癌、肝纤维化和肝硬化、酒精性和非酒精性脂肪性肝病以及衰老相关的假毛细血管化)的发生和发展相关的失调情况。