Knittel T, Aurisch S, Neubauer K, Eichhorst S, Ramadori G
Department of Internal Medicine, University of Göttingen, Germany.
Am J Pathol. 1996 Aug;149(2):449-62.
Ito cells (lipocytes, stellate cells) are regarded as the principle matrix-producing cell of the liver and have been shown recently to express glial fibrillary acidic protein, an intermediate filament typically found in glia cells of the nervous system. The present study examines 1) whether Ito cells of rat liver express central nervous system typical adhesion molecules, namely, neural cell adhesion molecule (N-CAM), in a cell-type-specific manner and 2) whether N-CAM expression is affected by activation of Ito cells in vitro and during rat liver injury in vivo. As assessed by reverse transcriptase polymerase chain reaction, Northern blotting, Western blotting, and immunocytochemistry of freshly isolated and cultivated hepatic cells, N-CAM expression was restricted to Ito cells and was absent in hepatocytes, Kupffer cells, and sinusoidal endothelial cells. Ito cells expressed predominantly N-CAM-coding transcripts of 6.1 and 4.8 kb in size and 140-kd isoforms of the N-CAM protein, which was localized on the cell surface membrane of Ito cells. In parallel to glial fibrillary acidic protein down-regulation and smooth muscle alpha-actin up-regulation, N-CAM expression was increased during in vitro transformation of Ito cells from resting to activated (myofibroblast-like) cells and by the fibrogenic mediator transforming growth factor-beta 1. By immunohistochemistry, N-CAM was detected in normal rat liver in the portal field as densely packed material and in a spot as well as fiber-like pattern probably representing nerve structures. However, after liver injury, N-CAM expression became detectable in mesenchymal cells within and around the necrotic area and within fibrotic septae. In serially cut tissue sections, N-CAM-positive cells were predominantly co-distributed with smooth muscle alpha-actin-positive cells rather than glial fibrillary acidic protein-positive cells, especially in fibrotic livers. The experimental results illustrate that N-CAM positivity in the liver cannot be solely ascribed to nerve endings as, among the different types of resident liver cells, Ito cells specifically express N-CAM in vitro and presumably in vivo. In addition to its role as potential cell-type-specific marker protein for activated Ito cells, the induction of N-CAM expression might illustrate a mechanism by which mesenchymal cell proliferation might be inhibited when tissue repair is concluded.
肝星状细胞(贮脂细胞、星状细胞)被视为肝脏中主要的基质产生细胞,最近研究表明其可表达胶质纤维酸性蛋白,这是一种通常在神经系统胶质细胞中发现的中间丝。本研究旨在探讨:1)大鼠肝脏的肝星状细胞是否以细胞类型特异性方式表达中枢神经系统典型的黏附分子,即神经细胞黏附分子(N-CAM);2)N-CAM的表达在体外肝星状细胞激活过程以及体内大鼠肝损伤过程中是否受到影响。通过对新鲜分离和培养的肝细胞进行逆转录聚合酶链反应、Northern印迹、Western印迹及免疫细胞化学分析,发现N-CAM的表达仅限于肝星状细胞,在肝细胞、库普弗细胞和肝血窦内皮细胞中未检测到。肝星状细胞主要表达大小为6.1和4.8 kb的N-CAM编码转录本以及140-kd的N-CAM蛋白异构体,该蛋白定位于肝星状细胞的细胞膜表面。随着胶质纤维酸性蛋白下调和平滑肌α-肌动蛋白上调,在体外肝星状细胞从静止状态转变为激活状态(成肌纤维细胞样)的过程中以及在致纤维化介质转化生长因子-β1作用下,N-CAM的表达增加。通过免疫组织化学方法,在正常大鼠肝脏的门管区检测到N-CAM,表现为密集堆积的物质,呈点状及纤维状分布,可能代表神经结构。然而,肝损伤后,在坏死区域内及周围的间充质细胞以及纤维化间隔中可检测到N-CAM的表达。在连续切片的组织中,N-CAM阳性细胞主要与平滑肌α-肌动蛋白阳性细胞而非胶质纤维酸性蛋白阳性细胞共同分布,尤其是在纤维化肝脏中。实验结果表明,肝脏中的N-CAM阳性不能仅归因于神经末梢,因为在不同类型的肝脏驻留细胞中,肝星状细胞在体外以及推测在体内特异性表达N-CAM。除了作为激活的肝星状细胞潜在的细胞类型特异性标记蛋白外,N-CAM表达的诱导可能说明了一种机制,即组织修复完成时间充质细胞增殖可能受到抑制。