Expression of CINC-2beta is related to the state of differentiation of alveolar epithelial cells.
Expression of CINC-2beta is related to the state of differentiation of alveolar epithelial cells.
复制标题
CINC-2β的表达与肺泡上皮细胞的分化状态有关。
DOI：
10.1165/rcmb.2005-0113oc
复制
发表时间：
2005
影响因子：
6.4
通讯作者：
Mason,RobertJ
中科院分区：
文献类型：
--
作者：
Nishina,Kahoru;Zhang,Feijie;Nielsen,LarryD;Edeen,Karen;Wang,Jieru;Mason,RobertJ
肺泡上皮细胞是最先遇到吸入颗粒或生物体的细胞之一。这些细胞可能通过产生趋化因子参与炎症反应的启动和调节。然而，关于这些细胞趋化因子产生的程度或调节的信息很少。在分化和去分化条件下研究大鼠 II 型细胞，以确定其表达和分泌 CXC 趋化因子的能力。分化和去分化的 II 型细胞均分泌 MIP-2、MCP-1 和 CINC-2，以响应 IL-1β、TNF-α 和 IFN-γ 的细胞因子混合物或单独的 IL-1β。细胞因子混合物还诱导 iNOS 表达和亚硝酸盐分泌。分化和去分化的 II 型细胞均表达 CINC-1 (GRO)、CINC-2α、CINC-3 (MIP-2) 和 MCP-1 mRNA，并且细胞因子混合物或单独的 IL-1β 可以增加它们的表达。然而，CINC-2β（CINC-2的剪接变体）仅在KGF刺激的分化条件下表达，并且不会被细胞因子混合物或IL-1β增加。正常肺和滴注Ad-KGF的肺的原位杂交证明CINC-2β在体内由肺泡和细支气管上皮细胞表达。我们得出的结论是，CINC-2β 的调节方式与大多数其他趋化因子不同，并且其表达与肺泡 II 型细胞分化的状态有关。
Alveolar epithelial cells are among the first cells to encounter inhaled particles or organisms. These cells likely participate in the initiation and modulation of the inflammatory response by production of chemokines. However, there is little information on the extent or regulation of chemokine production by these cells. Rat type II cells were studied under differentiated and dedifferentiated conditions to determine their ability to express and secrete CXC chemokines. Both differentiated and dedifferentiated type II cells secreted MIP-2, MCP-1, and CINC-2 in response to a cytokine mixture of IL-1β, TNF-α, and IFN-γ or to IL-1β alone. The cytokine mixture also induced iNOS expression and nitrite secretion. Both differentiated and dedifferentiated type II cells expressed CINC-1 (GRO), CINC-2α, CINC-3 (MIP-2), and MCP-1 mRNA, and their expression was increased by the cytokine mixture or by IL-1β alone. However, CINC-2β, a splice variant of CINC-2, was only expressed under differentiated conditions stimulated by KGF and was not increased by the cytokine mixture or by IL-1β.In situhybridization of normal lung and lung instilled with Ad-KGF demonstrated that CINC-2β was expressed by alveolar and bronchiolar epithelial cellsin vivo. We conclude that CINC-2β is regulated differently from most other chemokines and that its expression is related to the state of alveolar type II cell differentiation.