GM-CSF and GM-CSF receptor have regulatory role in transforming rat mesenteric mesothelial cells into macrophage-like cells
GM-CSF and GM-CSF receptor have regulatory role in transforming rat mesenteric mesothelial cells into macrophage-like cells
复制标题
DOI：
10.1007/s00011-016-0967-5
复制
发表时间：
2016-10-01
影响因子：
6.7
通讯作者：
Kiss, Anna L.
中科院分区：
文献类型：
--
作者：
Katz, Sandor;Zsiros, Viktoria;Kiss, Anna L.
腹膜炎期间，间皮细胞呈现巨噬细胞特征，表达巨噬细胞标志物，表明它们可能分化为巨噬细胞样细胞。使用25只雄性大鼠进行体内实验。对于体外实验，开发了原代肠系膜培养模型。通过研究 ED1 表达来跟踪间皮细胞向巨噬细胞样细胞的转变。用粒细胞-巨噬细胞集落刺激因子（GM-CSF，1 ng/ml）处理体外原代肠系膜培养物。使用Dynasore (80 A mu M)来阻断受体-配体复合物的内化。腹腔注射弗氏佐剂(1ml)诱发急性腹膜炎。免疫组织化学：GM-CSF体外处理导致转化间皮细胞中ED1显着表达。阻断内化，无法检测到 ED1 表达。 GM-CSF 受体（α 和 β）在体外（即使 GM-CSF 不存在）和体内的间皮细胞中表达。炎症导致间皮细胞裂解液中 GM-CSF 和 GM-CSF 受体水平增加。间皮细胞可以分化为巨噬细胞样细胞，而由间皮细胞产生的 GM-CSF 可能在这一转变中具有自分泌调节作用。我们的结果提供了有关间皮细胞可塑性的新数据，并支持炎症期间巨噬细胞也可以来自非造血来源的观点。
During peritonitis, mesothelial cells assume macrophage characteristics, expressing macrophage markers, indicating that they might differentiate into macrophage-like cells.Twenty-five male rats were used for in vivo experiments. For in vitro experiments, a primary mesentery culture model was developed. The mesothelial cell to macrophage-like cell transition was followed by studying ED1 expression.In vitro primary mesenteric culture was treated with granulocyte-macrophage colony-stimulating factor (GM-CSF, 1 ng/ml). Blocking internalization of receptor-ligand complex, Dynasore (80 A mu M) was used. Acute peritonitis was induced by Freund's adjuvant's (1 ml) intraperitoneal injection.Immunohistochemistry: GM-CSF in vitro treatment resulted in a prominent ED1 expression in transformed mesothelial cells. Blocking the internalization, ED1 expression could not be detected. GM-CSF receptor (both alpha and beta) was expressed in mesothelial cells in vitro (even if the GM-CSF was not present) and in vivo. Inflammation resulted in an increasing GM-CSF and GM-CSF-receptor level in the lysate of mesothelial cells.Mesothelial cells can differentiate into macrophage-like cells, and GM-CSF, produced by the mesothelial cells, has probably an autocrine regulatory role in this transition. Our results provide new data about the plasticity of mesothelial cell and support the idea that during inflammation macrophages can derive from non-hematopoietic sources as well.