Schrader J W, Moyer C, Ziltener H J, Reinisch C L
Biomedical Research Centre, University of Brittish Columbia, Vancouver, Canada.
J Immunol. 1991 Jun 1;146(11):3799-808.
Vascular smooth muscle cells were cultured from the mesenteric arteries of MRL lpr/lpr, MRL +/+, CBA/J, or C3H/HeJ mice and evaluated for their ability to synthesize a range of cytokines. Vascular smooth muscle cells of MRL +/+, MRL lpr/lpr, and CBA/J origin released biologically significant amounts of CSF-1 and IL-6 and relatively low but detectable amounts of granulocyte macrophage-CSF (GM-CSF) but not IL-2, IL-3, or IL-4. Vascular smooth muscle cells of C3H/HeJ origin produced lower amounts of CSF-1 and IL-6, and GM-CSF was barely detectable. Production of these cytokines did not require the exogenous growth factors present in FCS and occurred, although at lower levels, in serum-free medium supplemented with insulin, transferrin, and albumin. Cloned lines of MRL +/+ vascular smooth muscle cells, with electron microscopic and immunochemical properties of vascular smooth muscle cells, produced CSF-1, IL-6, and GM-CSF, establishing that vascular smooth muscle cells were a direct source of CSF-1, IL-6, and GM-CSF. These observations highlight the need for experiments to directly address the question of whether vascular smooth muscle cells constitutively produce these cytokines under physiologic conditions in vivo and suggest that vascular smooth muscle cells may participate actively in inflammation by releasing cytokines that are active on lympho-hemopoietic and other cells.
从MRL lpr/lpr、MRL +/+、CBA/J或C3H/HeJ小鼠的肠系膜动脉中培养血管平滑肌细胞,并评估它们合成一系列细胞因子的能力。源自MRL +/+、MRL lpr/lpr和CBA/J的血管平滑肌细胞释放出具有生物学意义的大量集落刺激因子-1(CSF-1)和白细胞介素-6(IL-6),以及相对较低但可检测到的粒细胞巨噬细胞集落刺激因子(GM-CSF),但不释放IL-2、IL-3或IL-4。源自C3H/HeJ的血管平滑肌细胞产生的CSF-1和IL-6量较低,GM-CSF几乎检测不到。这些细胞因子的产生不需要胎牛血清(FCS)中存在的外源性生长因子,并且在补充有胰岛素、转铁蛋白和白蛋白的无血清培养基中也会产生,尽管水平较低。具有血管平滑肌细胞电子显微镜和免疫化学特性的MRL +/+血管平滑肌细胞克隆系产生CSF-1、IL-6和GM-CSF,证实血管平滑肌细胞是CSF-1、IL-6和GM-CSF的直接来源。这些观察结果突出了进行实验以直接解决血管平滑肌细胞在体内生理条件下是否组成性产生这些细胞因子这一问题的必要性,并表明血管平滑肌细胞可能通过释放对淋巴细胞造血和其他细胞有活性的细胞因子而积极参与炎症反应。