Walker D G
Kinsmen Laboratory of Neurological Research, Department of Psychiatry, University of British Columbia, Vancouver, Canada.
Mol Chem Neuropathol. 1998 Jun-Aug;34(2-3):197-218. doi: 10.1007/BF02815080.
The regulation of C1q expression was examined in the human monocytic cell line THP-1. Since these cells can be differentiated into cells with macrophage properties and induced to express C1q, they were used as models for mature human monocyte/macrophages and indirectly microglia. Interferon-gamma (IFN-gamma) and the anti-inflammatory steroid agents dexamethasone and prednisone were powerful stimulators of C1q production, alone or in combination. Interleukin-6 (IL-6) and lipopolysaccharide (LPS) also had significant stimulatory activity. Phorbol myristate acetate, a protein kinase C activator, reduced C1q expression. Four additional classes of pharmacological agents were tested for their effect on C1q secretion. Tacrine, but not indomethacin, cimetidine, or propentofylline, showed activity in inhibiting C1q secretion by IFN-gamma treated THP-1-derived macrophages.
在人单核细胞系THP-1中研究了C1q表达的调控。由于这些细胞可分化为具有巨噬细胞特性的细胞并被诱导表达C1q，因此它们被用作成熟人单核细胞/巨噬细胞以及间接小胶质细胞的模型。干扰素-γ（IFN-γ）以及抗炎类固醇药物地塞米松和泼尼松，单独或联合使用时都是C1q产生的强大刺激剂。白细胞介素-6（IL-6）和脂多糖（LPS）也具有显著的刺激活性。蛋白激酶C激活剂佛波酯肉豆蔻酸酯降低了C1q的表达。测试了另外四类药物对C1q分泌的影响。他克林，而非吲哚美辛、西咪替丁或丙戊茶碱，在抑制IFN-γ处理的THP-1衍生巨噬细胞分泌C1q方面表现出活性。
