Monk P N, Barker M D, Partridge L J
Department of Molecular Biology and Biotechnology, University of Sheffield, UK.
Biochim Biophys Acta. 1994 Apr 28;1221(3):323-9. doi: 10.1016/0167-4889(94)90257-7.
The CD11/CD18 family of leukocyte glycoproteins is essential in the process of adherence to endothelial and other cells that occurs during the acute inflammatory response. The cell surface expression of one member of this family, CD11b/CD18, or Mac-1, is increased on monocytes, neutrophils and other cell types by a number of agents, including chemotactic peptides and lipid mediators. The intracellular signalling mechanisms which control Mac-1 expression are not fully understood. In this report we have investigated the role of G proteins and extracellular Ca2+ in the stimulation of Mac-1 upregulation by the chemoattractant C5a in the human monocyte-like cell line, U937. Two signal transduction pathways are apparently involved and can be distinguished by their sensitivity to pertussis toxin, which inhibits activation of the Gi class of G proteins. The results indicate that a pertussis toxin-insensitive influx of extracellular Ca2+ may be one part of a network of signals leading to Mac-1 upregulation on U937 cells. This is in contrast to the stimulation of this process in neutrophils by chemotactic peptide, which is reported to be entirely dependent on pertussis toxin sensitive G proteins and independent of extracellular Ca2+.
白细胞糖蛋白CD11/CD18家族在急性炎症反应期间发生的与内皮细胞及其他细胞的黏附过程中至关重要。该家族一个成员CD11b/CD18（即Mac-1）在单核细胞、中性粒细胞及其他细胞类型上的细胞表面表达可被多种因子上调，包括趋化肽和脂质介质。控制Mac-1表达的细胞内信号传导机制尚未完全明确。在本报告中，我们研究了G蛋白和细胞外Ca2+在趋化因子C5a刺激人单核细胞样细胞系U937中Mac-1上调过程中的作用。显然涉及两条信号转导途径，且可通过它们对百日咳毒素的敏感性加以区分，百日咳毒素可抑制Gi类G蛋白的激活。结果表明，细胞外Ca2+不依赖百日咳毒素的内流可能是导致U937细胞上Mac-1上调的信号网络的一部分。这与趋化肽对中性粒细胞中该过程的刺激形成对比，据报道趋化肽对中性粒细胞的刺激完全依赖于对百日咳毒素敏感的G蛋白且不依赖细胞外Ca2+。
