肺泡巨噬细胞中巨噬细胞炎性蛋白-1α的分子克隆及转录后调控
Molecular cloning and posttranscriptional regulation of macrophage inflammatory protein-1 alpha in alveolar macrophages.
作者信息
Shi M M, Godleski J J, Paulauskis J D
机构信息
Department of Environmental Health, Harvard School of Public Health, Boston, MA 02115, USA.
出版信息
Biochem Biophys Res Commun. 1995 Jun 6;211(1):289-95. doi: 10.1006/bbrc.1995.1809.
Macrophage inflammatory protein-1 alpha (MIP-1 alpha) belongs to the "chemokine" superfamily of chemoattractant pro-inflammatory cytokines. MIP-1 alpha is chemotactic for monocytes and neutrophils and thus, plays an important role in initiation and control of inflammation. We have isolated and sequenced a cDNA clone encoding rat MIP-1 alpha. This 0.75 kb cDNA includes a single open reading frame of 92 amino acids. Expression of MIP-1 alpha mRNA was characterized in NR8383, a rat alveolar macrophage cell line (RAM). In resting RAM cells, MIP-1 alpha mRNA decayed rapidly, with a half life of less than 2 hours. Lipopolysaccharide (LPS) treatment of RAM cells resulted in a dose-dependent increase in MIP-1 alpha steady state mRNA expression. The induction of MIP-1 alpha mRNA by LPS was partially the result of mRNA stabilization, as half life increased to over 6 hours.
巨噬细胞炎性蛋白-1α（MIP-1α）属于趋化性促炎细胞因子的“趋化因子”超家族。MIP-1α对单核细胞和中性粒细胞具有趋化作用，因此在炎症的启动和控制中发挥重要作用。我们已经分离并测序了一个编码大鼠MIP-1α的cDNA克隆。这个0.75kb的cDNA包含一个由92个氨基酸组成的单一开放阅读框。在大鼠肺泡巨噬细胞系NR8383（RAM）中对MIP-1α mRNA的表达进行了表征。在静息的RAM细胞中，MIP-1α mRNA迅速降解，半衰期不到2小时。用脂多糖（LPS）处理RAM细胞导致MIP-1α稳态mRNA表达呈剂量依赖性增加。LPS对MIP-1α mRNA的诱导部分是mRNA稳定化的结果，因为半衰期增加到超过6小时。
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