ADP-核糖基化在活化单核细胞/巨噬细胞中的作用。

Role of ADP-ribosylation in activated monocytes/macrophages.

作者信息

Hauschildt S, Scheipers P, Bessler W, Schwarz K, Ullmer A, Flad H D, Heine H

机构信息

Institut für Zoologie Immunobiologie, Universität Leipzig.

出版信息

Adv Exp Med Biol. 1997;419:249-52. doi: 10.1007/978-1-4419-8632-0_31.

DOI:10.1007/978-1-4419-8632-0_31

PMID:9193661

Abstract

Stimulating monocytes/macrophages with bacterial lipopolysaccharide (LPS) results in TNF-alpha, IL-1, IL-6 and nitrite (NO2-) formation. Inhibitors of poly(ADP-ribose)polymerase inhibit release of these mediators by preventing mRNA expression indicating that ADP-ribosylation plays a crucial role in the synthesis of these mediators. Furthermore we present evidence that ADP-ribosylation is involved in modifying cellular proteins. In murine macrophages a 33 kDa cytosolic protein could be identified that in response to LPS changed its state of ADP-ribosylation, and in human monocytes we showed that the inhibitor nicotinamide prevents LPS induced phosphorylation of two cytosolic proteins of 36 kDa and 38 kDa (p36/38) LPS. Taken together these data indicate that protein modification by ADP-ribosylation may control cellular processes involved in distinct steps of monocyte/macrophage activation.

摘要

用细菌脂多糖（LPS）刺激单核细胞/巨噬细胞会导致肿瘤坏死因子-α（TNF-α）、白细胞介素-1（IL-1）、白细胞介素-6（IL-6）和亚硝酸盐（NO2-）的形成。聚（ADP-核糖）聚合酶抑制剂通过阻止mRNA表达来抑制这些介质的释放，这表明ADP-核糖基化在这些介质的合成中起关键作用。此外，我们提供证据表明ADP-核糖基化参与修饰细胞蛋白。在小鼠巨噬细胞中，可以鉴定出一种33 kDa的胞质蛋白，其在对LPS的反应中改变了其ADP-核糖基化状态，并且在人类单核细胞中，我们表明抑制剂烟酰胺可防止LPS诱导的两种36 kDa和38 kDa胞质蛋白（p36/38）LPS的磷酸化。综上所述，这些数据表明ADP-核糖基化对蛋白质的修饰可能控制单核细胞/巨噬细胞激活不同步骤中涉及的细胞过程。