Eps8 是上皮生長因子接受器 (epidermal growth factor receptor ； EGFR) 的受質，它不僅會受到 EGFR 的磷酸化，也會受到其他酪胺酸激接受器 (例如：PDGFR、FGFR) 與non-receptor tyrosine kinases (例如：Src) 的磷酸化。Eps8 被認為參與了 EGF-induced 而且當其過量表達時，會促進腫瘤的形成。但 Eps8在haemopoietic cells 的功能，迄今仍不清楚。以巨噬細胞為研究材料時，我們發現 LPS可誘發 Eps8 表現量增加。另外在老鼠的 thioglycolate-elicited peritoneal macrophages (PEMs) 上也發現， 有類似的現象。初步發現利用不同的訊息傳遞抑制劑，NF-κB及 PI-3K可能參與LPS-mediated Eps8 induction。有趣的是當巨噬細胞表達 eps8 的 siRNA時，LPS-induced NO release及 migration 均受到抑制。因此我們認為 Eps8 在 LPS 活化巨噬細胞過程中，扮演一個重要角色。 Eps8 is a substrate for epidermal growth factor receptor (EGFR) and can be phosphorylated by receptor and nonreceptor tyrosine kinases . Eps8 is involved in EGF-induced mitogenesis and its overexpression can promote tumor formation. However to date, the function of Eps8 in haemopoietic cells is still unclear. In this study, we observed that LPS could increase Eps8 expression in RAW 264.7 cells and thioglycolate-elicited peritoneal macrophages (PEMs). And this LPS-mediated Eps8 induction could be inhibited by PDTC and LY294002, suggesting the participation of NF-κB and PI-3K in this signaling pathway. Intriguingly, LPS-induced NO release and migration was suppressed in macrophages expressing eps8 siRNA. And to our knowledge, this is the first report indicating that Eps8 is an important player in LPS-induced macrophages activation.
