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Special (비정기세미나)
2004.04.23 19:10

제8회 정기세미나

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1. 연사 및 연제
① 송동근 교수 : 한림의대
(Therapeutic effects of lysophosphatidylcholine in experimental sepsis)
② 김성진 박사 : NIH
(Cross-talk of TGF-β signaling with other signaling pathways)
2. 일시 : 2004년 4월 27일 (화) 오후 4:00
3. 장소 : 의과학센터 원격강의실

※ 문의 : 고규영 교수님 (2638), 정안식 (2625)

※ ①'s Abstract
Sepsis represents a major cause of death in intensive care units. Here we show that administration of lysophosphatidylcholine (LPC), an endogenous lysophospholipid, protected mice against lethality after cecal ligation and puncture (CLP) or intraperitoneal injection of Escherichia coli. In vivo treatment with LPC markedly enhanced clearance of intraperitoneal bacteria and blocked CLP-induced deactivation of neutrophils. In vitro, LPC increased bactericidal activity of neutrophils, but not macrophages, by enhancing H(2)O(2) production in neutrophils that ingested E. coli. Incubation with an antibody to the LPC receptor, G2A, inhibited LPC-induced protection from CLP lethality and inhibited the effects of LPC in neutrophils. G2A-specific antibody also blocked the inhibitory effects of LPC on certain actions of lipopolysaccharides (LPS), including lethality and the release of tumor necrosis factor-alpha (TNF-alpha) from neutrophils. These results suggest that LPC can effectively prevent and treat sepsis and microbial infections.

※ ②'s Abstract
Transforming growth factor-bs (TGF-bs) regulate pivotal cellular processes such as proliferation, differentiation and apoptosis. Following receptor-induced activation, heteromeric Smad complexes translocate into the nucleus, where they act as transcription factors. Many different cell surface receptors and intracellular proteins influence the TGF-b pathway, demonstrating that signal transduction does not proceed in a linear fashion but rather through a complex network of cascades that mutually influence each other. The intracellular signaling events mediating the effects of TGF-b are multiple, involving extensive cross-talk between Smad-dependent and MAP-kinase-dependent pathways. In addition, the Smads regulate transcription through functional cooperativity and physical interactions with other transcription factors. We are only beginning to understand the importance of the balance between these cascades as a determinant of the response to TGF-b, and have yet to determine the roles that alterations in these pathways might play in cancer. It is logical to predict that any functional impairment in the TGF-b pathway may predispose to cancer. I will discuss the molecular mechanisms of inactivation of TGF-b signaling during carcinogenesis.

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