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11/12疾患生命工学センター宮崎徹博士

日時:11月12日(金)午後5時-6時
場所:医学部図書館大学院ゼミ室(地下一階)
演者:宮崎徹博士(東京大学医学部疾患生命工学センター教授。現、
Associate Professor&s_comma; Center for Immunology University of Texas
Southwestern Medical Center at Dallas)
演題:マクロファージ由来アポトーシス阻害因子と動脈硬化
A role for the apoptosis inhibitory factor AIM in atherosclerosis development
Macrophages are the most prominent cell type in atherosclerotic
lesions. The apoptosis inhibitor&s_comma; AIM (/Spア/Api6)&s_comma; is induced in
macrophages by oxidative lipids via activation of the nuclear Liver X
receptor/Retinoid X receptor (LXR/RXR) complex. Consistent with
this induction&s_comma; AIM is highly expressed in lipid-laden macrophages
within the atherosclerotic lesions. AIM-null (AIM-/-) macrophages
are more susceptible to oxLDL-induced apoptosis&s_comma; and hence&s_comma; the
lesions that developed in AIM-/-LDL-receptor (LDLR)-/- double
knockout mice after a high-fat diet contain a markedly higher number
of apoptotic macrophages than those in AIM+/+LDLR-/- controls.
Interestingly&s_comma; the lesions in double knockout mice are dramatically
smaller in size during the early and developing disease stages when
compared to AIM+/+LDLR-/- littermate mice. Thus&s_comma; we conclude AIM
production is an important mechanism by which the resistance of
macrophages to apoptosis within the atherosclerotic lesions is
increased&s_comma; and this response in turn supports the development of
atherosclerosis. These findings imply that AIM suppression may be
useful in the prevention of atherosclerosis development. In
addition to this physiological involvement of AIM in
atherosclerogenesis&s_comma; we will discuss about a clue for the molecular
mechanism of how AIM supports the cell survival.
主催:東大医学部細胞情報  清水孝雄 (内線23448)
来聴歓迎します
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東京大学大学院医学系研究科 分子細胞生物学専攻
生化学分子生物学(細胞情報研究部門)
教授 清 水 孝 雄
〒113-0033 東京都文京区本郷7-3-1
電話 03-5802-2925(研究室)、03-3813-8964(教授室直通)
ファックス 03-3813-8732
e-mail tshimizu@m.u-tokyo.ac.jp
URL http://biochem2.umin.jp/index_j.html
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