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開催日時: 平成19 年 10月10日(水)1

開催場所:  東京大学医科学研究所アムジェンホール大会議室

講師氏名:  Dr. Kenneth Kun-Yu Wu&s_comma; M.D.&s_comma; Ph.D.
Distinguished investigator and president
Acting director&s_comma;
National Health Research Institutes&s_comma; Zhu-nan&s_comma; Miaoli&s_comma; Taiwan

演  題: Cyclooxygenase-2 (COX-2) derived prostaglandins in
embryo and embryonic stem cell (ESC) development and survival

概  要: 

COX-2 occupies a pivotal position in synthesis of biologically active
prostaglandins. Overexpression of COX-2 has been causally linked to
inflammatory disorders&s_comma;
cancer&s_comma; atherosclerosis and neurodegenerative disorders. On the other
hand&s_comma; COX-2 derived PGS such as PGI2 protects cells from apoptosis.
Our recent work shows that PGI2 production by endothelial cells (EC)
via COX-2 protects ECs from apoptosis via PPARα-mediated
14-3-3ε upregulation. COX-2 derived PGI2 plays a crucial role
in murine embryo development in vitro. The action of PGI2 is also
mediated via PPARα as two-cell embryos derived from
PPARα knockout mice exhibit a retarded development into mature
blastocytes and has impaired implantation. PGI2-type membrane
receptor&s_comma; IP is less important. However&s_comma; two-cell embryos from IP-/-
mice develop in a slower rate than two-cell embryos from wild-type
mice. COX-2 plays a crucial role in protecting mouse ESC from
apoptosis. However&s_comma; mESCs do not have detectable PGI synthase and do
not produce PGI2. In contrast&s_comma; they express PGE synthases and produce
abundant PGE2. Our recent work suggests that COX-2 derived PGE2
protects ESC from apoptosis via EP2 receptor-mediated Akt activation.
Work is in progress to determine whether PGE2 and PGD2 are involved
in regulating ESC renewal&s_comma; proliferation and differentiation.

世話人:清木 元治、○渡辺 すみ子