ࡱ> Root EntryRoot Entry&,?ҦFileHeaderZDocInfoI&BodyText 0(?Ҧ0(?Ҧ HwpSummaryInformation.@-PrvImage PrvTextDocOptions p+?Ҧ&,?ҦScripts &,?Ҧ&,?ҦJScriptVersion a DefaultJScript^_LinkDocb  !"#$%&'()*+,-./0123456789:;<=>?ABCDEFGHJKLMNOPQRSTUVWXY[\]_`cdefghijlmnopqrstuvwxyz{|}~Strategies for Overcoming Pulmonary Fibrosis Yun-Sil Lee Graduate School of Pharmaceutical Sciences, Ewha Womans University We have previously developed a mouse model simulating clinical SBRT and have used the model to validate the induction of lung fibrosis by high-dose ionizing radiation (IR). The regimen was similar to that used for human therapy reflecting the understanding of the clinically related IR-mediated normal cell damage like fibrosis. To identify molecular signatures for lung fibrosis, we further examined the fibrosis process at 4 weeks from irradiated region from mouse lung tissues after IR and identified targets for lung fibrosis. Moreover, we also identified another molecular targets in lung fibrosis development. Hsp27 expression was increased during IR-induced lung fibrosis, and functional inhibition of Hsp27 using a small molecule ameliorated lung fibrosis. While investigating mechanisms of Hsp27 in the development of lung fibrosis, we found that IkB-NFkB signaling activationGIF89aɻxxxkkk]]]PPPCCC555((( d`LH00`Hذ̘`H0|pdXL@`0H `H0`dHL`H0xp`XH@0d LȰ``HH00dLؘȀ`H0xp`XH@d0L `H0d`LH`H0|pdXL@0`$H`dHL00`HذȘdL0xp`XH@0` HdH0ȳ``HHdL0xp`XH@`0H Ը̰ĠऀؘpȈXxHp@h@d8`8X0xT0pH dxddxd`d`p`|``x`p``x`!, H*\ȰÇ#JHŋ3jȱǏ CIɓ(S\ɲ˗0cʜI͛8sɳϟ@ JѣH*]ʴӧPJJիXjʵׯ`ÊKٳv@jU6nܷkڅv`]zEo޼\a ]X.aw3fnϠCM鱋'> S2\Ȭc˞M۸Vlf߅z3E8c.Wt[w>=wG:wӫ_Ͼ˟Or .nw~r_aEoU6q!HsycQgF"p%!ԟ__.ޗͤ]sǠdaIHYN8L7}$(`Th݌,!b"QΘM@7X]t'c-]2yUۗȕdfr#b9$edvu6f 7`=Q *hmE8)g馔RX)&z*9ic.i;^ju9xNjfQ:RʙUc֔]bof>vZj W+ E8lu"EY jflJ ۺ\r $?a+&+12cc2a>h1/w%#|GGw)lbb[ՅʪX+`V?|yBknC{F}#5R8[5ࡷ_׽ް:ywGV$ tMj*,[yۤ>%Y=p׆֜"o&D^c{'׽vxSl͎_~:TB }.K8s)3U|.Ⱥ냏gUMYZpbΙz+vn>{Y"<9f֮eNgz;)NTl_愩-I^XJP 5DӦkD2%k:rQ8!ĵb/bHy( IBL"F:򑐌$'IJZ̤&7Nz (GIRL*WV򕰌,gIZ̥.w^ 0IbL2f:Ќ4IjZ3=;`a``a`0x,8D X   %Identificationofnoveltargetsandtreatuser2018D 8 25| є| $ 1:22:30yslee-8, 5, 8, 1677 WIN32LEWindows_Unknown_Version@=+<@0(?Ҧ@WKkQޓw4qL-`vZbjE]h-EJMt(R"BYHE L3m2 "3d;9ih=X8ki)٨Yq |}3!͑"B#%c ˈ Vqi[i 5O*;L#hJKɄa ^mcZU:<؀_hye5+[_(^Q"%k~L7gXϰEkqa Z%5#Tvp۫kd-;/PϠT*A[}Xo/xmޚo}Nj[ӛWL^ܞ" 53<У.@' )jSo'~jp2:EՂ |(<6噿 B]؄ 6i]I,~wxV,w|@C=>_풿KPǿ?TPI;fPA)X-T:kEZ6E(pq(% FZowqr<bf֨04Hљ#`XRB["K62B!hg>n[u?fܜS TX IՔ!660)4mK/U.aJ-HnI@$U #bt7b/#Ͼ!rgI#MI9w'[H9=V1&IcX[Qk\ǷݩqaTKL%֜a/:W/'#YeI%k,Yg G*d//HWP Document Fileu@DO 6C,H,#GB!k0~ 6*7=M*Z:ҙ#?*?ӿT@Y~X+mj3'm[v|:j)%C$Mϼ5#cd߈ion was increased during IR-induced lung fibrosis, and functional inhibition of Hsp27 using a small molecule ameliorated lung fibrosis. While investigating mechanisms of Hsp27 in the development of lung fibrosis, we found that IkB-NFkB signaling activationWoE~koh$TU-R"pU !I mcMũ8 ġ' 7ȍC$$#ofqƆ\M_<_d *9/zexI oxi{ϝaoyQ, 5 d K|xvY4/nMd` fc,065¬N}fu{ ېOxO :v5cǯ,NH_H Ε=4=O^i˅}(oZ*: 6qӐP 1Wl|:9-&Msi1@71KX.#0sJX/C3xX5;͖W$䰮vM4}S5~àB|LRN-mU4ʳ:sbkBoJ'S*.9Q;1)":(~u[ɊZ,+)>-n=?iM!;E'1:nVe跨Uts"6RR9-/uO3ź7hQ12KO?-2:*8Yx#+3㱁37g)6Ϟvh3ύ4c‰Z.&7'4\gco}W>w[Ծ~{g[sO}MuǼ7|ƶ- 6[u[&֏t|u_:/UN:Ov:BgЭ:w!y Gn?!;:7 ?u _ܭ/W