Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 전대원 | - |
dc.date.accessioned | 2019-12-03T04:19:17Z | - |
dc.date.available | 2019-12-03T04:19:17Z | - |
dc.date.issued | 2017-12 | - |
dc.identifier.citation | ONCOTARGET, v. 8, no. 58, page. 97965-97976 | en_US |
dc.identifier.issn | 1949-2553 | - |
dc.identifier.uri | http://www.oncotarget.com/index.php?journal=oncotarget&page=article&op=view&path[]=18967&path[]=60800 | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/116757 | - |
dc.description.abstract | Protective effects of granulocyte colony stimulating factor (G-CSF) in acute liver injury via marrow cell mobilization have been reported in several studies. But exact mode of action and optimal protocol of G-CSF has been still doubt in chronic disease. Here we investigated mode of action and optimization of G-CSF as a treatment for nonalcoholic fatty liver disease (NAFLD). Various doses of conventional G-CSF (30 mu g/kg once weekly, once daily for 5 days, twice weekly) and long acting G-CSF (30 mu g/kg once a month) were evaluated in two kinds of NAFLD animal models to optimize the G-CSF protocol. G-CSF receptor expression highest increased in NAFLD model among various liver diseases compare to control (NAFLD: 14.7 times, alcohol hepatitis: 7.1 times, cirrhosis: 2.4 times, and ischemia reperfusion: 6.8 times). G-CSF treatment reduced intrahepatic fat accumulation, and inflammation in two kinds of NAFLD animal models. G-CSF increased PI3K/Akt expression in hepatocyte as well as decreased apoptotic drive (increased Bcl-2 expression and decreased Bax expression) in animal model. Five day consecutive G-CSF treatment and once a month long acting G-CSF increased marrow derived stem cell marker in peripheral blood. But twice a week conventional G-CSF treatment did not increased CD34+ cell in peripheral blood and liver neither. Not only high dose G-CSF (once daily for 5 days) but also hepatotropic dose G-CSF (twice a week) significantly reduced hepatocyte apoptosis via PI3K and Akt pathway activation without marrow cell mobilization in NAFLD animal model. | en_US |
dc.description.sponsorship | This work was supported by a grant from National Research Foundation of Korea 2011-0007127. | en_US |
dc.language.iso | en_US | en_US |
dc.publisher | IMPACT JOURNALS LLC | en_US |
dc.subject | non-alcoholic fatty liver | en_US |
dc.subject | granulocyte colony stimulating factor | en_US |
dc.subject | apoptosis | en_US |
dc.title | Granulocyte colony stimulating factor treatment in non-alcoholic fatty liver disease: Beyond marrow cell mobilization | en_US |
dc.type | Article | en_US |
dc.relation.no | 58 | - |
dc.relation.volume | 8 | - |
dc.identifier.doi | 10.18632/oncotarget.18967 | - |
dc.relation.page | 97965-97976 | - |
dc.relation.journal | ONCOTARGET | - |
dc.contributor.googleauthor | Nam, Ho Hyun | - |
dc.contributor.googleauthor | Jun, Dae Won | - |
dc.contributor.googleauthor | Jang, Kiseok | - |
dc.contributor.googleauthor | Saeed, Waqar Khalid | - |
dc.contributor.googleauthor | Lee, Jai Sun | - |
dc.contributor.googleauthor | Kang, Hyeon Tae | - |
dc.contributor.googleauthor | Chae, Yeon Ji | - |
dc.relation.code | 2017009424 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | noshin | - |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.