Hepatic progenitor cell resistance to TGF-β1's proliferative and apoptotic effects

被引：16

作者：

Clark, JB ^{[1
]}

Rice, L ^{[1
]}

Sadiq, T ^{[1
]}

Brittain, E ^{[1
]}

Song, LJ ^{[1
]}

Wang, J ^{[1
]}

Gerber, DA ^{[1
]}

机构：

[1] Univ N Carolina, Dept Surg, Chapel Hill, NC 27599 USA

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2005年 / 329卷 / 01期

关键词：

liver; hepatocyte; cytokines; apoptosis; stem cells; progenitor cell; caspase; proliferation;

D O I：

10.1016/j.bbrc.2005.01.129

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The success of hepatocellular therapies using stem or progenitor cell populations is dependent upon multiple factors including the donor cell. microenviromnent, and etiology of the liver injury. The following experiments investigated the impact of TGF-beta1 on a previously described population of hepatic progenitor cells (HPC). The majority of the hepatic progenitor cells were resistant to endoeenously produced TGF-beta1's proapoptotic and anti-proliferative effects unlike more well-differentiated cellular populations (e.g., mature hepatocytes). Surprisingly, in vitro TGF- l supplementation significantly inhibited de novo hepatic progenitor cell colony formation possibly via an indirect mechanism(s). Therefore despite the HPC's direct resistance to supplemental TGF-beta1, this cytokine's inhibitory effect on colony formation could have a potential negative impact on the use of these cells as a therapy for patients with liver disease. (C) 2005 Elsevier Inc. All rialits reserved.

引用

页码：337 / 344

页数：8

共 43 条

[1] Activation of a caspase-dependent oxidative damage response mediates TGFβ1 in rat hepatocytes [J].