Dysregulation of PARP1 is involved in development of Barrett's esophagus.
Dysregulation of PARP1 is involved in development of Barrett's esophagus.
复制标题
PARP1 失调与巴雷特食管的发育有关
DOI：
10.3748/wjg.v24.i9.982
复制
发表时间：
2018-03-07
影响因子：
4.3
通讯作者：
Li F
中科院分区：
文献类型：
--
作者：
Zhang C;Ma T;Luo T;Li A;Gao X;Wang ZG;Li F
To investigate the potential role of poly(ADP-ribose) polymerase 1 (PARP1) in the development of Barrett’s esophagus (BE). A BE mouse model was established to examine the esophageal morphological changes and molecular changes. Microarray analysis was performed to compare the gene expression profiles between BE patients and healthy controls. qPCR was used to examine the PARP1 expression in cell lines after treatment with H2O2 and bile acids (pH 4). Immunofluorescence staining, comet assay, and annexin V staining were used to evaluate the impact of PARP1 activity on cell survival and DNA damage response after oxidative stress. The gene expression profile in normal and BE esophageal epithelial cells showed that PARP1, the major poly(ADP-ribose) polymerase, was overexpressed in BE. In the mouse model of BE, positive staining for NF-κB, γH2AX, and poly(ADP-ribose) (PAR) was observed. H2O2 and bile acids (pH 4) increased the PARP1 mRNA expression level in normal esophageal epithelial cells. Using shRNA-PARP1 to suppress PARP1 activity decreased the cell viability after treatment with H2O2 and bile acids (pH 4), and increased the oxidative damage as demonstrated by an increase in the levels of H2O2, intracellular reactive oxygen species (ROS), oxidative DNA damage, double-strand breaks, and apoptosis (P < 0.01). The dysfunction of PARP1 in esophageal epithelial cells increases the levels of ROS and oxidative DNA damage, which could be common risk factors for BE and esophageal adenocarcinoma.
登录
查看更多内容
DOI：
10.1158/1078-0432.ccr-13-0601
发表时间：
2013-08-01
期刊：
Clinical cancer research : an official journal of the American Association for Cancer Research
影响因子：
--
作者：
Streppel MM;Pai S;Campbell NR;Hu C;Yabuuchi S;Canto MI;Wang JS;Montgomery EA;Maitra A
通讯作者：
Maitra A
影响因子：
6.5
作者：
Brunyanszki, Attila;Hegedus, Csaba;Bai, Peter
通讯作者：
Bai, Peter
影响因子：
3.7
作者：
Hassa, PO;Hottiger, MO
通讯作者：
Hottiger, MO
影响因子：
2.3
作者：
Farinati, Fabio;Piciocchi, Marika;Cardin, Romilda
通讯作者：
Cardin, Romilda
影响因子：
29.4
作者：
Vaezi, MF;Richter, JE
通讯作者：
Richter, JE