Expression of tissue factor and forkhead box transcription factor O-1 in a rat model for chronic thromboembolic pulmonary hypertension
Expression of tissue factor and forkhead box transcription factor O-1 in a rat model for chronic thromboembolic pulmonary hypertension
复制标题
组织因子和叉头盒转录因子O-1在慢性血栓栓塞性肺动脉高压大鼠模型中的表达
DOI:
10.1007/s11239-016-1413-9
复制
发表时间:
2016-11-01
影响因子:
4
通讯作者:
Wu, Shuang
中科院分区:
文献类型:
--
作者:
Deng, Chaosheng;Wu, Dawen;Wu, Shuang
Few reports have examined tissue factor (TF) and forkhead box transcription factor O-1 (FoxO1) expression in chronic thromboembolic pulmonary hypertension (CTEPH) animal models. To investigate the role of TF and FoxO1 and their interactions during CTEPH pathogenesis in a rat model. Autologous blood clots were repeatedly injected into the pulmonary arteries through right jugular vein to induce a rat model of CTEPH. Hemodynamic parameters, histopathology, and TF and FoxO1expression levels were detected. The mean pulmonary arterial pressure (mPAP), pulmonary vascular resistance and vessel wall area/total area (WA/TA) ratio in the experiment group increased significantly than sham group (P< 0.05). The cardiac output in the 1-, 2-, and 4-week groups decreased significantly (P< 0.05) when compared to sham group. TF mRNA expression levels in the experiment group increased significantly than sham group (P< 0.05). FoxO1 mRNA and protein expression levels were lower in the experiment group than sham group (P< 0.05). The mPAP had a positive correlation with WA/TA ratio (r= 0.45,P= 0.01). TF mRNA expression had a positive correlation with WA/TA ratio (r= 0.374,P= 0.035) and a positive correlation with mPAP (r= 0.48,P= 0.005). FoxO1 mRNA expression had a negative correlation trend with the WA/TA ratio (r= −0.297,P= 0.099) and a negative correlation trend with mPAP (r= −0.34,P= 0.057). TF mRNA expression had a negative correlation with FoxO1 mRNA expression (r= −0.62,P< 0.001). A rat model of CTEPH can be successfully established by the injection of autologous blood clots into the pulmonary artery. TF and FoxO1 may play a key role in vascular remodeling during CTEPH pathogenesis.