The role of tissue factor and autophagy in pulmonary vascular remodeling in a rat model for chronic thromboembolic pulmonary hypertension.
The role of tissue factor and autophagy in pulmonary vascular remodeling in a rat model for chronic thromboembolic pulmonary hypertension.
复制标题
组织因子和自噬在慢性血栓栓塞性肺动脉高压大鼠模型肺血管重塑中的作用
DOI：
10.1186/s12931-016-0383-y
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发表时间：
2016-05-27
影响因子：
5.8
通讯作者：
Liu K
中科院分区：
文献类型：
--
作者：
Deng C;Wu D;Yang M;Chen Y;Ding H;Zhong Z;Lian N;Zhang Q;Wu S;Liu K
很少有报告研究组织因子(TF)和自噬在慢性肺血栓栓塞性高血压(CTEPH)动物模型中的表达。目的：探讨组织因子(TF)、自噬及其相互作用在慢性血栓栓塞性肺动脉高压(CTEPH)发病机制中的作用。大鼠左颈静脉注射内源性纤溶抑制剂氨甲环酸(TXA)，反复注入自体血栓。检测平均肺动脉压(MPAP)、组织病理学及组织因子、Beclin-1和微管相关蛋白1轻链(LC3)的表达水平。实验组平均动脉压和管壁面积/总面积比(Wa/Ta)明显升高(P< <； <0.05)。实验组TFm RNA和蛋白表达水平显著升高(P <； 0.05)。实验组BECLIN-1和LC3BmRNA和蛋白表达水平低于对照组(P <； 0.05)。MPAP与Wa/TA比值呈正相关(r = 0.955，P <； 0.0 5)。BECLIN-1和LC3B蛋白表达与WA/TA比值呈负相关(r = -0.963，P <； 0.05，r = -0.965，P <； 0.05)。Tf蛋白表达与Beclin-1、LC3B蛋白表达呈负相关(r = -0.995，P<；0.05，r = -0972，P <； 0.05)。用TXA反复向大鼠肺动脉内注入自体血凝块，可建立大鼠CTEPH模型。Tf和自噬可能在CTEPH的发病机制中起关键作用，尤其是在血管重塑过程中。
Few reports have examined tissue factor (TF) and autophagy expression in chronic pulmonary thromboembolic hypertension (CTEPH) animal models. Objectives: To investigate the role of tissue factor (TF), autophagy and their interactions during chronic thromboembolic pulmonary hypertension (CTEPH) pathogenesis in a rat model. Autologous blood clots were repeatedly injected into the left jugular vein of rats with injecting endogenous fibrinolysis inhibitor tranexamic acid (TXA). Mean pulmonary arterial pressure (mPAP), histopathology and TF, Beclin-1 and microtubule-associated protein 1 light chain (LC3) expression levels were detected. The mPAP and vessel wall area/total area (WA/TA) ratio in the experiment group increased significantly (P < 0.05). TF mRNA and protein expression levels in the experiment group increased significantly (P < 0.05). Beclin-1 and LC3B mRNA and protein expression levels were lower in the experiment group (P < 0.05). The mPAP had a positive correlation with WA/TA ratio (r = 0.955, P < 0.05). Beclin-1 and LC3B protein expression had a negative correlation with the WA/TA ratio (r = -0.963, P < 0.05, r = -0.965, P < 0.05, respectively). TF protein expression had a negative correlation with both Beclin-1 and LC3B protein expression (r = -0.995, P <0.05, r = -0972, P < 0.05, respectively). A rat model of CTEPH can be established by repeatedly introducing autologous blood clots into the pulmonary artery with injecting TXA. TF and autophagy may play a key role during CTEPH pathogenesis, especially in vascular remodeling.