Abnormal expression of vesicular transport proteins in pulmonary arterial hypertension in monocrotaline-treated rats  

作　　者：Hongliang Zhang Qin Luo Zhihong Liu YongWang Zhihui Zhao 

机构地区：[1]Center for Pulmonary Vascular Diseases, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, NationalCenter for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College,Beijing 100037, China

出　　处：《Acta Biochimica et Biophysica Sinica》2015年第3期156-163,共8页生物化学与生物物理学报（英文版）

摘　　要：Intracellular vesicular transport is shown to be dysfunctional in pulmonary arterial hypertension （PAH）. However, the expression of intracellular vesicular transport proteins in PAH remains unclear. To elucidate the possible role of these proteins in the development of PAH, the changes in the expres- sions of N-ethyl-maleimide-sensitive factor （NSF）, a-soluble NSF attachment protein （a-SNAP）, synaptosome-associated membrane protein 23 （SNAP23）, type 2 bone morphogenetic receptor （BMPR2）, caveolin-1 （cav-1）, and endothelial nitric oxide synthase （eNOS） were examined in lung tis- sues of monocrotaline （MCT）-treated rats by real-time polymerase chain reaction and western blot analysis. In addition, caspase-3, also examined by western blot analysis, was used as an indicator of apoptosis. Our data showed that during the development of PAH, the expressions of NSF, a-SNAP, and SNAP23 were significantly increased before pulmonary arterial pressure started to increase and then significantly decreased after PAH was established. The expressions of BMPR2 and eNOS were similar to those of NSF, a-SNAP, and SNAP23; however, the expression of cav-1 was down-regulated after MCT treatment. Caspase-3 expression was increased after exposure to MCT. In conclusion, the expressions of NSF, a-SNAP, and SNPA23 changed greatly during the onset of PAH, which was ac- companied by abnormal expressions of BMPR2, cav-1, and eNOS, as well as an increase in apop- tosis. Thus, changes in NSF, a-SNAP, and SNAP23 expressions appear to be mechanistically associated with the development of PAH in MCT-treated rats.Intracellular vesicular transport is shown to be dysfunctional in pulmonary arterial hypertension （PAH）. However, the expression of intracellular vesicular transport proteins in PAH remains unclear. To elucidate the possible role of these proteins in the development of PAH, the changes in the expres- sions of N-ethyl-maleimide-sensitive factor （NSF）, a-soluble NSF attachment protein （a-SNAP）, synaptosome-associated membrane protein 23 （SNAP23）, type 2 bone morphogenetic receptor （BMPR2）, caveolin-1 （cav-1）, and endothelial nitric oxide synthase （eNOS） were examined in lung tis- sues of monocrotaline （MCT）-treated rats by real-time polymerase chain reaction and western blot analysis. In addition, caspase-3, also examined by western blot analysis, was used as an indicator of apoptosis. Our data showed that during the development of PAH, the expressions of NSF, a-SNAP, and SNAP23 were significantly increased before pulmonary arterial pressure started to increase and then significantly decreased after PAH was established. The expressions of BMPR2 and eNOS were similar to those of NSF, a-SNAP, and SNAP23; however, the expression of cav-1 was down-regulated after MCT treatment. Caspase-3 expression was increased after exposure to MCT. In conclusion, the expressions of NSF, a-SNAP, and SNPA23 changed greatly during the onset of PAH, which was ac- companied by abnormal expressions of BMPR2, cav-1, and eNOS, as well as an increase in apop- tosis. Thus, changes in NSF, a-SNAP, and SNAP23 expressions appear to be mechanistically associated with the development of PAH in MCT-treated rats.

关 键 词：pulmonary arterial hypertension MONOCROTALINE vesicular transport 

分 类 号：Q954.434[生物学—动物学] S858.31[农业科学—临床兽医学]