PDF(Pubmed)
Abstract：
OBJECTIVE: Pulmonary hypertension (PH) is a pathological process mainly characterized by the progressive increase in pulmonary vascular resistance. The degradation of pulmonary artery smooth muscle cells (PASMCs) from contractile/differentiated phenotype to synthetic/dedifferentiated phenotype is a key factor for hypoxic pulmonary hypertension.
METHODS: In this study, qPCR was performed to evaluate the gene expression of mRNAs. Western blot, immunofluorescence and RNA pull down were used to detect gene expression levels.
RESULTS: We found that the gene expression of polypyrimidine tract-binding protein1 (PTBP1) was increased significantly in a time-dependent manner in rats PA tissues and PASMCs after hypoxia. PTBP1 knockdown can inhibit the phenotypic transition of PASMCs. PTBP1 inhibits the phenotypic transition of PASMCs. In addition, PTBP1 inhibits the integrin-linked kinase (ILK) expression under hypoxic conditions, thereby down-regulating the expression of downstream proteins. It inhibits the phenotypic transition of PASMCs and alleviates pulmonary hypertension.
CONCLUSIONS: In conclusion, PTBP1/ILK axis promotes the development of PH via inducing phenotypic transition of PASMCs. This may provide a novel therapy for PH.
METHODS: In this study, qPCR was performed to evaluate the gene expression of mRNAs. Western blot, immunofluorescence and RNA pull down were used to detect gene expression levels.
RESULTS: We found that the gene expression of polypyrimidine tract-binding protein1 (PTBP1) was increased significantly in a time-dependent manner in rats PA tissues and PASMCs after hypoxia. PTBP1 knockdown can inhibit the phenotypic transition of PASMCs. PTBP1 inhibits the phenotypic transition of PASMCs. In addition, PTBP1 inhibits the integrin-linked kinase (ILK) expression under hypoxic conditions, thereby down-regulating the expression of downstream proteins. It inhibits the phenotypic transition of PASMCs and alleviates pulmonary hypertension.
CONCLUSIONS: In conclusion, PTBP1/ILK axis promotes the development of PH via inducing phenotypic transition of PASMCs. This may provide a novel therapy for PH.
摘要：
目的：肺动脉高压（PH）是以肺血管阻力进行性增加为主要特征的病理过程。肺动脉平滑肌细胞（PASMC）从收缩/分化表型降解为合成/去分化表型是低氧性肺动脉高压的关键因素。
方法：在本研究中，进行qPCR以评估mRNA的基因表达。蛋白质印迹,免疫荧光和RNA下拉法检测基因表达水平。
结果：我们发现，缺氧后大鼠PA组织和PASMCs中聚嘧啶束结合蛋白1（PTBP1）的基因表达呈时间依赖性明显增加。PTBP1敲低可以抑制PASMCs的表型转变。PTBP1抑制PASMC的表型转变。此外,PTBP1在低氧条件下抑制整合素连接激酶（ILK）的表达，从而下调下游蛋白的表达。它抑制PASMC的表型转变并减轻肺动脉高压。
结论：结论：PTBP1/ILK轴通过诱导PASMC的表型转变促进PH的发展。这可能为PH提供新的疗法。
方法：在本研究中，进行qPCR以评估mRNA的基因表达。蛋白质印迹,免疫荧光和RNA下拉法检测基因表达水平。
结果：我们发现，缺氧后大鼠PA组织和PASMCs中聚嘧啶束结合蛋白1（PTBP1）的基因表达呈时间依赖性明显增加。PTBP1敲低可以抑制PASMCs的表型转变。PTBP1抑制PASMC的表型转变。此外,PTBP1在低氧条件下抑制整合素连接激酶（ILK）的表达，从而下调下游蛋白的表达。它抑制PASMC的表型转变并减轻肺动脉高压。
结论：结论：PTBP1/ILK轴通过诱导PASMC的表型转变促进PH的发展。这可能为PH提供新的疗法。
