Zhang Meng-Jie, Kou Jie-Jian, Zhang Hong-Da, Xie Xin-Mei, Zhou Yun-Feng, Yuan Ping, Pang Xiao-Bin, Zhao Lu-Ling, Qiu Jing, He Yang-Yang
School of Pharmacy, Henan University, Kaifeng, China.
Department of Pharmacy, Huaihe Hospital of Henan University, Kaifeng, China.
Animal Model Exp Med. 2025 Jul;8(7):1268-1276. doi: 10.1002/ame2.12486. Epub 2024 Oct 28.
Metabolic abnormalities are considered to play a key regulatory role in vascular remodeling of pulmonary arterial hypertension. However, to date, there is a paucity of research documenting the changes in metabolome profiles within the supernatants of pulmonary artery smooth muscle cells (PASMC) during their transition from a contractile to a synthetic phenotype.
CCK-8 and Edu staining assays were used to evaluate the cell viability and proliferation of human PASMCs. IncuCyte ZOOM imaging system was used to continuously and automatically detect the migration of the PASMCs. A targeted metabolomics profiling was performed to quantitatively analyze 121 metabolites in the supernatant. Orthogonal partial least squares discriminant analysis was used to discriminate between PDGF-BB-induced PASMCs and controls. Metabolite set enrichment analysis was adapted to exploit the most disturbed metabolic pathways.
Human PASMCs exhibited a transformation from contractile phenotype to synthetic phenotype after PDGF-BB induction, along with a significant increase in cell viability, proliferation, and migration. Metabolites in the supernatants of PASMCs treated with or without PDGF-BB were well profiled. Eleven metabolites were found to be significantly upregulated, whereas seven metabolites were downregulated in the supernatants of PASMCs induced by PDGF-BB compared to the vehicle-treated cells. Fourteen pathways were involved, and pyruvate metabolism pathway was ranked first with the highest enrichment impact followed by glycolysis/gluconeogenesis and pyrimidine metabolism.
Significant and extensive metabolic abnormalities occurred during the phenotypic transformation of PASMCs. Disturbance of pyruvate metabolism pathway might contribute to pulmonary vascular remodeling.
代谢异常被认为在肺动脉高压的血管重塑中起关键调节作用。然而,迄今为止,缺乏研究记录肺动脉平滑肌细胞(PASMC)从收缩表型转变为合成表型过程中其培养上清液中代谢组谱的变化。
采用CCK-8和Edu染色试验评估人PASMC的细胞活力和增殖。使用IncuCyte ZOOM成像系统连续自动检测PASMC的迁移。进行靶向代谢组分析以定量分析上清液中的121种代谢物。采用正交偏最小二乘法判别分析区分PDGF-BB诱导的PASMC和对照组。采用代谢物集富集分析来探究受干扰最严重的代谢途径。
PDGF-BB诱导后人PASMC表现出从收缩表型向合成表型的转变,同时细胞活力、增殖和迁移显著增加。对有无PDGF-BB处理的PASMC上清液中的代谢物进行了很好的分析。与载体处理的细胞相比,发现PDGF-BB诱导的PASMC上清液中有11种代谢物显著上调,而7种代谢物下调。涉及14条途径,丙酮酸代谢途径的富集影响最大,位居第一,其次是糖酵解/糖异生和嘧啶代谢。
PASMC表型转化过程中发生了显著且广泛的代谢异常。丙酮酸代谢途径的紊乱可能导致肺血管重塑。