Backgrounds

To investigate the biological functions and the molecular mechanisms of PTTG1 in PDGF-BB-induced ASMCs.

Objectives

QPCR and western blotting were used to detect PTTG1 levels in PDGF-BB-induced ASMCs. MTT, BrdU incorporation, cell apoptosis and cell invasion assays were performed to evaluate the effect of PTTG1 on cell proliferation, invasion and apoptosis, respectively. Western blotting was also used to assess the extracellular matrix and PI3K/AKT/mTOR signaling pathway components in PDGF-BB-induced ASMCs.

Results

PTTG1 was highly expressed in PDGF-BB-induced ASMCs. The depletion of PTTG1 suppressed the proliferation and motility of PDGF-BB-induced ASMCs. The data further showed that PTTG1 ablation stimulated cell apoptosis, and inhibited the production of extracellular matrix by PDGF-BB-induced ASMCs. Mechanically, PTTG1 depletion inhibited the PI3K/AKT/mTOR signaling pathway, thereby inhibiting proliferation, motility, and extracellular matrix production.

Conclusions

PTTG1 could serve as a promising molecular target for the treatment of asthma.

中文翻译：

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下调PTTG1通过调节PI3K/AKT/mTOR信号通路抑制PDGF-BB诱导的气道平滑肌细胞（ASMCs）增殖、迁移和细胞外基质产生

背景

研究 PTTG1 在 PDGF-BB 诱导的 ASMC 中的生物学功能和分子机制。

目标

QPCR 和蛋白质印迹用于检测 PDGF-BB 诱导的 ASMC 中的 PTTG1 水平。进行MTT、BrdU掺入、细胞凋亡和细胞侵袭测定以分别评价PTTG1对细胞增殖、侵袭和凋亡的影响。蛋白质印迹还用于评估 PDGF-BB 诱导的 ASMC 中的细胞外基质和 PI3K/AKT/mTOR 信号通路组分。

结果

PTTG1 在 PDGF-BB 诱导的 ASMC 中高度表达。PTTG1 的消耗抑制了 PDGF-BB 诱导的 ASMC 的增殖和运动。数据进一步表明，PTTG1 消融刺激细胞凋亡，并抑制 PDGF-BB 诱导的 ASMC 产生细胞外基质。从机制上讲，PTTG1 耗竭会抑制 PI3K/AKT/mTOR 信号通路，从而抑制增殖、运动和细胞外基质的产生。

结论

PTTG1 可以作为治疗哮喘的有希望的分子靶点。