Few studies about nucleotide‐oligomerization domain‐like receptor subfamily C3 (NLRC3) in PASMCs have been conducted. This research aimed to investigate the role of NLRC3 on platelet‐derived growth factor (PDGF)‐induced proliferation of pulmonary artery smooth muscle cells (PASMCs) and its underlying mechanism. We found that the proliferation of PASMCs stimulated with PDGF decreased when phosphoinositide 3‐kinase (PI3K) or mammalian target of rapamycin (mTOR) inhibitors pretreatment. Overexpression of NLRC3 inhibited the proliferation of PASMCs and the phosphorylation of PI3K and mTOR while knocking down NLRC3 reversed this effect. Targeted to PI3K or mTOR can also reverse the effect of NLRC3. Activation of PI3K increased the phosphorylation of mTOR while inhibition of PI3K reduced it. Our data suggest that PDGF can induce abnormal proliferation of PASMCs, and NLRC3 suppresses activation of the PI3K‐mTOR signaling thus inhibits PASMCs proliferation. These findings unveiled the effect of NLRC3 as an inhibitor of the PI3K‐mTOR pathway mediating protection against PASMCs proliferation.

中文翻译：

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NLRC3通过PI3K-mTOR途径抑制PDGF诱导的PASMCs增殖。

在PASMC中，关于核苷酸寡聚化域样受体亚家族C3（NLRC3）的研究很少。这项研究旨在探讨NLRC3在血小板衍生生长因子（PDGF）诱导的肺动脉平滑肌细胞（PASMC）增殖中的作用及其潜在机制。我们发现，当磷酸肌醇3激酶（PI3K）或哺乳动物雷帕霉素（mTOR）抑制剂靶标预处理时，PDGF刺激的PASMCs增殖减少。NLRC3的过表达抑制了PASMCs的增殖，而PI3K和mTOR的磷酸化则降低了NLRC3的表达。以PI3K或mTOR为目标也可以逆转NLRC3的作用。PI3K的激活增加了mTOR的磷酸化，而PI3K的抑制则降低了它的磷酸化。我们的数据表明PDGF可以诱导PASMCs异常增殖，而NLRC3抑制PI3K-mTOR信号的激活，从而抑制PASMCs增殖。这些发现揭示了NLRC3作为PI3K-mTOR途径抑制剂的作用，介导了针对PASMC增殖的保护作用。