Department of Pulmonary and Critical Care Medicine, Peking University Shenzhen Hospital, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, P.R. China.
Department of Pulmonary and Critical Care Medicine, Peking University Shenzhen Hospital, Shenzhen, P.R. China.
Epigenetics. 2023 Dec;18(1):2195305. doi: 10.1080/15592294.2023.2195305.
Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease with an unclear pathogenesis. This study aimed to elucidate the function and potential mechanisms of TUG1 in IPF progression. Cell viability and migration were detected by CCK-8 and transwell assays. Autophagy, fibrosis, or EMT-related proteins were measured by Western blotting. Pro-inflammatory cytokine levels were assessed by ELISA kits. The subcellular localization of TUG1 was observed by FISH assay. RIP assay detected the interaction between TUG1 and CDC27. TUG1 and CDC27 was up-regulated in TGF-β1-induced RLE-6TN cells. TUG1 depletion suppressed pulmonary fibrosis via attenuating inflammation, EMT, inducing autophagy and inactivating PI3K/Akt/mTOR pathway in vitro and in vivo. TUG1 knockdown prevented CDC27 expression. TUG1 silencing ameliorated pulmonary fibrosis by reducing CDC27 expression and inhibiting PI3K/Akt/mTOR pathway.
特发性肺纤维化（IPF）是一种病因不明的致命性肺间质疾病。本研究旨在阐明 TUG1 在 IPF 进展中的功能和潜在机制。通过 CCK-8 和 Transwell 测定法检测细胞活力和迁移。通过 Western blot 测定自噬、纤维化或 EMT 相关蛋白。通过 ELISA 试剂盒评估促炎细胞因子水平。通过 FISH 测定观察 TUG1 的亚细胞定位。RIP 测定检测 TUG1 和 CDC27 之间的相互作用。TUG1 和 CDC27 在 TGF-β1 诱导的 RLE-6TN 细胞中上调。TUG1 耗竭通过体外和体内减轻炎症、EMT、诱导自噬和失活 PI3K/Akt/mTOR 通路来抑制肺纤维化。TUG1 敲低可防止 CDC27 表达。TUG1 沉默通过降低 CDC27 表达和抑制 PI3K/Akt/mTOR 通路来改善肺纤维化。
