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Calpain 1 Regulates TGF-β1-induced Epithelial-Mesenchymal Transition in Human Lung Epithelial Cells via PI3K/Akt Signaling Pathway

Calpain 1 Regulates TGF-β1-induced Epithelial-Mesenchymal Transition in Human Lung Epithelial Cells via PI3K/Akt Signaling Pathway

Wei-Jun Tan, Qiu-Yue Tan, Ting Wang, Min Lian, Li Zhang, Zhen-Shun Cheng

Am J Transl Res. 2017 Mar 15;9(3):1402-1409.

PMID: 28386365

Abstract:

Cell proliferation, transformation, and epithelial-mesenchymal transition (EMT) are key processes involved in the development of idiopathic pulmonary fibrosis (IPF). This study investigated the regulatory factors and signaling pathways that mediate EMT in the human type II alveolar epithelial A549 cell line. A549 cells were cultured in RPMI-1640 medium and allocated to the following four groups: blank control group or treated with transforming growth factor-β1 (TGF-β1), TGF-β1 + PD 150606 (a calpain 1 inhibitor), or PD 150606. We examined E-cadherin (E-cad), α-smooth muscle actin (α-SMA), and calpain 1 mRNA transcript and protein expression levels in these four groups by performing RT-PCR and western blot analyses. The results indicated that TGF-β1 treatment significantly downregulated E-cad and upregulated α-SMA expression compared with that of the blank control group (P<0.05). TGF-β1 also enhanced calpain 1 expression compared with that of the blank control group (P<0.05). By contrast, treatment with the calpain 1 inhibitor PD 150606 increased E-cad expression and decreased α-SMA expression. Furthermore, PD 150606 treatment antagonized TGF-β1-mediated increase in Akt/phospho-Akt in A549 epithelial cells. However, TGF-β1-induced ETM was not correlated with the ERK and JNK signaling pathways. These combined results indicate that calpain 1 could regulate EMT in TGF-β1-treated A549 epithelial cells via the PI3K/Akt signaling pathway.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP179528451	PD 150606		179528-45-1	Price

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