Abstract：
:Idiopathic pulmonary fibrosis (IPF) is a chronic progressive interstitial lung disease characterized by progressive lung scarring and excessive extracellular matrix depositon. When stimulated, alveolar epithelial cells (AECs) are aberrantly activated, the expression of profibrotic molecules is enhanced, and lung fibrosis is promoted, but the mechanism for this is unclear. It has been reported that a downregulation of the Na,K‑ATPase β1 subunit in renal epithelial cells is involved in renal fibrosis development, but the role of this protein in lung fibrosis remains unknown. In the present study, the expression of the Na,K‑ATPase β1 subunit was revealed to be markedly decreased in AECs of patients with IPF and a bleomycin‑induced pulmonary fibrosis mouse model. Treatment with transforming growth factor β‑1 led to significantly downregulation of the Na,K‑ATPase β1 subunit in lung adenocarcioma A549 cells. Furthermore, the knockdown of the Na,K‑ATPase β1 subunit in A549 cells resulted in the upregulation of profibrotic molecules, activation of the neurogenic locus notch homolog protein 1 and extracellular signal‑regulated kinase 1/2 signaling pathways and induction of endoplasmic reticulum stress. These findings reveal that the downregulation of the Na,K‑ATPase β1 subunit enhances the expression of profibrotic molecules in AECs and may contribute to IPF pathogenesis.
journal_name
Int J Mol Medjournal_title
International journal of molecular medicineauthors
Li B,Huang X,Xu X,Ning W,Dai H,Wang Cdoi
10.3892/ijmm.2019.4201subject
Has Abstractpub_date
2019-07-01 00:00:00pages
273-280issue
1eissn
1107-3756issn
1791-244Xjournal_volume
44pub_type
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