PTEN enhances nasal epithelial cell resistance to TNFα‑induced inflammatory injury by limiting mitophagy via repression of the TLR4‑JNK‑Bnip3 pathway
Abstract
Nasal epithelial cell inflammatory injury is associated with chronic obstructive pulmonary disease development. However, the mechanism by which inflammation triggers nasal epithelial cell damage remains unclear. In the present study, tumor necrosis factor (TNF)α was used to induce an inflammatory injury and explore the underlying pathogenesis for nasal epithelial cell apoptosis in vitro, with a focus on mitochondrial homeostasis. Then, cellular apoptosis was detected via a terminal deoxynucleotidyl‑transferase‑mediated dUTP nick end labeling assay and western blotting. Mitochondrial function was evaluated via JC‑1 staining, mPTP opening measurement and western blotting. The results demonstrated that TNFα treatment induced nasal epithelial cell apoptosis, proliferation arrest and migration inhibition via downregulating phosphatase and tensin homolog (PTEN) levels. Increased PTEN expression was associated with reduce Toll‑like receptor (TLR)4‑c‑Jun kinase (JNK)‑Bcl2‑interacting protein 3 (Bnip3) pathway signaling, leading to reductions in mitophagy activity. Excessive mitophagy resulted in ATP deficiencies, mitochondrial dysfunction, caspase‑9 activation and cellular apoptosis. By contrast, PTEN overexpression in nasal epithelial...Continue Reading
References
Importance of ROS-mediated autophagy in determining apoptotic cell death induced by physapubescin B.
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