[No authors listed]
Intermittent hypoxia/reoxygenation (IHR), characterized by repeated episodes of hypoxia interspersed with periods of reoxygenation, has been found to induce proâinflammatory cytokine production and is increasingly recognized as a major pathophysiological factor in various disease processes with distinct cell and molecular responses. The present study is the first, to the best of our knowledge, to investigate the effects of ubiquitinâspecific peptidase 8 (USP8) on IHRâinduced inflammation in renal tubular epithelial cells and examine the underlying mechanism. Following transfection of plasmids, HKâ2 and TCMKâ1 cells were incubated for eight cycles of IHR treatment including 3 h of hypoxic incubation followed by 3 h of normoxic culture. It was demonstrated that the expression of USP8 was decreased in IHR conditions but not in normoxic or continuous hypoxic conditions. In addition, IHRâinduced inflammation was suppressed in USP8âoverexpressinh renal tubular epithelial cells, and the silencing of USP8 markedly aggravated inflammation. Furthermore, it was found that the overexpression of USP8 inhibited the IHRâinduced activation of nuclear factorâκB and it was demonstrated that USP8 interacted with transforming growth factorâβâactivated kinaseâ1 (TAK1) and deubiquitinated the K63âlinked ubiquitination of TAK1. Taken together, the results demonstrated the role of USP8 in IHRâinduced inflammation and suggested USP8 as a potential and specific therapeutic target for IHRârelated diseases.
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