Knockdown of lncRNA TTTY15 alleviates ischemia/reperfusion‑induced inflammation and apoptosis of PC12 cells by targeting miR‑766‑5p
- Chenguang Hao
- Shibao Chen
Affiliations: Department of Neurology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang 830054, P.R. China, Department of Neurology, Bayingolin Mongolian Autonomous Prefecture People's Hospital, Korla, Xinjiang 841000, P.R. China
- Published online on: March 19, 2021 https://doi.org/10.3892/etm.2021.9942
Copyright: © Hao
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
The pathogenesis of ischemic stroke is extremely complex and has a significant impact on the quality of life of the patients. Accumulating studies have reported that long non‑coding RNAs (lncRNAs) may be associated with the progression of ischemic stroke. However, the role and underlying mechanism of action of the lncRNA testis‑specific transcript Y‑linked 15 (TTTY15) in ischemic stroke remains unknown. The present study analyzed the expression levels of TTTY15 in PC12 cells injured by oxygen‑glucose deprivation/reperfusion (OGD/R). The effects of the knockdown of TTTY15 expression on the levels of the inflammatory cytokines TNF‑α, IL‑1β, IL‑18 and IL‑10, cell apoptosis and the expression levels of the apoptosis‑associated proteins Bcl‑2, Bax, cleaved caspase‑3, caspase‑3, cleaved caspase‑9 and caspase‑9, were subsequently analyzed in OGD/R‑treated PC12 cells using ELISA, flow cytometry and western blotting, respectively. In addition, the downstream target gene of TTTY15 was verified using a dual luciferase reporter assay. The effects of TTTY15 on the inflammation and apoptosis of PC12 cells treated with OGD/R were determined by targeting miR‑766‑5p. The results of the present study revealed that TTTY15 expression was upregulated in OGD/R‑treated PC12 cells. The knockdown of TTTY15 significantly decreased the concentrations of the proinflammatory factors TNF‑α, IL‑1β and IL‑18, while it increased the concentration of the anti‑inflammatory cytokine IL‑10 in OGD/R‑treated PC12 cells. Apoptosis was also suppressed following gene silencing of TTTY15. Subsequently, miR‑766‑5p was identified as a target gene of TTTY15 using a dual luciferase reporter assay and the expression levels of TTTY15 and miR‑766‑5p were found to be negatively correlated. The overexpression of miR‑766‑5p alleviated the stimulatory effect of TTTY15 overexpression on the inflammation and apoptosis of PC12 cells treated with OGD/R. Therefore, the present study revealed that TTTY15 knockdown improved the OGD/R‑induced injury of PC12 cells by upregulating miR‑766‑5p expression.