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Upregulated LINC00319 aggravates neuronal injury induced by oxygen‑glucose deprivation via modulating miR‑200a‑3p

  • Authors:
    • Hui Yang
    • He Wang
    • Xiaodan Zhang
    • Yuehan Yang
    • Hongbin Li
  • View Affiliations / Copyright

    Affiliations: Department of Neurology, The First Affiliated Hospital of Jiamusi University, Jiamusi, Heilongjiang 154001, P.R. China, Department of Neurosurgery, The First Affiliated Hospital of Jiamusi University, Jiamusi, Heilongjiang 154001, P.R. China
    Copyright: © Yang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 844
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    Published online on: June 7, 2021
       https://doi.org/10.3892/etm.2021.10276
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Abstract

Ischemic stroke is one of the main causes of physical disability and mortality worldwide. Long non‑coding RNAs (lncRNAs) are reported to be dysregulated in various biological progressions and serve important roles in pathological processes of cerebral ischemia. However, their biological actions and potential mechanisms in the progression of ischemic stroke remain unknown. The present study aimed to investigate the functions of LINC00319 on ischemic brain injury. It was identified that LINC00319 was significantly upregulated in the Gene Expression Omnibus profile of ischemic stroke. Furthermore, LINC00319 overexpression elevated caspase‑3 activity and increased the apoptotic rate of neuronal cells, as well as decreased cell viability and glucose uptake. It was also demonstrated that LINC00319 participated in oxygen‑glucose deprivation (OGD)‑induced cerebral ischemic injury. LINC00319 could competitively bind with microRNA (miR)‑200a‑3p and decrease its expression. Moreover, miR‑200a‑3p could partly offset the negative effects of LINC00319 overexpression on neuronal injury caused by OGD. Collectively, the present results suggested that LINC00319 promoted apoptosis and aggravated neuronal injury induced by OGD by regulating miR‑200a‑3p, which may be important for ischemic stroke treatment.
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Copy and paste a formatted citation
Spandidos Publications style
Yang H, Wang H, Zhang X, Yang Y and Li H: Upregulated LINC00319 aggravates neuronal injury induced by oxygen‑glucose deprivation via modulating miR‑200a‑3p. Exp Ther Med 22: 844, 2021.
APA
Yang, H., Wang, H., Zhang, X., Yang, Y., & Li, H. (2021). Upregulated LINC00319 aggravates neuronal injury induced by oxygen‑glucose deprivation via modulating miR‑200a‑3p. Experimental and Therapeutic Medicine, 22, 844. https://doi.org/10.3892/etm.2021.10276
MLA
Yang, H., Wang, H., Zhang, X., Yang, Y., Li, H."Upregulated LINC00319 aggravates neuronal injury induced by oxygen‑glucose deprivation via modulating miR‑200a‑3p". Experimental and Therapeutic Medicine 22.2 (2021): 844.
Chicago
Yang, H., Wang, H., Zhang, X., Yang, Y., Li, H."Upregulated LINC00319 aggravates neuronal injury induced by oxygen‑glucose deprivation via modulating miR‑200a‑3p". Experimental and Therapeutic Medicine 22, no. 2 (2021): 844. https://doi.org/10.3892/etm.2021.10276
Copy and paste a formatted citation
x
Spandidos Publications style
Yang H, Wang H, Zhang X, Yang Y and Li H: Upregulated LINC00319 aggravates neuronal injury induced by oxygen‑glucose deprivation via modulating miR‑200a‑3p. Exp Ther Med 22: 844, 2021.
APA
Yang, H., Wang, H., Zhang, X., Yang, Y., & Li, H. (2021). Upregulated LINC00319 aggravates neuronal injury induced by oxygen‑glucose deprivation via modulating miR‑200a‑3p. Experimental and Therapeutic Medicine, 22, 844. https://doi.org/10.3892/etm.2021.10276
MLA
Yang, H., Wang, H., Zhang, X., Yang, Y., Li, H."Upregulated LINC00319 aggravates neuronal injury induced by oxygen‑glucose deprivation via modulating miR‑200a‑3p". Experimental and Therapeutic Medicine 22.2 (2021): 844.
Chicago
Yang, H., Wang, H., Zhang, X., Yang, Y., Li, H."Upregulated LINC00319 aggravates neuronal injury induced by oxygen‑glucose deprivation via modulating miR‑200a‑3p". Experimental and Therapeutic Medicine 22, no. 2 (2021): 844. https://doi.org/10.3892/etm.2021.10276
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