Document Type : Original Article
Authors
- Mahnaz Bayat 1
- Etrat Hooshmandi 1
- Najmeh Karimi 2
- Moosa Rahimi 3
- Reza Tabrizi 4
- Tahereh Asadabadi 1
- Mohammad Saied Salehi 1
- Seyedeh Shaghayegh Zafarmand 1
- Maryam Owjfard 1
- Carlos Garcia Esperon 5
- Neil Spratt 5
- Christopher Levi 6
- Afshin Borhani-Haghighi 1
1 Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
2 Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran Department of Neurology, Shiraz University of Medical Sciences, Shiraz, Iran
3 Laboratory of Basic Sciences, Mohammad Rasul Allah Research Tower, Shiraz University of Medical Sciences, Shiraz, Iran
4 Noncommunicable Diseases Research Center, Fasa University of Medical Sciences, Fasa, Iran
5 Department of Neurology, John Hunter Hospital, Newcastle, Newcastle, Australia
6 Hunter Medical Research Institute, University of Newcastle, Newcastle, Australia
Abstract
Background: Inflammation is the major contributor to the pathophysiology of ischemic stroke (IS). Long non-coding ribonucleic acids (lncRNAs) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and tumor necrosis factor and heterogeneous nuclear ribonucleoprotein L-related immunoregulatory (THRIL) have been demonstrated to be up-regulated in inflammation and atherosclerosis. Therefore, we aimed to study the expression profile of these lncRNAs after IS.
Methods: This observational case-control study was conducted in Namazi Hospital, Shiraz, Iran. The real-time polymerase chain reaction (RT-PCR) measured the sequential changes in circulating levels of MALAT1 and THRIL on days 1, 3, and 5 after IS. The receiver operating characteristic (ROC) curve analysis was used to estimate the diagnostic and prognostic potential of lncRNAs with the area under the curve (AUC).
Results: In patients with IS, the relative MALAT1 and THRIL expressions were significantly higher than the controls (P < 0.001 and P < 0.01, respectively), on days 1, 3, and 5 after stroke.
We showed a significantly increase in lncRNAs expression on day five compared to days 1 and 3 after stroke. Moreover, a positive correlation was detected between MALAT1 expression and time within the first 24 hours after stroke (r = 0.27, P = 0.03). Logistic regression analysis showed a significant positive association between MALAT1 and THRIL and the risk of stroke evolution. We found a potential diagnostic marker for MALAT1 with an AUC of 0.78.
Conclusion: We demonstrated the significant sequential upregulation in MALAT1 and THRIL expression on days 1, 3, and 5 after IS with a significant positive association with the risk of stroke. MALAT1 also significantly correlated with time within the first 24 hours after stroke.
Keywords
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