Inhibition of long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 attenuates high glucose-induced cardiomyocyte apoptosis via regulation of miR-181a-5p
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- Cheng Yongxia
- Pathology Diagnosis Center, The First Clinical Medical School of Mudanjiang Medical College, No. 3 Tongxiang Street, Aimin District, Mudanjiang, Heilongjiang 157011, P.R.China Key Laboratory of Cancer Prevention and Treatment of Heilongjiang Province, Mudanjiang Medical College, No. 3 Tongxiang Street, Aimin District, Mudanjiang, Heilongjiang 157011, P.R.China Institute of Stem Cells, Mudanjiang Medical College, No. 3 Tongxiang Street, Aimin District, Mudanjiang, Heilongjiang 157011, P.R.China
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- Li Jingchao
- Department of Neurology, Hongqi Hospital of Mudanjiang Medical College, No. 3 Tongxiang Street, Aimin District, Mudanjiang, Heilongjiang 157011, P.R.China
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- Wang Chong
- Pathology Diagnosis Center, The First Clinical Medical School of Mudanjiang Medical College, No. 3 Tongxiang Street, Aimin District, Mudanjiang, Heilongjiang 157011, P.R.China
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- Yang Heran
- Department of Laboratory Medicine, Hongqi Hospital of Mudanjiang Medical College, No. 3 Tongxiang Street, Aimin District, Mudanjiang, Heilongjiang 157011, P.R.China
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- Wang Ying
- Department of Anatomy, School of Basic Medical Sciences, Mudanjiang Medical College, No. 3 Tongxiang Street, Aimin District, Mudanjiang, Heilongjiang 157011, P.R.China Institute of Neural Tissue Engineering, Mudanjiang Medical College, No. 3 Tongxiang Street, Aimin District, Mudanjiang, Heilongjiang 157011, P.R.China
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- Zhan Tao
- Pathology Diagnosis Center, The First Clinical Medical School of Mudanjiang Medical College, No. 3 Tongxiang Street, Aimin District, Mudanjiang, Heilongjiang 157011, P.R.China
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- Guo Sufen
- Pathology Diagnosis Center, The First Clinical Medical School of Mudanjiang Medical College, No. 3 Tongxiang Street, Aimin District, Mudanjiang, Heilongjiang 157011, P.R.China
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- Liang Jun
- Institute of Stem Cells, Mudanjiang Medical College, No. 3 Tongxiang Street, Aimin District, Mudanjiang, Heilongjiang 157011, P.R.China Department of Histology and Embryology, School of Basic Medical Sciences, Mudanjiang Medical College, No. 3 Tongxiang Street, Aimin District, Mudanjiang, Heilongjiang 157011, P.R.China
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- Bai Yuxin
- Pathology Diagnosis Center, The First Clinical Medical School of Mudanjiang Medical College, No. 3 Tongxiang Street, Aimin District, Mudanjiang, Heilongjiang 157011, P.R.China
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- Yu Jianbo
- Pathology Diagnosis Center, The First Clinical Medical School of Mudanjiang Medical College, No. 3 Tongxiang Street, Aimin District, Mudanjiang, Heilongjiang 157011, P.R.China Key Laboratory of Cancer Prevention and Treatment of Heilongjiang Province, Mudanjiang Medical College, No. 3 Tongxiang Street, Aimin District, Mudanjiang, Heilongjiang 157011, P.R.China
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- Liu Guibo
- Department of Anatomy, School of Basic Medical Sciences, Mudanjiang Medical College, No. 3 Tongxiang Street, Aimin District, Mudanjiang, Heilongjiang 157011, P.R.China Institute of Neural Tissue Engineering, Mudanjiang Medical College, No. 3 Tongxiang Street, Aimin District, Mudanjiang, Heilongjiang 157011, P.R.China
抄録
<p> Diabetic cardiomyopathy (DCM) is one of the cardiovascular complications of diabetes mellitus independent of hypertension, coronary disease, and other heart diseases. The development of DCM is multifactorial and hard to detect at an early stage. Long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (Malat1) is emerging as a regulator of DCM, the underlying mechanism of its role in DCM has not been elaborated yet. In this study, we established a mouse DCM model via streptozocin injection as evidenced by cell hypertrophy and cell apoptosis of myocardial tissue, and found that Malat1 expression was upregulated in the myocardium in DCM mice. Meanwhile, elevated expression of pro-apoptotic factors p53, p21, cleaved caspase 3, cleaved caspase 9 and BAX, and down-regulation of anti-apoptotic BCL-2 were observed in DCM myocardium. We further investigated the effect of Malat1 on cardiomyocytes under high glucose condition by silencing Malat1 with its specific short-hairpin RNA. Like in vivo, expression of Malat1 in cardiomyocytes was notably raised, remarkable cell apoptosis and changes in apoptosis-related factors were also observed following high glucose treatment. Besides, we validated that Malat1 acted as a sponge of miR-181a-5p. Inhibition of miR-181a-5p could, at least partially, abolish Malat1 knockdown-induced alteration in cardiomyocytes. In addition, p53, a critical regulator of apoptosis, was validated to be a downstream target of miR-181a-5p. In summary, our findings reveal that Malat1 knockdown attenuates high glucose-induced cardiomyocyte apoptosis via releasing miR-181a-5p, and this mechanism may provide us with new diagnosis target of DCM.</p>
収録刊行物
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- Experimental Animals
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Experimental Animals 69 (1), 34-44, 2020
公益社団法人 日本実験動物学会