Knockdown of MicroRNA-1 in the Hippocampus Ameliorates Myocardial Infarction Induced Impairment of Long-Term Potentiation
Backgrounds/Aims: It has been reported that myocardial infarction (MI) is a risk factor for vascular dementia. However, the molecular mechanism remains largely unknown. Methods: MI mice were generated by ligation of the left coronary artery (LCA) for 4 weeks. Passive and active avoidance tests were...
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Cell Physiol Biochem Press GmbH & Co KG
2018-10-01
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Online Access: | https://www.karger.com/Article/FullText/494657 |
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author | Ji-Chao Ma Ming-Jing Duan Ke-Xin Li Das Biddyut Shuai Zhang Mei-Ling Yan Lin Yang Zhuo Jin Hong-Mei Zhao Si-Yu Huang Qiang Sun Dan Su Yi Xu Yong-Hui Pan Jing Ai |
author_facet | Ji-Chao Ma Ming-Jing Duan Ke-Xin Li Das Biddyut Shuai Zhang Mei-Ling Yan Lin Yang Zhuo Jin Hong-Mei Zhao Si-Yu Huang Qiang Sun Dan Su Yi Xu Yong-Hui Pan Jing Ai |
author_sort | Ji-Chao Ma |
collection | DOAJ |
description | Backgrounds/Aims: It has been reported that myocardial infarction (MI) is a risk factor for vascular dementia. However, the molecular mechanism remains largely unknown. Methods: MI mice were generated by ligation of the left coronary artery (LCA) for 4 weeks. Passive and active avoidance tests were performed to evaluate the cognitive ability of MI mice. A theta-burst stimulation (TBS) protocol was applied to elicit long-term potentiation (LTP) of the perforant pathway-dentate gyrus synapse (PP-DG). Western blot analysis was employed to assess protein levels. Results: In this study, we demonstrated that after 4 weeks of MI, C57BL/6 mice had significantly impaired memory. Compared with the sham group, in vivo physiological recording in the MI group revealed significantly decreased amplitude of population spikes (PS) with no effect on the latency and duration of the stimulus-response curve. The amplitude of LTP was markedly decreased in the MI group compared with the sham group. Further examination showed that the expression of the TBS-LTP-related proteins BDNF, GluA1 and phosphorylated GluA1 were all decreased in the MI group compared with those in the sham group. Strikingly, all these changes were prevented by hippocampal stereotaxic injection of an anti-miR-1 oligonucleotide fragment carried by a lentivirus vector (lenti-pre-AMO-1). Conclusion: MI induced cognitive decline and TBS-LTP impairment, and decreased BDNF and GluA1 phosphorylation levels from overexpression of miR-1ated were involved in this process. |
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language | English |
last_indexed | 2024-12-12T19:53:53Z |
publishDate | 2018-10-01 |
publisher | Cell Physiol Biochem Press GmbH & Co KG |
record_format | Article |
series | Cellular Physiology and Biochemistry |
spelling | doaj.art-716293e0414644f6936c982cb38a4dd52022-12-22T00:13:56ZengCell Physiol Biochem Press GmbH & Co KGCellular Physiology and Biochemistry1015-89871421-97782018-10-015041601161610.1159/000494657494657Knockdown of MicroRNA-1 in the Hippocampus Ameliorates Myocardial Infarction Induced Impairment of Long-Term PotentiationJi-Chao MaMing-Jing DuanKe-Xin LiDas BiddyutShuai ZhangMei-Ling YanLin YangZhuo JinHong-Mei ZhaoSi-Yu HuangQiang SunDan SuYi XuYong-Hui PanJing AiBackgrounds/Aims: It has been reported that myocardial infarction (MI) is a risk factor for vascular dementia. However, the molecular mechanism remains largely unknown. Methods: MI mice were generated by ligation of the left coronary artery (LCA) for 4 weeks. Passive and active avoidance tests were performed to evaluate the cognitive ability of MI mice. A theta-burst stimulation (TBS) protocol was applied to elicit long-term potentiation (LTP) of the perforant pathway-dentate gyrus synapse (PP-DG). Western blot analysis was employed to assess protein levels. Results: In this study, we demonstrated that after 4 weeks of MI, C57BL/6 mice had significantly impaired memory. Compared with the sham group, in vivo physiological recording in the MI group revealed significantly decreased amplitude of population spikes (PS) with no effect on the latency and duration of the stimulus-response curve. The amplitude of LTP was markedly decreased in the MI group compared with the sham group. Further examination showed that the expression of the TBS-LTP-related proteins BDNF, GluA1 and phosphorylated GluA1 were all decreased in the MI group compared with those in the sham group. Strikingly, all these changes were prevented by hippocampal stereotaxic injection of an anti-miR-1 oligonucleotide fragment carried by a lentivirus vector (lenti-pre-AMO-1). Conclusion: MI induced cognitive decline and TBS-LTP impairment, and decreased BDNF and GluA1 phosphorylation levels from overexpression of miR-1ated were involved in this process.https://www.karger.com/Article/FullText/494657HeartHippocampusCognitive impairmentMicroRNA-1BDNFlong-term potentiation |
spellingShingle | Ji-Chao Ma Ming-Jing Duan Ke-Xin Li Das Biddyut Shuai Zhang Mei-Ling Yan Lin Yang Zhuo Jin Hong-Mei Zhao Si-Yu Huang Qiang Sun Dan Su Yi Xu Yong-Hui Pan Jing Ai Knockdown of MicroRNA-1 in the Hippocampus Ameliorates Myocardial Infarction Induced Impairment of Long-Term Potentiation Cellular Physiology and Biochemistry Heart Hippocampus Cognitive impairment MicroRNA-1 BDNF long-term potentiation |
title | Knockdown of MicroRNA-1 in the Hippocampus Ameliorates Myocardial Infarction Induced Impairment of Long-Term Potentiation |
title_full | Knockdown of MicroRNA-1 in the Hippocampus Ameliorates Myocardial Infarction Induced Impairment of Long-Term Potentiation |
title_fullStr | Knockdown of MicroRNA-1 in the Hippocampus Ameliorates Myocardial Infarction Induced Impairment of Long-Term Potentiation |
title_full_unstemmed | Knockdown of MicroRNA-1 in the Hippocampus Ameliorates Myocardial Infarction Induced Impairment of Long-Term Potentiation |
title_short | Knockdown of MicroRNA-1 in the Hippocampus Ameliorates Myocardial Infarction Induced Impairment of Long-Term Potentiation |
title_sort | knockdown of microrna 1 in the hippocampus ameliorates myocardial infarction induced impairment of long term potentiation |
topic | Heart Hippocampus Cognitive impairment MicroRNA-1 BDNF long-term potentiation |
url | https://www.karger.com/Article/FullText/494657 |
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