Cardiac over-expression of microRNA-1 induces impairment of cognition in mice

Ma, Jing; Duan, Mengjie; Sun, Lihua; Yan, Meiling; Liu, T.; Wang, Q.; Liu, C.-D.; Wang, X.; Kang, Xujuan; Pei, Shuang-Chao; Zong, De-Kang; Chen, X.; Wang, N.; Ai, Jing

doi:10.1016/j.neuroscience.2015.04.061

Cited by 21 publications

(30 citation statements)

References 54 publications

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“…Although all cardiovascular diseases share similar pathological changes, e.g., changes due to diabetes and/or hyperlipidaemia, the clinical trial results of the benefits of antihypertensive, anti-diabetic and antihyperlipidaemia treatments on cognitive impairment are controversial [12,40,41]. Our previous study demonstrated that a mouse model with the cardiac-specific over-expression of miR-1-2 driven by α-MHC showed impaired cognition, which was associated with increased miR-1 levels mediating downregulation of BDNF expression in the hippocampus [20]. Because miR-1 levels were increased in the heart and blood of MI mice [21,42,43], MIinduced brain damage was apparent on the 15 th day and cognitive deficiency was observed at 3 months after LCA [13], we hypothesized that miR-1 might be involved in MI induced brain dysfunction.…”

Section: Discussionmentioning

confidence: 99%

“…These It has been demonstrated that the molecular basis of TBS-LTP is related to BDNF signalling by binding with the TrkB receptor and phosphorylating GluA1 [38,39]. Our previous study demonstrated that cardiac over-expression of miR-1 downregulated BDNF expression in the hippocampus [20]. Thus, we speculated that the reduced LTP in Tg mice might be associated with BDNF, which mediated the decreased phosphorylation of GluA1 (p-GluA1).…”

Section: Cellular Physiology and Biochemistrymentioning

confidence: 91%

“…Previously, miR-1 has been reported to be increased in the blood of both AMI rats and patients [23,25,37], and cardiac-specific over-expression of miR-1 could induce cognitive impairment compared with age-matched WT mice using the Morris water maze test [20]. We hypothesized that the attenuation of TBS-LTP following 4 weeks of MI might be associated with miR-1.…”

Section: Attenuation Of Cognition and Tbs-ltp In Cardiac-specific Ovementioning

confidence: 95%

“…Total protein samples for western blot analysis were extracted from the hippocampi of the mice or from primary cultured NRNs, and the procedure for the preparation of total protein has been described previously [20]. Frozen brain tissues were lysed in a solution containing 10 % SDS, 60 % RIPA, 1 % protease inhibitor and 10 % phosphatase inhibitor.…”

Section: Western Blot Analysismentioning

confidence: 99%

“…Our previous study demonstrated that heart-specific microRNA-1 (miR-1) overexpression in transgenic mice, induced an increase in miR-1 levels in the hippocampus and cognitive impairment by exerting direct effects on the brain [20]. Because it has been reported that miR-1 plays an important role in MI-induced arrhythmia [21] and heart failure [22], and plasma miR-1 was found to be increased in the blood of patients suffering from acute myocardial infarction (AMI) [23][24][25], we hypothesized that miR-1 may participate in MI mediated brain dysfunction.…”

Section: Introductionmentioning

confidence: 99%

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Knockdown of MicroRNA-1 in the Hippocampus Ameliorates Myocardial Infarction Induced Impairment of Long-Term Potentiation

Duan

et al. 2018

Cell Physiol Biochem

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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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Section: Discussionmentioning

confidence: 99%

Section: Cellular Physiology and Biochemistrymentioning

confidence: 91%

Section: Attenuation Of Cognition and Tbs-ltp In Cardiac-specific Ovementioning

confidence: 95%

Section: Western Blot Analysismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Knockdown of MicroRNA-1 in the Hippocampus Ameliorates Myocardial Infarction Induced Impairment of Long-Term Potentiation

Duan

et al. 2018

Cell Physiol Biochem

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Cerebral derailment after myocardial infarct: mechanisms and effects of the signaling from the ischemic heart to brain

et al. 2021

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Myocardial infarction (MI) is the leading cause of death among ischemic heart diseases and is associated with several long-term cardiovascular complications, such as angina, re-infarction, arrhythmias, and heart failure. However, MI is frequently accompanied by non-cardiovascular multiple comorbidities, including brain disorders such as stroke, anxiety, depression, and cognitive impairment. Accumulating experimental and clinical evidence suggests a causal relationship between MI and stroke, but the precise underlying mechanisms have not yet been elucidated. Indeed, the risk of stroke remains a current challenge in patients with MI, in spite of the improvement of medical treatment among this patient population has reduced the risk of stroke. In this review, the effects of the signaling from the ischemic heart to the brain, such as neuroinflammation, neuronal apoptosis, and neurogenesis, and the possible actors mediating these effects, such as systemic inflammation, immunoresponse, extracellular vesicles, and microRNAs, are discussed.

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Cognitive impairment in patients with heart failure: molecular mechanism and therapy

Chen

Feng

et al. 2023

Heart Fail Rev

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Cardiac over-expression of microRNA-1 induces impairment of cognition in mice

Cited by 21 publications

References 54 publications

Knockdown of MicroRNA-1 in the Hippocampus Ameliorates Myocardial Infarction Induced Impairment of Long-Term Potentiation

Knockdown of MicroRNA-1 in the Hippocampus Ameliorates Myocardial Infarction Induced Impairment of Long-Term Potentiation

Cerebral derailment after myocardial infarct: mechanisms and effects of the signaling from the ischemic heart to brain

Cognitive impairment in patients with heart failure: molecular mechanism and therapy

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