Downregulated microRNA‐330 suppresses left ventricular remodeling via the TGF‐β1/Smad3 signaling pathway by targeting SRY in mice with myocardial ischemia–reperfusion injury

Liu, Zhengyu; Cao, Yan; Zheng, Jiao; Tang, Yi; He, Jin; Hu, Yongjun; Wang, Changlu; Zou, Qiong-Chao; Fu, Qinghua; Zhang, Le; Peng, Jianqiang; Jing, Ling; Ning, Peng; Rong, Jingjing; Zheng, Zhaofen

doi:10.1002/jcp.27800

Cited by 18 publications

(11 citation statements)

References 40 publications

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“…A recent study reported that miRNA-330 overexpression in Alzheimer's disease contributed to the reduction of amyloid β, oxidative stress, and mitochondrial dysfunction by targeting VAV1 through the MAPK pathway (Zhou et al, 2018). In addition, downregulated miRNA-330 could reduce myocardial infarction size through suppressing left ventricular remodeling (Liu Z. Y. et al, 2019). The discrepancy in miRNA-330 biological effects may result from the different diseases, tissues, and experimental conditions used.…”

Section: Discussionmentioning

confidence: 99%

Exosomal MicroRNAs Contribute to Cognitive Impairment in Hypertensive Patients by Decreasing Frontal Cerebrovascular Reactivity

Cao

Chen

et al. 2021

Front. Neurosci.

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Mechanisms underlying cognitive impairment (CI) in hypertensive patients remain relatively unclear. The present study aimed to explore the relationship among serum exosomal microRNAs (miRNAs), cerebrovascular reactivity (CVR), and cognitive function in hypertensive patients. Seventy-three hypertensive patients with CI (HT-CI), 67 hypertensive patients with normal cognition (HT-NC), and 37 healthy controls underwent identification of exosomal miRNA, multimodal magnetic resonance imaging (MRI) scans, and neuropsychological tests. CVR mapping was investigated based on resting-state functional MRI data. Compared with healthy subjects and HT-NC subjects, HT-CI subjects displayed decreased serum exosomal miRNA-330-3p. The group difference of CVR was mainly found in the left frontal lobe and demonstrated that HT-CI group had a lower CVR than both HT-NC group and control group. Furthermore, both the CVR in the left medial superior frontal gyrus and the miRNA-330-3p level were significantly correlated with executive function (r = −0.275, P = 0.021, and r = −0.246, P = 0.04, respectively) in HT-CI subjects, and the CVR was significantly correlated with the miRNA-330-3p level (r = 0.246, P = 0.040). Notably, path analysis showed that the CVR mediated the association between miRNA-330-3p and executive function. In conclusion, decreased miRNA-330-3p might contribute to CI in hypertensive patients by decreasing frontal CVR and could be a biomarker of early diagnosis.

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Section: Discussionmentioning

confidence: 99%

Exosomal MicroRNAs Contribute to Cognitive Impairment in Hypertensive Patients by Decreasing Frontal Cerebrovascular Reactivity

Cao

Chen

et al. 2021

Front. Neurosci.

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“…A previous study reported that the TGF-β/Smad3 signaling pathway was activated and promoted ventricular remodeling after IR injury in rats (17), while mediating the protection of myocardial cells against IR injury via the stimulation of sphingosine-1-phosphate (S1P)/S1P receptor 1. TGF-β1/Smad3 has also been reported to exert an important effect on cerebral ischemia.…”

Section: Aggravation Of Hepatic Ischemia-reperfusion Injury With Increased Inflammatory Cell Infiltration Is Associated With the Tgf-β/smmentioning

confidence: 99%

Aggravation of hepatic ischemia‑reperfusion injury with increased inflammatory cell infiltration is associated with the TGF‑β/Smad3 signaling pathway

Shen

Tong

et al. 2021

Mol Med Rep

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Ischemia-reperfusion (IR) injury is a major challenge influencing the outcomes of hepatic transplantation. Transforming growth factor-β (TGF-β) and its downstream gene, SMAD family member 3 (Smad3), have been implicated in the pathogenesis of chronic hepatic injuries, such as hepatic fibrosis. Thus, the present study aimed to investigate the role of the TGF-β/Smad3 signaling pathway on hepatic injury induced by IR in vivo. In total, 20 129S2/SvPasCrl wild-type (WT) mice were randomized into two groups; 10 mice underwent IR injury surgery and 10 mice were sham-operated. Histopathological changes in liver tissues and serum levels of alanine aminotransferase (ALT) were examined to confirm hepatic injury caused by IR surgery. The expression levels of TGF-β1, Smad3 and phosphorylated-Smad3 (p-Smad3) were detected via western blotting. Furthermore, a total of five Smad3 -/-129S2/SvPasCrl mice (Smad3 -/mice) and 10 Smad3 +/+ littermates received IR surgery, while another five Smad3 -/mice and 10 Smad3 +/+ littermates received the sham operation. Histopathological changes in liver tissues and serum levels of ALT were then compared between the groups. Furthermore, hepatic apoptosis and inflammatory cell infiltration after IR were evaluated in the liver tissues of Smad3 -/mice and Smad3 +/+ mice. The results demonstrated that the expression levels of TGF-β1, Smad3 and p-Smad3 were elevated in hepatic tissue from WT mice after IR injury. Aggravated hepatic injury, increased apoptosis and enhanced inflammatory cell infiltration induced by hepatic IR injury were observed in the Smad3 -/mice compared with in Smad3 +/+ mice. Collectively, the current findings suggested that activation of the TGF-β/Smad3 signaling pathway was present alongside the hepatic injury induced by IR. However, the TGF-β/Smad3 signaling pathway may have an effect on protecting against liver tissue damage caused by IR injury in vivo.

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“…The MI mouse model was established in accordance with a previous study [18] and speci c methods were illustrated as follows. Healthy adult C57BL/6 mice of the same age were purchased from Beijing Beike Huaxia Biomedical Technology Co., Ltd. [SYXK (Beijing) 2017-0044, Beijing, China].…”

Section: Establishment and Grouping Of MI Micementioning

confidence: 99%

“…The cardiac function of mice and its correlation with the above indexes were analyzed. TTC staining TTC staining method was as previously mentioned [18]. Following TTE, the hearts were taken out from the mice and frozen for half an h at -80°C, and then the transverse section across the left ventricular long axis from the apex to the bottom was obtained using a vibrating blade.…”

Section: Transthoracic Echocardiography (Tte)mentioning

confidence: 99%

“…Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) RT-qPCR was performed as mentioned in the reference [18].The TRIzol one-step method was employed to extract total RNA of myocardial tissues based on the instructions of TRIzol reagent (Invitrogen Inc., Carlsbad, CA). RNA was dissolved in ultrapure water treated by diethyl pyrocarbonate.…”

Section: Masson Stainingmentioning

confidence: 99%

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MicroRNA-17-5p Downregulation Inhibits Autophagy and Myocardial Remodeling after Myocardial Infarction by Targeting STAT3

Chen¹,

Yang²,

et al. 2021

Preprint

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Objective: Myocardial infarction (MI) is acknowledged as a major cause of heart disease related death in the world. This study aims to explore the function and mechanism of miR-17-5p-induced STAT3 in myocardial remodeling after MI.Methods: MI mice were infected by lentivirus antago-miR-17-5p vector. The expression of miR-17-5p in myocardial tissues was detected. The levels of STAT3 and specific markers of autophagy LC3-II/LC3-I, Beclin-1 and p62 were measured. Myocardial remodeling and scar size were assessed and cell apoptosis was determined. The binding of miR-17-5p and STAT3 was analyzed. The functions of miR-17-5p and STAT3 in autophagy and myocardial remodeling after MI were confirmed by functional rescue experiment after injecting STAT3 inhibitor S31-20.Results: Decreased fractional shortening, increased left ventricular systolic diameter and ventricular filling velocity were detected in MI mice. High expression of miR-17-5p was found in myocardial tissues after MI. The inhibition of miR-17-5p expression led to reduction of fibrosis of myocardial tissues, scarring, cardiomyocyte apoptosis, and expressions of LC3-II/LC3-I and Beclin-1, and increased p62 expression after MI. miR-17-5p targeted STAT3 and negatively regulated its expression. Inhibition of STAT3 level reversed the improving effect of antago-miR-17-5p on MI.Conclusion: Inhibition of miR-17-5p can inhibit myocardial autophagy through targeting STAT3, and then inhibit myocardial remodeling, thereby protecting myocardium after MI.

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Downregulated microRNA‐330 suppresses left ventricular remodeling via the TGF‐β1/Smad3 signaling pathway by targeting SRY in mice with myocardial ischemia–reperfusion injury

Cited by 18 publications

References 40 publications

Exosomal MicroRNAs Contribute to Cognitive Impairment in Hypertensive Patients by Decreasing Frontal Cerebrovascular Reactivity

Exosomal MicroRNAs Contribute to Cognitive Impairment in Hypertensive Patients by Decreasing Frontal Cerebrovascular Reactivity

Aggravation of hepatic ischemia‑reperfusion injury with increased inflammatory cell infiltration is associated with the TGF‑β/Smad3 signaling pathway

MicroRNA-17-5p Downregulation Inhibits Autophagy and Myocardial Remodeling after Myocardial Infarction by Targeting STAT3

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