MiR-143-3p targets ATG2B to inhibit autophagy and promote endothelial progenitor cells tube formation in deep vein thrombosis

Zhang, Wangao; Chen, Pengju; Zong, Huimin; Ding, Yikun; Yan, Ruhu

doi:10.1016/j.tice.2020.101453

Cited by 9 publications

(7 citation statements)

References 39 publications

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“…In addition, miR-143-3p was found to be of high diagnostic value for the screening of VD patients. Moreover, aberrant miR-143-3p expression has been shown to be involved in other diseases, such as ovarian cancer (Shi et al, 2018) and deep vein thrombosis (Zhang et al, 2020). Thus, we suggested that the upregulated miR-143-3p might be involved in the progression of VD.…”

Section: Discussionmentioning

confidence: 61%

Acupuncture attenuates cognitive impairments in vascular dementia through inhibiting miR-143-3p

Yang

Huang

2022

Acta Biochim Pol

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Background: Acupuncture can be used to treat vascular dementia (VD), but the underlying mechanism remains unclear. This study aimed to investigate the expression and clinical significance of microRNA-143-3p (miR-143-3p) in VD patients and explore whether acupuncture ameliorates VD by regulating miR-143-3p. Methods: Cognitive function and daily living ability in VD patients were assessed by mini-mental state examination, Hasegawa’s dementia scale and activities of daily living scale, respectively. VD model of male Wistar rats was established using permanent bilateral common carotid artery occlusion. The expression level of miR-143-3p was measured by quantitative real-time PCR. Morris water maze test was used to assess the cognitive function of VD rat model. Receiver operating characteristic analysis was used to assess the diagnostic value of miR-143-3p in VD patients. Correlations between variables were analyzed by Pearson’s correlation analysis. Results: Increased serum miR-143-3p expression in VD patients had a high diagnostic value to screen VD patients. Serum miR-143-3p level in VD patients after acupuncture treatment was decreased. After acupuncture treatment, serum miR-143-3p was negatively correlated with cognitive function and daily living ability in VD patients. miR-143-3p level was increased in VD rats, and the suppressive effects of acupuncture on miR-143-3p levels were relieved by miR-143-3p mimic. Overexpression of miR-143-3p reversed the ameliorative effect of acupuncture on cognitive functions of VD rats. Conclusion: Serum miR-143-3p expression is upregulated in VD patients and downregulated in VD patients after acupuncture treatment. Additionally, acupuncture treatment may attenuate cognitive impairments in VD by suppressing miR-143-3p.

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Section: Discussionmentioning

confidence: 61%

Acupuncture attenuates cognitive impairments in vascular dementia through inhibiting miR-143-3p

Yang

Huang

2022

Acta Biochim Pol

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“…Previous studies have demonstrated that autophagy could either negatively or positively regulate cell proliferation, migration, and angiogenesis [ 40 ]. For example, miR-143-3p targets autophagy-related 2B (ATG2B) to suppress autophagy and thereby promotes EPC viability, migration, and tube formation [ 14 ]. miR-195 inhibits autophagy and thereby attenuates EPC proliferation, migration, and angiogenesis via targeting GABA type A receptor-associated protein-like 1 (GABARAPL1) [ 12 ].…”

Section: Discussionmentioning

confidence: 99%

“…MicroRNAs (miRNAs) are small noncoding RNAs of 21-24 nucleotide long, which participate in posttranscriptional modulation of gene expression through suppressing RNA translation or facilitating mRNA degradation [ 11 ]. Numerous miRNAs including miR-143-3p, miR-195, and miR-130a-3p play pivotal roles in modulating the functions of EPCs such as cell proliferation, migration, angiogenesis, and autophagy and further influencing DVT recanalization and resolution [ 12 – 14 ]. miR-206 was reported to be implicated in the pathogenesis of many cardiovascular disorders, such as atherosclerosis, pulmonary arterial hypertension, and coronary artery disease (CAD) [ 15 – 18 ].…”

Section: Introductionmentioning

confidence: 99%

Upregulated miR-206 Aggravates Deep Vein Thrombosis by Regulating GJA1-Mediated Autophagy of Endothelial Progenitor Cells

Yin

et al. 2022

Cardiovascular Therapeutics

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Background. Deep vein thrombosis (DVT) is the third most prevalent vascular disease worldwide. MicroRNAs (miRNAs) play regulatory roles in functions of endothelial progenitor cells (EPCs), which is becoming a promising therapeutic choice for thrombus resolution. Nevertheless, the role of miR-206 in EPCs is unclear. Methods. EPCs were isolated from the peripheral blood of patients with DVT. In DVT mouse models, DVT was induced by stenosis of the inferior vena cava (IVC). The levels of miR-206 and gap junction protein alpha 1 (GJA1) in EPCs and vascular tissues of DVT mice were detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The proliferation, migration, apoptosis, and angiogenesis were tested by cell counting kit-8 (CCK-8) assay, Transwell assay, flow cytometry analysis, and in vitro tube formation assay. The levels of autophagy-related proteins as well as the level of GJA1 in EPCs and vascular tissues were evaluated by western blotting. DVT formation in vivo was observed through hematoxylin-eosin (HE) staining. The expression of thrombus resolution markers, CD34 molecule (CD34) and matrix metallopeptidase 2 (MMP2), in the thrombi was measured by immunofluorescence staining. Results. miR-206 overexpression inhibited proliferation, migration, and angiogenesis and promoted apoptosis of EPCs, while miR-206 knockdown exerted an opposite effect on EPC phenotypes. Downregulation of GJA1, the target of miR-206, abolished the influence of miR-206 on EPC phenotypes. Furthermore, silencing of miR-206 suppressed the autophagy of EPCs via upregulating GJA1. miR-206 knockdown repressed thrombus formation, enhanced the homing ability of EPCs to the thrombosis site, and facilitated thrombus resolution in DVT mouse models. Additionally, miR-206 was upregulated while GJA1 was downregulated in vascular tissues of DVT mice. miR-206 knockdown elevated GJA1 expression in vascular tissues of DVT mice. The expression of miR-206 was negatively correlated with that of GJA1 in DVT mice. Conclusion. miR-206 knockdown upregulates GJA1 to inhibit autophagy of EPCs and then promote EPC proliferation, migration, and angiogenesis, thereby enhancing EPC homing to thrombi and facilitating thrombus resolution.

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“…Furthermore, inhibition of xCT (encoded by slc7a11 ), a cystine/glutamate antiporter that relies on autophagy machinery to import cystine, could deprive the pathogen of cysteine, an amino acid essential to its growth (55, 60, 61). Finally, although this needs to be confirmed in macrophages, overexpression of miR-143-3p in human endothelial progenitor cells decreased LC3-II and increased p62 levels, two phenotypes that strongly imply a role for miR-143-3p in dampening autophagic flux (62). Cumulatively, our data suggest that down-regulation of miR-143-3p during C. burnetii infection promotes intracellular growth of the pathogen by delaying apoptosis and promoting autophagy.…”

Section: Discussionmentioning

confidence: 99%

MicroRNAs contribute to the host response to Coxiella burnetii

Sachan

Brann

Voth

et al. 2022

Preprint

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MicroRNAs (miRNAs), a class of small non-coding RNAs, are critical to gene regulation in eukaryotes. They are involved in modulating a variety of physiological processes, including the host response to intracellular infections. Little is known about miRNA functions during infection by Coxiella burnetii, the causative agent of human Q fever. This bacterial pathogen establishes a large replicative vacuole within macrophages by manipulating host processes such as apoptosis and autophagy. We investigated miRNA expression in C. burnetii-infected macrophages and identified several miRNAs that were down- or up-regulated during infection. We further explored the functions of miR-143-3p, an miRNA whose expression is down-regulated in macrophages infected with C. burnetii, and show that increasing the abundance of this miRNA in human cells results in increased apoptosis and reduced autophagy – conditions that are unfavorable to C. burnetii intracellular growth. In sum, this study demonstrates that C. burnetii infection elicits a robust miRNA-based host response, and because miR-143-3p promotes apoptosis and inhibits autophagy, down-regulation of miR-143-3p expression during C. burnetii infection likely benefits the pathogen.

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MiR-143-3p targets ATG2B to inhibit autophagy and promote endothelial progenitor cells tube formation in deep vein thrombosis

Cited by 9 publications

References 39 publications

Acupuncture attenuates cognitive impairments in vascular dementia through inhibiting miR-143-3p

Acupuncture attenuates cognitive impairments in vascular dementia through inhibiting miR-143-3p

Upregulated miR-206 Aggravates Deep Vein Thrombosis by Regulating GJA1-Mediated Autophagy of Endothelial Progenitor Cells

MicroRNAs contribute to the host response to Coxiella burnetii

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