Elevated Plasma miR-29a Levels Are Associated with Increased Carotid Intima-Media Thickness in Atherosclerosis Patients

Liu, Cuizhong; Zhong, Qi; Huang, Yu-Qing

doi:10.1620/tjem.241.183

Cited by 14 publications

(11 citation statements)

References 39 publications

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“…Our study was aimed to link miRNA regulation with lipid overload and the immunoinflammatory mechanism of AS. Many recent studies have found that miR-29a was involved in numerous biological processes, including AS (Liu et al, 2017), hepatocellular carcinoma (Parpart et al, 2014), myocardial fibrosis (Dai et al, 2014), glucose handling (Dooley et al, 2016), and so on. Nowadays, researchers have found that plasma miR-29a was a new biomarker that could play a role in the pathophysiology of AS (Hulsmans and Holvoet, 2013;Huang et al, 2016;Liu et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

“…Many recent studies have found that miR-29a was involved in numerous biological processes, including AS (Liu et al, 2017), hepatocellular carcinoma (Parpart et al, 2014), myocardial fibrosis (Dai et al, 2014), glucose handling (Dooley et al, 2016), and so on. Nowadays, researchers have found that plasma miR-29a was a new biomarker that could play a role in the pathophysiology of AS (Hulsmans and Holvoet, 2013;Huang et al, 2016;Liu et al, 2017). Previous studies also revealed that miR-29a plays important roles in the development of AS by regulating ox-LDL increases miR-29a transcription in macrophages D. Jian et al types I and III collagens, and the usage of miR-29 antagonists may prevent plaque remodeling (Ulrich et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

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ox‐LDL increases microRNA‐29a transcription through upregulating YY1 and STAT1 in macrophages

Jian

Dai

Yao

et al. 2017

Cell Biology International

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Macrophages and oxidized low-density lipoprotein (ox-LDL) have been verified playing vital roles in the pathogenesis of atherosclerosis (AS). Previous studies demonstrated that microRNA-29a (miR-29a) was upregulated in many atherogenic process and cells, thus acting as an important participant in AS. But the detailed regulation mechanism of miR-29a in AS has not been fully understood. In our study, we demonstrated a positive feedback loop of ox-LDL-SRA-miR-29a. Furthermore, we found that YY1 and STAT1 were upregulated in ox-LDL-stimulating macrophages followed by translocation in the nucleus and binding to the transcriptional promoter region of miR-29a, thus leading to the increase of miR-29a expression. In addition, we demonstrated that JAK1/2 signaling was involved in miR-29a upregulation. Finally, we found that miR-29a played important roles in the secretion of proinflammation factors and lipid uptake in macrophages. We uncovered the molecular mechanism and provide novel insights into the function and regulatory network of miR-29a expression regulated by ox-LDL in macrophages.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

ox‐LDL increases microRNA‐29a transcription through upregulating YY1 and STAT1 in macrophages

Jian

Dai

Yao

et al. 2017

Cell Biology International

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“…miRNA-22 regulates inflammation and angiogenesis by targeting VE-cadherin [ 61 ], and miRNA-29a can modulate the angiogenic properties of human endothelial cells [ 19 ] and be upregulated by proinflammatory cytokine transforming growth factor- β (TGF- β ) [ 62 ]. The miRNA is also involved in neuron growth [ 63 ] and atherosclerosis formation [ 64 ]. An in vitro study found that miRNA-29a overexpression promoted the formation of new blood vessels, while miR-29a suppression completely blocked TGF- β 1-stimulated angiogenesis [ 62 ].…”

Section: Discussionmentioning

confidence: 99%

Vascular Inflammation Is a Risk Factor Associated with Brain Atrophy and Disease Severity in Parkinson’s Disease: A Case-Control Study

Chen

et al. 2020

Oxidative Medicine and Cellular Longevity

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Introduction. Systemic inflammation with elevated oxidative stress causing neuroinflammation is considered a major factor in the pathogenesis of Parkinson’s disease (PD). The interface between systemic circulation and the brain parenchyma is the blood-brain barrier (BBB), which also plays a role in maintaining neurovascular homeostasis. Vascular cell adhesion molecule-1 (VCAM-1) and microRNAs (miRNAs) regulate brain vessel endothelial function, neoangiogenesis, and, in turn, neuronal homeostasis regulation, such that their dysregulation can result in neurodegeneration, such as gray matter atrophy, in PD. Objective. Our aim was to evaluate the associations among specific levels of gray matter atrophy, peripheral vascular adhesion molecules, miRNAs, and clinical disease severity in order to achieve a clearer understanding of PD pathogenesis. Methods. Blood samples were collected from 33 patients with PD and 27 healthy volunteers, and the levels of VCAM-1 and several miRNAs in those samples were measured. Voxel-based morphometry (VBM) analysis was performed using 3 T magnetic resonance imaging (MRI) and SPM (Statistical Parametric Mapping software program). The associations among the vascular parameter, miRNAs, gray matter volume, and clinical disease severity measurements were evaluated by partial correlation analysis. Results. The levels of VCAM-1, miRNA-22, and miRNA-29a expression were significantly elevated in the PD patients. The gray matter volume atrophy in the left parahippocampus, bilateral posterior cingulate gyrus, fusiform gyrus, left temporal gyrus, and cerebellum was significantly correlated with increased clinical disease severity, the upregulation of miRNA levels, and increased vascular inflammation. Conclusion. Patients with PD seem to have abnormal levels of vascular inflammatory markers and miRNAs in the peripheral circulation, and these levels are correlated with specific brain volume changes. This study reinforces the associations among peripheral inflammation, the BBB interface, and gray matter atrophy in PD and further demonstrates that BBB dysfunction with neurovascular impairment may play an important role in PD progression.

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“…In this study, the angiogenesis-related miRNA-29a and miRNA-22 were up-regulated in the PD patients, suggesting an underlying and ongoing angiogenesis process. MiRNA-22 regulates inflammation and angiogenesis by targeting VEcadherin [53] and miRNA-29a can modulate the angiogenic properties of human endothelial cells [19] and be upregulated by proinflammatory cytokine transforming growth factor β (TGF-β) [54].The miRNA is also involved in neuron growth [55] and atherosclerosis formation [56].An in vitro study found that miRNA-29a overexpression promoted the formation of new blood vessels, while miR-29a suppression completely blocked TGF-β1-stimulated angiogenesis [54]. TGF-β1 expression was increased in striatal neurons and in activated microglia on the lesion side of a 6-hydroxydopamineinduced PD mouse model in one in vivo study [57] and was elevated in the CSF fluid of PD patients in an in vitro study, indicating that it acts as a neuroprotective factor in injured brains.…”

Section: Vcam-1 and Mirna Profiles As Vascular Inflammation Indicatormentioning

confidence: 99%

Vascular inflammation is a risk factor associated with brain atrophy and disease severity in Parkinson’s disease: a case-control study

Chen

et al. 2019

Preprint

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Background: Systemic inflammation with elevated oxidative stress causing neuroinflammation is considered a major factor in the pathogenesis of Parkinson’s disease (PD).The interface between systemic circulation and the brain parenchyma is the blood - brain barrier (BBB), which also plays a role in maintaining neurovascular homeostasis. Relatedly, intermediate vascular inflammation causing BBB dysfunction is a key component of PD pathogenesis. Vascular cell adhesion molecule-1 (VCAM-1) and microRNAs (miRNAs) regulate brain endothelial function, neoangiogenesis, and, in turn, neuronal homeostasis regulation, such that their dysregulation can result in neurodegeneration, such as gray matter atrophy, in PD. In this study, our aim was to evaluate the associations among specific levels of gray matter atrophy, peripheral vascular adhesion molecules, miRNAs, and clinical disease severity in order to achieve a clearer understanding of PD pathogenesis.Methods: Blood samples were collected from 33 patients with PD and 27 healthy volunteers, and the levels of VCAM-1 and several miRNAs in those samples were measured. Voxel-based morphometry (VBM) analysis was performed using 3T magnetic resonance imaging (MRI) and SPM (Statistical Parametric Mapping software program). The associations among the vascular parameter, miRNAs, gray matter volume and clinical disease severity measurements were evaluated by partial correlation analysis.Results: The levels of VCAM-1, miRNA-22 and miRNA-29a expression were significantly elevated in the PD patients. The gray matter volume atrophy in the left parahippocampus, bilateral posterior cingulate gyrus, fusiform gyrus, left temporal gyrus, and cerebellum was significantly correlated with increased clinical disease severity, the upregulation of miRNA levels, and increased vascular inflammation.Conclusions: Patients with PD seem to have abnormal levels of vascular inflammatory markers and miRNAs in the peripheral circulation, and these levels are correlated with specific brain volume changes. This study reinforces the associations among peripheral inflammation, the BBB interface, and gray matter atrophy in PD, and further demonstrates that BBB dysfunction with neurovascular impairment may play an important role in PD progression.

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Elevated Plasma miR-29a Levels Are Associated with Increased Carotid Intima-Media Thickness in Atherosclerosis Patients

Cited by 14 publications

References 39 publications

ox‐LDL increases microRNA‐29a transcription through upregulating YY1 and STAT1 in macrophages

ox‐LDL increases microRNA‐29a transcription through upregulating YY1 and STAT1 in macrophages

Vascular Inflammation Is a Risk Factor Associated with Brain Atrophy and Disease Severity in Parkinson’s Disease: A Case-Control Study

Vascular inflammation is a risk factor associated with brain atrophy and disease severity in Parkinson’s disease: a case-control study

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