MicroRNA-765 influences arterial stiffness through modulating apelin expression

Liao, Yi‐Chu; Wang, Yung‐Song; Hsi, Edward; Chang, Ming-Hung; You, Yun-Zhen; Juo, Suh‐Hang Hank

doi:10.1016/j.mce.2015.04.006

Cited by 24 publications

(22 citation statements)

References 35 publications

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“…In recent years, aberrant miRNA expression has been suggested to be involved in vascular dysfunction [42, 43]. Specifically, miRNA-induced vascular dysfunction increased arterial stiffness in the study by Liao et al [44]. Freedman et al reported that miR-1185 was expressed at high levels in plasma and predicted to modulate both transcription factor expression and the cell cycle [45].…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA-1185 Promotes Arterial Stiffness though Modulating VCAM-1 and E-Selectin Expression

Deng

Song

et al. 2017

Cell Physiol Biochem

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Background/Aims: Atherosclerosis is the primary cause of cardiovascular ischaemic events; arterial stiffness is a characteristic of the atherosclerotic process. MicroRNAs (miRNAs) have been revealed as crucial modulators of atherosclerosis. However, the role of arterial stiffness-related miRNAs in the atherosclerotic process is still unclear. Methods: Four hundred six participants from Northern China were enrolled in this study. Circulating miR-1185 and adhesion molecule levels were measured. Multiple linear regression models were used to evaluate the association of miR-1185 levels with brachial-ankle pulse wave velocity (baPWV) and adhesion molecule levels. A mediation analysis was also performed to examine the mediating effect. Cell adhesion molecule levels were measured in primary human umbilical vein endothelial cells (pHUVECs) and human umbilical vein smooth cells (HUVSMCs) transfected with miR-1185 or co-transfected with a miR-1185 inhibitor. Results: miR-1185 was independently correlated with arterial stiffness. A positive relationship between miR-1185 and vascular cell adhesion molecule-1 (VCAM-1) and E-selectin levels was observed. VCAM- 1 and E-selectin partially mediated the correlation between miR-1185 and arterial stiffness. miR-1185 induced a significant increase in the VCAM-1 and E-selectin levels in pHUVECs and HUVSMCs in vitro. According to our mechanistic analysis, VCAM-1 and E-selectin mediated miR-1185-induced arterial stiffening. Conclusions: miR-1185 modulated the expression of VCAM-1 and E-selectin to promote arterial stiffening, suggesting that miR-1185 plays a crucial role in the development of atherosclerosis and may serve as a novel therapeutic target for atherosclerosis.

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Section: Discussionmentioning

confidence: 99%

“…Arterial stiffness arises from a complex process involving structural alterations in the extracellular matrix (ECM) and changes in vascular tone [44]. Adhesion molecules have been shown to increase the arterial stiffness by participating in the remodelling of the ECM [35, 47].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-1185 Promotes Arterial Stiffness though Modulating VCAM-1 and E-Selectin Expression

Deng

Song

et al. 2017

Cell Physiol Biochem

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“…However, this result was not evaluated statistically because of the small sample size. A recent study showed that rs3115758, which is in LD with rs3115757, is located in a miR-765 binding site in the 3'-UTR of APLN [122]. A reporter assay confirmed that the different alleles of rs3115758 interfered with miR-765 binding and modified APLN expression [122].…”

Section: Further Adipokinesmentioning

confidence: 90%

“…A recent study showed that rs3115758, which is in LD with rs3115757, is located in a miR-765 binding site in the 3'-UTR of APLN [122]. A reporter assay confirmed that the different alleles of rs3115758 interfered with miR-765 binding and modified APLN expression [122]. This was investigated in context with arterial stiffness, but remains to be investigated in adipocytes.…”

Section: Further Adipokinesmentioning

confidence: 98%

Genetic Determination of Serum Levels of Diabetes-Associated Adipokines

Schleinitz¹

2016

Rev Diabet Stud

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■ AbstractAdipose tissue secretes an abundance of proteins. Some of these proteins are known as adipokines and adipose-derived hormones which have been linked with metabolic disorders, including type 2 diabetes, and even with cancer. Variance in serum adipokine concentration is often closely associated with an increase (obesity) or decrease (lipodystrophy) in fat tissue mass, and it is affected by age, gender, and localization of the adipose tissue. However, there may be genetic variants which, in consequence, influence the serum concentration of a certain adipokine, and thereby promote metabolic disturbances or, with regard to the "protective" allele, exert beneficial effects. This review focuses on the genetic determination of serum levels of the following adipokines: adiponectin, chemerin, leptin, progranulin, resistin, retinol binding protein 4, vaspin, adipsin, apelin, and omentin. The article reports on the latest findings from genome-wide association studies (GWAS) and candidate gene studies, showing variants located in/nearby the adipokine genes and other (non-receptor) genes. An extra chapter highlights adipokine-receptor variants. Epigenetic studies on adipokines are also addressed.

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“…This observation led Liao et al to overexpress miR-765-which interferes with apelin gene expression-in ECs to further elucidate the underlying mechanism of arterial stiffness. They found that overexpression of miR-765 reduces mRNA and protein levels of apelin, consequently inhibiting the phosphorylation of eNOS and ERK/Akt/AMPK signaling pathways [342].…”

Section: Apelinmentioning

confidence: 99%

Insights into the molecular mechanisms of diabetes-induced endothelial dysfunction: focus on oxidative stress and endothelial progenitor cells

et al. 2015

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Diabetes mellitus is a heterogeneous, multifactorial, chronic disease characterized by hyperglycemia owing to insulin insufficiency and insulin resistance (IR). Recent epidemiological studies showed that the diabetes epidemic affects 382 million people worldwide in 2013, and this figure is expected to be 600 million people by 2035. Diabetes is associated with microvascular and macrovascular complications resulting in accelerated endothelial dysfunction (ED), atherosclerosis, and cardiovascular disease (CVD). Unfortunately, the complex pathophysiology of diabetic cardiovascular damage is not fully understood. Therefore, there is a clear need to better understand the molecular pathophysiology of ED in diabetes, and consequently, better treatment options and novel efficacious therapies could be identified. In the light of recent extensive research, we re-investigate the association between diabetes-associated metabolic disturbances (IR, subclinical inflammation, dyslipidemia, hyperglycemia, dysregulated production of adipokines, defective incretin and gut hormones production/action, and oxidative stress) and ED, focusing on oxidative stress and endothelial progenitor cells (EPCs). In addition, we re-emphasize that oxidative stress is the final common pathway that transduces signals from other conditions-either directly or indirectly-leading to ED and CVD.

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MicroRNA-765 influences arterial stiffness through modulating apelin expression

Cited by 24 publications

References 35 publications

MicroRNA-1185 Promotes Arterial Stiffness though Modulating VCAM-1 and E-Selectin Expression

MicroRNA-1185 Promotes Arterial Stiffness though Modulating VCAM-1 and E-Selectin Expression

Genetic Determination of Serum Levels of Diabetes-Associated Adipokines

Insights into the molecular mechanisms of diabetes-induced endothelial dysfunction: focus on oxidative stress and endothelial progenitor cells

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