14-3-3 mediates apelin-13-induced enhancement of adhesion of monocytes to human umbilical vein endothelial cells

Li, Xin; Zhang, Xianhui; Li, Fang; Chen, Linxi; Li, Lanfang; Qin, Xu; Gao, Jing; Su, Tao; Zeng, Yi-Xin; Liao, Duan‐Fang

doi:10.1093/abbs/gmq036

Cited by 30 publications

(22 citation statements)

References 40 publications

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“…Our previous studies also showed that apelin-13 induced the expression of 14-3-3 in concentrationand time-dependent manners [24]. Furthermore, the potent 14-3-3 inhibitor difopein significantly reduced the expression of 14-3-3 and VCAM-1 in apelin-13-stimulated HUVECs, and extremely inhibited the effect of apelin-13 on induction of MCs adhesion to HUVECs [24]. The apelin/ APJ system in endothelial cells is involved in the expression of adhesion molecules and chemokines, which is essential for the initiation of endothelial inflammation-related AS.…”

Section: Apelin Induces Adhesion Of Monocytes-endothelial Cells By Inmentioning

confidence: 69%

“…Lu et al [23] reported similar results that the expression of intercellular adhesion molecule-1, VCAM-1, and monocyte chemoattractant protein-1 (MCP-1) in HUVECs is significantly increased when treated with apelin. Our previous studies also showed that apelin-13 induced the expression of 14-3-3 in concentrationand time-dependent manners [24]. Furthermore, the potent 14-3-3 inhibitor difopein significantly reduced the expression of 14-3-3 and VCAM-1 in apelin-13-stimulated HUVECs, and extremely inhibited the effect of apelin-13 on induction of MCs adhesion to HUVECs [24].…”

Section: Apelin Induces Adhesion Of Monocytes-endothelial Cells By Inmentioning

confidence: 81%

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Apelin and APJ, a novel critical factor and therapeutic target for atherosclerosis

Lv¹,

Li²,

Chen³

2013

ABBS

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Apelin is a bioactive peptide discovered recently that has been proved to be an endogenous ligand of the APJ receptor. Apelin and APJ are widely distributed in the central nervous system and peripheral tissues. Researches have confirmed that apelin/APJ involved in a wide range of physiological and pathological functions in the cardiovascular system. Investigations indicated that apelin is a novel critical factor in the development of atherosclerosis (AS). In this review, we discuss the roles of apelin in the vascular smooth muscle cell proliferation, monocytes-endothelial cell adhesion, and angiogenesis that potentially reveals a new cellular mechanism of AS. Considering these roles, apelin and APJ may be novel therapeutic targets of AS.

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Section: Apelin Induces Adhesion Of Monocytes-endothelial Cells By Inmentioning

confidence: 69%

Section: Apelin Induces Adhesion Of Monocytes-endothelial Cells By Inmentioning

confidence: 81%

Apelin and APJ, a novel critical factor and therapeutic target for atherosclerosis

Lv¹,

Li²,

Chen³

2013

ABBS

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“…It is knowledgeable that adhesion, proliferation [53][54][55] , migration [56] and autophagy [57,58] are the characteristics of cells [59][60][61] . [61] .…”

Section: Endoplasmic Reticulum Stress Regulates Cardiovascular Physiomentioning

confidence: 99%

“…Their new effects were identified recently. For example, Guan et al [53] discovered that telmisartan reduced ERS and thereby attenuated both apoptosis and cardiac hypertrophy. Telmisartan significantly reduced LVH and interstitial fibrosis, thus improving left ventricular function compared with AAC alone.…”

Section: Endoplasmic Reticulum Stress Is Involved In the Development mentioning

confidence: 99%

Endoplasmic reticulum stress: a novel mechanism and therapeutic target for cardiovascular diseases

2016

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Endoplasmic reticulum is a principal organelle responsible for folding, post-translational modifications and transport of secretory, luminal and membrane proteins, thus palys an important rale in maintaining cellular homeostasis. Endoplasmic reticulum stress (ERS) is a condition that is accelerated by accumulation of unfolded/misfolded proteins after endoplasmic reticulum environment disturbance, triggered by a variety of physiological and pathological factors, such as nutrient deprivation, altered glycosylation, calcium depletion, oxidative stress, DNA damage and energy disturbance, etc. ERS may initiate the unfolded protein response (UPR) to restore cellular homeostasis or lead to apoptosis. Numerous studies have clarified the link between ERS and cardiovascular diseases. This review focuses on ERS-associated molecular mechanisms that participate in physiological and pathophysiological processes of heart and blood vessels. In addition, a number of drugs that regulate ERS was introduced, which may be used to treat cardiovascular diseases. This review may open new avenues for studying the pathogenesis of cardiovascular diseases and discovering novel drugs targeting ERS.

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“…But Hashimoto et al [13] demonstrated that apelin/APJ system is the mediator of oxidative stress-linked AS in vascular tissue. Although apelin-13 is possibly a novel risk factor for AS occurrence and development by promoting vascular smooth muscle cell proliferation [14] and monocytes-endothelial cell adhesion [15], the mechanism of apelin on AS are still unclear. Further experiments are necessary to clarify the effect of apelin on AS, and miRNA is an excellent research strategy [16].…”

mentioning

confidence: 99%

Unanticipated role of apelin: regulation of miRNA generation

Lv¹,

Lu²,

Cao³

et al. 2013

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14-3-3 mediates apelin-13-induced enhancement of adhesion of monocytes to human umbilical vein endothelial cells

Cited by 30 publications

References 40 publications

Apelin and APJ, a novel critical factor and therapeutic target for atherosclerosis

Apelin and APJ, a novel critical factor and therapeutic target for atherosclerosis

Endoplasmic reticulum stress: a novel mechanism and therapeutic target for cardiovascular diseases

Unanticipated role of apelin: regulation of miRNA generation

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