Facilitatory effects of fetuin-A on atherosclerosis

Naito, C; H, Mio; Watanabe, K.; Shirai, Ryuichi; Takahashi, Yasuhiro; Kojima, Miho; Watanabe, Ryoji; Sato, Kengo; Iso, Yoshitaka; Matsuyama, Taka‐aki; Suzuki, Hiroshi; Ishibashi‐Ueda, Hatsue; Watanabe, Takuya

doi:10.1016/j.atherosclerosis.2016.01.037

Cited by 52 publications

(71 citation statements)

References 47 publications

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“…The increase or the decrease of the fetuin-A level is linked to the pathogenesis of multiple disorders such as atherosclerosis. 22 Naito et al 23 found that fetuin-A contributes to atherosclerosis through a proinflammatory effect on endothelial cells of the human umbilical vein. Fetuin-A stimulates macrophage to form foam cell and trigger proliferation and production of collagen in human aortic smooth muscle cells.…”

Section: Discussionmentioning

confidence: 99%

Usefulness of serum fetuin-A level as a marker of erectile dysfunction

et al. 2017

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This study aimed to evaluate the correlation between serum levels of fetuin-A and the presence and severity of erectile dysfunction (ED) in Egyptian population. The study was performed on 60 ED patients and 20 age-matched healthy controls. A comprehensive medical history and complete physical examination were obtained and performed in all participants. ED and its severity were assessed via International Index of Erectile Function (IIEF-5). Doppler ultrasound, fasting blood glucose level, complete lipid profile, serum total testosterone (TT) and serum fetuin-A were performed. Our results revealed that there were no statistically significant differences between the ED group and the controls regarding body mass index, fetal bovine serum, cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL) and triglyceride (TG). However, IIEF-5 and serum TT levels were significantly lower in ED patients than controls. Regarding serum fetuin-A, our data demonstrated that ED patients had significantly lower serum fetuin-A levels than controls. In addition, patients with severe ED had lower fetuin-A levels than moderate and mild ED (P<0.001). Serum fetuin-A levels are positively correlated with cholesterol, LDL, TG and IIEF-5 and negatively correlated with HDL. In conclusion, serum fetuin-A level could be a potentially useful and sensitive biomarker for ED diagnosis.

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Section: Discussionmentioning

confidence: 99%

Usefulness of serum fetuin-A level as a marker of erectile dysfunction

et al. 2017

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“…Ethical approval was from the Tokyo University of Pharmacy and Life Sciences (Tokyo, Japan), with written informed consent obtained from all participants before blood draws. Human peripheral mononuclear cells were isolated from the blood of 20 healthy volunteers (8 male, 12 female; aged [19][20][21][22][23][24][25]. Monocytes were purified using anti-CD14 antibodyconjugated magnetic microbeads (Miltenyi Biotec, Cambridge, MA).…”

Section: Methods Human Monocyte Primary Culturementioning

confidence: 99%

“…The mRNAs for TNF-a, IL-6, MCP-1, ICAM-1, VCAM-1, E-selectin, and glyceraldehyde-3-dehydrogenase were detected as described previously. [21][22][23]…”

Section: Reverse-transcription Polymerase Chain Reactionmentioning

confidence: 99%

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Potent Vasoconstrictor Kisspeptin‐10 Induces Atherosclerotic Plaque Progression and Instability: Reversal by its Receptor GPR54 Antagonist

Sato

Shirai

Hontani

et al. 2017

JAHA

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BackgroundKisspeptin‐10 (KP‐10), a potent vasoconstrictor and inhibitor of angiogenesis, and its receptor, GPR54, have currently received much attention in relation to pre‐eclampsia. However, it still remains unknown whether KP‐10 could affect atherogenesis.Methods and ResultsWe evaluated the effects of KP‐10 on human umbilical vein endothelial cells, human monocyte‐derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E–deficient (ApoE−/−) mice in vivo. KP‐10 significantly increased the adhesion of human monocytes to human umbilical vein endothelial cells, which was significantly inhibited by pretreatment with P234, a GPR54 antagonist. KP‐10 stimulated mRNA expression of tumor necrosis factor‐α, interleukin‐6, monocyte chemotactic protein‐1, intercellular adhesion molecule‐1, vascular adhesion molecule‐1, and E‐selectin in human umbilical vein endothelial cells. KP‐10 significantly enhanced oxidized low‐density lipoprotein–induced foam cell formation associated with upregulation of CD36 and acyl‐CoA:cholesterol acyltransferase‐1 in human monocyte‐derived macrophages. In human aortic smooth muscle cells, KP‐10 significantly suppressed angiotensin II–induced migration and proliferation, but enhanced apoptosis and activities of matrix metalloproteinase (MMP)‐2 and MMP‐9 by upregulation of extracellular signal‐regulated kinase 1 and 2, p38, Bcl‐2‐associated X protein, and caspase‐3. Four‐week‐infusion of KP‐10 into ApoE−/− mice significantly accelerated the development of aortic atherosclerotic lesions with increased monocyte/macrophage infiltration and vascular inflammation as well as decreased intraplaque vascular smooth muscle cells contents. Proatherosclerotic effects of endogenous and exogenous KP‐10 were completely canceled by P234 infusion in ApoE−/− mice.ConclusionsOur results suggest that KP‐10 may contribute to accelerate the progression and instability of atheromatous plaques, leading to plaque rupture. The GPR54 antagonist may be useful for prevention and treatment of atherosclerosis. Thus, the KP‐10/GPR54 system may serve as a novel therapeutic target for atherosclerotic diseases.

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“…Fetuin-A is a multifunctional protein whose major physiological role is the inhibition of ectopic calcification [10]. It has also been implicated in metabolic syndromes such as diabetes where it modulates the insulin receptor thereby altering insulin sensitivity [11,12] and myocardial infarction where it plays a role in the maturation of atherosclerotic plaques [13,14]. We reported that PyMT + transgenic mice that also lacked fetuin-A, had reduced mammary tumor incidence and prolonged tumor latency via the TGF-beta signaling [15].…”

Section: Original Researchmentioning

confidence: 99%

Fetuin‐A (alpha 2HS glycoprotein) modulates growth, motility, invasion, and senescence in high‐grade astrocytomas

et al. 2016

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Glioblastomas (high‐grade astrocytomas) are highly aggressive brain tumors with poor prognosis and limited treatment options. In the present studies, we have defined the role of fetuin‐A, a liver‐derived multifunctional serum protein, in the growth of an established glioblastoma cell line, LN229. We hereby demonstrate that these cells synthesize ectopic fetuin‐A which supports their growth in culture in the absence of serum. We have demonstrated that a panel of tissue microarray (TMA) of glioblastomas also express ectopic fetuin‐A. Knocking down fetuin‐A using shRNA approach in LN229, significantly reduced their in vitro growth as well as growth and invasion in vivo. The fetuin‐A knockdown subclones of LN229 (A and D) also had reduced motility and invasive capacity. Treatment of LN229 cells with asialofetuin (ASF), attenuated their uptake of labeled fetuin‐A, and induced senescence in them. Interestingly, the D subclone that had ~90% reduction in ectopic fetuin‐A, underwent senescence in serum‐free medium which was blunted in the presence of purified fetuin‐A. Uptake of labeled exosomes was attenuated in fetuin‐A knockdown subclones A and D. Taken together, the studies demonstrate the impact of fetuin‐A as significant node of growth, motility, and invasion signaling in glioblastomas that can be targeted for therapy.

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Facilitatory effects of fetuin-A on atherosclerosis

Cited by 52 publications

References 47 publications

Usefulness of serum fetuin-A level as a marker of erectile dysfunction

Usefulness of serum fetuin-A level as a marker of erectile dysfunction

Potent Vasoconstrictor Kisspeptin‐10 Induces Atherosclerotic Plaque Progression and Instability: Reversal by its Receptor GPR54 Antagonist

Fetuin‐A (alpha 2HS glycoprotein) modulates growth, motility, invasion, and senescence in high‐grade astrocytomas

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