Perivascular adipose tissue-derived visfatin is a vascular smooth muscle cell growth factor: role of nicotinamide mononucleotide

Wang, Pei; Xu, Tao; Guan, Yongjun; Su, Ding‐Feng; Fan, Guorong; Miao, Chao‐Yu

doi:10.1093/cvr/cvn288

Cited by 276 publications

(271 citation statements)

References 26 publications

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“…In line with our observations, Wang et al have recently reported that exogenous NMN, at the same concentration used in this study, mimics the proliferative action of ePBEF/NAMPT/visfatin in rat vascular smooth muscle [18]. Here, we demonstrate that extracellular NMN can also be considered as a proinflammatory agent for human vascular smooth muscle.…”

Section: Discussionsupporting

confidence: 93%

“…Furthermore, other cellular effects triggered by ePBEF/NAMPT/visfatin, including the secretion of IL-8 and TNF-α by human peripheral blood mononuclear cells [23] and the uptake of glucose in rat mesangial cells [27], also seem to involve the insulin receptor. Other studies, however, have discarded a role for this receptor in mediating the actions of ePBEF/NAMPT/ visfatin in a wide range of cell types, including vascular cells, macrophages and pancreatic beta cells [11,14,18,28]. The results presented herein do not support a role for the insulin receptor in mediating the pro-inflammatory action of ePBEF/NAMPT/visfatin in human vascular smooth muscle cells.…”

Section: Discussioncontrasting

confidence: 83%

“…On the one hand, intracellular PBEF/NAMPT/visfatin has been reported to induce maturation [16] and to extend the lifespan of human vascular smooth muscle cells by activating members of the sirtuin family and restraining the accumulation of p53 [17]. On the other hand, ePBEF/ NAMPT/visfatin, released by different cells and tissues including the visceral and perivascular adipose tissue, can reach vascular smooth muscle and behave as a growth factor for this cell type [18]. In the present study, we have further identified ePBEF/NAMPT/visfatin as a proinflammatory factor for vascular smooth muscle cells.…”

Section: Discussionmentioning

confidence: 99%

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Extracellular PBEF/NAMPT/visfatin activates pro-inflammatory signalling in human vascular smooth muscle cells through nicotinamide phosphoribosyltransferase activity

et al. 2009

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Aims/hypothesis Extracellular pre-B cell colony-enhancing factor/nicotinamide phosphoribosyltransferase/visfatin (ePBEF/NAMPT/visfatin) is an adipocytokine, whose circulating levels are enhanced in metabolic disorders, such as diabetes mellitus and obesity. Here, we explored the ability of ePBEF/NAMPT/visfatin to promote vascular inflammation, as a condition closely related to atherothrombotic diseases. We specifically studied the ability of PBEF/ NAMPT/visfatin to directly activate pathways leading to inducible nitric oxide synthase (iNOS) induction in cultured human aortic smooth muscle cells, as well as the mechanisms involved. Methods iNOS levels and extracellular signal-regulated kinase (ERK) 1/2 activity were determined by western blotting. Nuclear factor (NF)-κB activity was assessed by electrophoretic mobility shift assay. Results ePBEF/NAMPT/visfatin (10-250 ng/ml) induced iNOS in a concentration-dependent manner. At a submaximal concentration (100 ng/ml), ePBEF/NAMPT/visfatin time-dependently enhanced iNOS levels up to 18 h after stimulation. Over this time period, ePBEF/NAMPT/visfatin elicited a sustained activation of NF-κB and triggered a biphasic ERK 1/2 activation. By using the respective ERK 1/2 and NF-κB inhibitors, PD98059 and pyrrolidine dithiocarbamate, we established that iNOS induction by ePBEF/NAMPT/visfatin required the consecutive upstream activation of ERK 1/2 and NF-κB. The pro-inflammatory action of ePBEF/NAMPT/visfatin was not prevented by insulin receptor blockade. However, exogenous nicotinamide mononucleotide, the product of NAMPT activity, mimicked NF-κB activation and iNOS induction by ePBEF/NAMPT/visfatin, while the NAMPT inhibitor APO866 prevented the effects of ePBEF/NAMPT/visfatin on iNOS and NF-κB. Conclusions/interpretation Through its intrinsic NAMPT activity, ePBEF/NAMPT/visfatin appears to be a direct contributor to vascular inflammation, a key feature of atherothrombotic diseases linked to metabolic disorders.

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Section: Discussionsupporting

confidence: 93%

Section: Discussioncontrasting

confidence: 83%

Section: Discussionmentioning

confidence: 99%

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Extracellular PBEF/NAMPT/visfatin activates pro-inflammatory signalling in human vascular smooth muscle cells through nicotinamide phosphoribosyltransferase activity

et al. 2009

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“…Revollo et al (11) have demonstrated that visfatin regulates insulin secretion in pancreatic β-cells through its intrinsic NAMPT enzymatic activity. Wang et al (27) have reported that visfatin stimulates vascular smooth muscle cell proliferation via the NMN-mediated ERK1/2 and p38 signaling. In a recent study, Romacho et al (10) have shown that NAMPT activity is involved in visfatin's pro-inflammatory action in smooth muscle cells.…”

Section: Discussionmentioning

confidence: 99%

Visfatin/PBEF/Nampt induces EMMPRIN and MMP-9 production in macrophages via the NAMPT-MAPK (p38, ERK1/2)-NF-κB signaling pathway

Fan

Meng²,

Wang³

et al. 2011

Int J Mol Med

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Abstract. The adipocytokine visfatin is closely associated with metabolic disorders. This study explored the effects of visfatin on macrophage-induced inflammation in atheroma. The ability of visfatin to enhance extracellular matrix metalloproteinase inducer (EMMPRIN) expression, matrix metalloproteinase-9 (MMP-9) production and enzymatic activity in THP-1 derived macrophages as well as the mechanisms involved were investigated. EMMPRIN and MMP-9 mRNA levels were investigated by RT-PcR. EMMPRIN and MMP-9 protein levels, nuclear factor (NF)-κB -p65 protein levels, peroxisome proliferator-activated receptor γ (PPARγ) protein levels, and mitogen-activated protein kinase (MAPK) phosphorylation were determined by Western blotting. MMP-9 enzymatic activity was assayed by gelatin zymography. Visfatin (50-400 ng/ml) induced EMMPRIN and MMP-9 depending on the dosage used. Visfatin elicited the activation of NF-κB and MAPK (p38, ERK1/2). Exogenous nicotinamide mononucleotide (NMN), the product of nicotinamide phosphoribosyltransferase (NAMPT) activity, mimicked the effects of visfatin on MAPK (p38, ERK1/2)-NF-κB activation and EMMPRIN/MMP-9 induction. Using the p38 inhibitor, SB203580, the ERK1/2 inhibitor Pd98059, the NF-κB inhibitor, pyrrolidine dithiocarbamate and the NAMPT inhibitor FK866, we demonstrated that the visfatin pro-inflammatory action was through the NAMPT-MAPK (p38, ERK1/2)-NF-κB pathway. Furthermore, the visfatin pro-inflammatory action was not prevented by insulin receptor blockade or by a PPARγ agonist. Visfatin did not modulate PPARγ expression. Retinoid X receptor (RXR) agonist suppressed the effects of visfatin on EMMPRIN/MMP-9, NF-κB, but not on MAPK activation. In conclusion, we have demonstrated that visfatin enhances atheroma inflammation through the NAMPT-MAPK (p38, ERK1/2)-NF-κB-EMMPRIN/MMP-9 pathway, a key feature of atherosclerotic diseases linked to metabolic disorders.

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“…Human osteosarcoma cell lines (Saos-2, U-2OS and MG-63), human malignant melanoma cell line A375 and human osteoblast cell line Hob were obtained from the American Type Culture Collection (ATCC; Manassas, VA, USA) and cultured in Iscove's modified Dulbecco's medium (IMDM; Invitrogen, Carlsbad, CA, USA), supplemented with 20 U/ml penicillin, 100 µg/ml streptomycin (Sigma, Beijing, China), and 10% heat-inactivated fetal bovine serum (FBS; Biowhittaker, Walkersville, MD, USA) at 37˚C in a humidified incubator supplied with 5% CO 2 (25).…”

Section: Methodsmentioning

confidence: 99%

Expression and clinical significance of extracellular matrix metalloproteinase inducer, EMMPRIN/CD147, in human osteosarcoma

Lü

Kim

et al. 2012

Oncology Letters

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Abstract. Osteosarcoma is the most common primary malignant bone tumor in children and adolescents. Recent studies have shown that extracellular matrix metalloproteinase inducer (EMMPRIN/CD147) promotes adhesion, invasion and metastasis of malignant tumor cells. The aim of this study was to investigate the impact of EMMPRIN/CD147 expression on prognosis and its correlation with clinicopathological characteristics in patients with osteosarcoma. The expression of EMMPRIN/CD147 in 55 surgical specimens from patients with osteosarcoma at stage IIA or above, 15 non-tumor rib bone tissues, three human osteosarcoma cell lines (Saos-2, U-2OS and MG-63), the human osteoblast cell line HOB and the malignant melanoma cell line A375 were examined by immunohistochemistry, western blot analysis and ELISA, respectively. The potential association of the levels of EMMPRIN/CD147 expression in osteosarcoma specimens with the overall survival of patients was statistically analyzed. We found that the EMMPRIN/CD147 was expressed in 45 out of 55 osteosarcomas, with immunoreactivity primarily within the membrane and cytoplasm of tumor cells, but not in the non-tumor bone tissues. We also observed that EMMPRIN/CD147 was expressed in Saos-2, U-2OS, MG-63 and A375, but not in HOB cells. The levels of EMMPRIN/CD147 expression correlated positively with the pathological degree of osteosarcoma and negatively with the survival period of patients with osteosarcoma. The expression of EMMPRIN/CD147 is a potential factor in the development and prognosis of osteosarcoma and may be a novel therapeutic target of human osteosarcoma.

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Perivascular adipose tissue-derived visfatin is a vascular smooth muscle cell growth factor: role of nicotinamide mononucleotide

Cited by 276 publications

References 26 publications

Extracellular PBEF/NAMPT/visfatin activates pro-inflammatory signalling in human vascular smooth muscle cells through nicotinamide phosphoribosyltransferase activity

Extracellular PBEF/NAMPT/visfatin activates pro-inflammatory signalling in human vascular smooth muscle cells through nicotinamide phosphoribosyltransferase activity

Visfatin/PBEF/Nampt induces EMMPRIN and MMP-9 production in macrophages via the NAMPT-MAPK (p38, ERK1/2)-NF-κB signaling pathway

Expression and clinical significance of extracellular matrix metalloproteinase inducer, EMMPRIN/CD147, in human osteosarcoma

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