Visfatin Promotes Wound Healing through the Activation of ERK1/2 and JNK1/2 Pathway

Lee, Byung Cheol; Song, Jisun; Lee, Arim; Cho, Daeho; Kim, Tae Sung

doi:10.3390/ijms19113642

Cited by 25 publications

(18 citation statements)

References 57 publications

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“…Intriguingly, our data support that Nampt is part of the Mos/ MAPK-dependent pathway, which regulates spindle length and division asymmetry in oocytes 7,27 . It is notable in this regard that Nampt function is well-known to overlap with the MAPK pathway in other cell-types [46][47][48][49] , and MAPK activity has recently been shown to be important for sustaining Nampt levels 30 .…”

Section: Discussionmentioning

confidence: 99%

Nampt-mediated spindle sizing secures a post-anaphase increase in spindle speed required for extreme asymmetry

et al. 2020

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Meiotic divisions in oocytes are extremely asymmetric and require pre-and post-anaphaseonset phases of spindle migration. The latter induces membrane protrusion that is moulded around the spindle thereby reducing cytoplasmic loss. Here, we find that depleting the NAD biosynthetic enzyme, nicotinamide phosphoribosyl-transferase (Nampt), in mouse oocytes results in markedly longer spindles and compromises asymmetry. By analysing spindle speed in live oocytes, we identify a striking and transient acceleration after anaphase-onset that is severely blunted following Nampt-depletion. Slow-moving midzones of elongated spindles induce cortical furrowing deep within the oocyte before protrusions can form, altogether resulting in larger oocyte fragments being cleaved off. Additionally, we find that Namptdepletion lowers NAD and ATP levels and that reducing NAD using small molecule Nampt inhibitors also compromises asymmetry. These data show that rapid midzone displacement is critical for extreme asymmetry by delaying furrowing to enable protrusions to form and link metabolic status to asymmetric division.

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Section: Discussionmentioning

confidence: 99%

Nampt-mediated spindle sizing secures a post-anaphase increase in spindle speed required for extreme asymmetry

et al. 2020

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“…This biomarker has been studied for several inflammatory diseases such as obesity, metabolic syndrome, type 2 DM, polycystic ovary syndrome, and RA, but the findings are controversial [10][11][12][13][16][17][18]. Subsequent studies described visfatin upregulation in several immune cells including monocytes, lymphocytes, dendritic cells and macrophages [19][20][21]. Visfatin was shown to activate pro-inflammatory pathways and induce other proinflammatory cytokines including TNF-α, IL-1β and IL-6.…”

Section: Discussionmentioning

confidence: 99%

The evaluation of serum biomarkers in patients with sarcoidosis: Can visfatin be a new biomarker for sarcoidosis?

Tanrıverdi

Iliaz

Çörtük

et al. 2017

Diffuse Parenchymal Lung Disease

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Objective: Sarcoidosis is a chronic systemic inflammatory disease which can affect multiple organ systems. The role of biomarkers in the diagnosis and prognosis of sarcoidosis is increasing. Interest in the role of adipose tissue mediated inflammation in the pathogenesis of the inflammatory diseases has increased in recent years. Visfatin is a proinflammatory adipocytokine which has been studied for several inflammatory diseases such as diabetes mellitus, obesity and metabolic syndrome. Our aim is to assess serum visfatin levels in sarcoidosis and its relation with other markers of inflammation (CRP, ACE and ESR). Material and Methods: We enrolled 59 patients with sarcoidosis and 21 healthy controls. We measured plasma levels of visfatin along with serum CRP, ESR, ACE using ELISA (enzyme-linked immunosorbent assay) kits (Blue Gene Biotech, Shanghai, China). Results: Visfatin levels were not significantly different between patients and control subjects (29.9±15.8 ng/ml for patients and 23.93±16.73 ng/ml for controls, p=0.15) and there was no correlation between visfatin and serum CRP, ACE or ESR in patients with sarcoidosis. Conclusion: Visfatin recently is being discussed as biomarker for inflammatory diseases in several studies and results are controversial. In our study, no differences were found in serum level of visfatin between patients with sarcoidosis and control group.

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“…Literature shows that visfatin augments gene expression and protein production of VEGF (Adya et al, 2007;Astern et al, 2013;Dambala et al, 2017;Park et al, 2011). This visfatin-induced VEGF expression has also been documented in other types of cells (B. C. Lee et al, 2018). The mechanism for this induced upregulation of VEGF appears to be mediated by the MAPK and PI3K/Akt pathways (Adya et al, 2007).…”

Section: Visfatin and Vegfmentioning

confidence: 76%

Visfatin: An emerging adipocytokine bridging the gap in the evolution of cardiovascular diseases

Dakroub

Nasser

Kobeissy

et al. 2021

Journal Cellular Physiology

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Visfatin/nicotinamide phosphoribosyltransferase (NAMPT) is an adipokine expressed predominately in visceral fat tissues. High circulating levels of visfatin/ NAMPT have been implicated in vascular remodeling, vascular inflammation, and atherosclerosis, all of which pose increased risks of cardiovascular events. In this context, increased levels of visfatin have been correlated with several upregulated pro-inflammatory mediators, such as IL-1, IL-1Ra, IL-6, IL-8, and TNF-α. Furthermore, visfatin is associated with leukocyte recruitment by endothelial cells and the production of adhesion molecules such as vascular cell adhesion molecule 1, intercellular cell adhesion molecule 1, and E-selectin, which are well known to mediate the progression of atherosclerosis. Moreover, diverse angiogenic factors have been found to mediate visfatin-induced angiogenesis. These include matrix metalloproteinases, vascular endothelial growth factor, monocyte chemoattractant protein 1, and fibroblast growth factor 2. This review aims to provide aThis is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Visfatin Promotes Wound Healing through the Activation of ERK1/2 and JNK1/2 Pathway

Cited by 25 publications

References 57 publications

Nampt-mediated spindle sizing secures a post-anaphase increase in spindle speed required for extreme asymmetry

Nampt-mediated spindle sizing secures a post-anaphase increase in spindle speed required for extreme asymmetry

The evaluation of serum biomarkers in patients with sarcoidosis: Can visfatin be a new biomarker for sarcoidosis?

Visfatin: An emerging adipocytokine bridging the gap in the evolution of cardiovascular diseases

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