Chronic Stretching of Amniotic Epithelial Cells Increases Pre-B Cell Colony-Enhancing Factor (PBEF/Visfatin) Expression and Protects Them from Apoptosis

Kendal-Wright, Claire E.; Hubbard, Daniela; Bryant‐Greenwood, Gillian D.

doi:10.1016/j.placenta.2007.12.008

Cited by 48 publications

(51 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Visfatin also participates in cellular resistance to genotoxic/oxidative stress, and enhances immune cell survival during stressful situations such as inflammation (Rongvaux et al 2008). In normal pregnancy, increased SIRT1 and decreased p53 expression in amniotic epithelial cells paralleled the changes induced by visfatin, which contributed to cell survival; moreover, the knockdown of visfatin with antisense probes abrogated this protective effect (Kendal et al 2008). FK866, a potent Nampt catalytic inhibitor, prevented visfatin-mediated cell protection, indicating that Nampt activity of visfatin is required for cell protection (Yang et al 2007).…”

Section: Discussionmentioning

confidence: 99%

Visfatin inhibits apoptosis of pancreatic β-cell line, MIN6, via the mitogen-activated protein kinase/phosphoinositide 3-kinase pathway

Cheng¹,

Weipin²,

Qian³

et al. 2011

Journal of Molecular Endocrinology

View full text Add to dashboard Cite

Visfatin is an adipocytokine that plays an important role in attenuating insulin resistance by binding to insulin receptor. It has been suggested that visfatin plays a role in the regulation of cell apoptosis and inflammation by an as yet unidentified mechanism. This study investigated the protective effects of visfatin on palmitate-induced islet b-cell apoptosis in the clonal mouse pancreatic b-cell line MIN6. The cells were treated with palmitate and/or recombinant visfatin. An 1-(4,5-dimethylthiazol-2-yl)-3,5-diphenylformazan assay was used to detect cell proliferation, V-FITC/propidium iodide staining was used to measure cell apoptosis and necrosis, and western blot analysis was used to detect the expression of proapoptotic proteins. The incubation of the cells with visfatin led to a concentration-dependent increase of cell proliferation (1 . 55-fold at 10 K7 M and 24 h compared with control, P!0 . 05). Visfatin significantly reduced the cell apoptosis induced by palmitate and caused a significant change in the expression of several proapoptotic proteins, including upregulation of Bcl-2 and a marked downregulation of cytochrome c and caspase 3. Visfatin also activated the ERK1/2 and the phosphoinositide 3-kinase (PI3K)/AKT signaling pathways in a time-and concentration-dependent manner, and the effect of visfatin on apoptosis was blocked by the specific ERK1/2 and PI3K/AKT inhibitors, PD098059 and LY294002. We conclude that visfatin can increase b-cell proliferation and prevent apoptosis, activate intracellular signaling, and regulate the expression of proapoptotic proteins. The antiapoptotic action of visfatin is mediated by activation of mitogen-activated protein kinase-dependent and PI3K-dependent signaling pathways.

show abstract

Section: Discussionmentioning

confidence: 99%

Visfatin inhibits apoptosis of pancreatic β-cell line, MIN6, via the mitogen-activated protein kinase/phosphoinositide 3-kinase pathway

Cheng¹,

Weipin²,

Qian³

et al. 2011

Journal of Molecular Endocrinology

View full text Add to dashboard Cite

show abstract

“…This was set up and used based on the parameters designed by the manufacturer. The 20% static stretching of these cells was performed as described in our previous studies [23] and represents the maximum amount of stretch achievable with this instrument. Cyclic stretch/release was performed using repetition of 23 secs of 20% stretch followed by 7 secs of release to 0% stretch.…”

Section: Methodsmentioning

confidence: 99%

“…However, PBEF also functions intracellularly as the enzyme nicotinamide phosphoribosyltranferase (Nampt) and increases the amount of NAD + available for metabolism [22]. Thus, the static stretch-induced increased production of PBEF [8, 23] may be a mechanism for providing the extra energy needed for the cell to successfully alter its cytoskeleton and gene expression profile required for adaptation to the stimulus and accommodation for the extra work required during labor. At the same time, its action to induce some key cytokines, such as TNFα [24] clearly involved in the parturition process [2], would further assist in the progression of labor.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Stretch and inflammation-induced Pre-B cell colony-enhancing factor (PBEF/Visfatin) and Interleukin-8 in amniotic epithelial cells☆

Kendal-Wright¹,

Hubbard²,

Gowin-Brown³

et al. 2010

Placenta

Self Cite

View full text Add to dashboard Cite

Preterm birth continues to be a growing problem in the USA. Although approximately half of preterm births are caused by intrauterine infection, uterine over-distension is also a cause. In this study we have compared the effects of static stretch, cyclic stretch/release and an inflammatory stimulus alone and in combination on the expression of Pre-B cell colony-enhancing factor (PBEF) and IL-8 in primary amniotic epithelial cells (AEC). We then sought to identify some of the mechanism(s) by which these cells respond to stretching stimuli. We show that cyclic stretch/release is a more robust stimulus for both PBEF and IL-8 than static stretch. Cyclic stretch/release increased both intracellular and secreted PBEF and a combination of both types of stretch was a more robust stimulus to PBEF that IL-8. However, when an inflammatory stimulus (IL-1β) was added to either kind of stretch, the effect on IL-8 was much greater than that on PBEF. Thus, different kinds of stretch affect the expression of these two cytokines from AEC, but inflammation is a much stronger stimulus of IL-8 than PBEF, agreeing with its primary role as a chemokine. Although the AEC showed morphological signs of increased cellular stress during stretching, blocking reactive oxygen species (ROS) had little effect. However, blocking integrin binding to fibronectin significantly reduced the responses of both PBEF and IL-8 to cyclic stretch/release. The increased PBEF, both intracellularly and secreted, suggests that it functions both to increase the metabolism of the cells, at the same time as stimulating further the cytokine cascade leading to parturition.

show abstract

“…It is also found in skeletal muscle, liver, bone marrow, lymphocytes [2] and placenta [3,4,5,6]. It has insulinomimetic effects by activating the insulin signal transduction pathway through binding to the same receptor [1].…”

Section: Introductionmentioning

confidence: 99%

Serum Levels of Visfatin and Possible Interaction with Iron Parameters in Gestational Diabetes Mellitus

Kaygusuz

Gümüş

Yılmaz

et al. 2013

Gynecol Obstet Invest

View full text Add to dashboard Cite

Background/Aims: Visfatin is a novel adipokine with insulinomimetic properties that increases in diabetes. However, for gestational diabetes mellitus (GDM) there are conflicting reports. Recent studies have reported a positive association of serum ferritin concentrations with insulin resistance. Thus, we assessed serum levels of visfatin in pregnant women with varying degrees of glucose tolerance and investigated the possible interaction of visfatin with parameters of iron metabolism. Methods: Visfatin levels were measured at 24-28 weeks of gestation in 88 women who were divided into three groups according to their response to a 50-gram glucose challenge test and a 100-gram oral glucose tolerance test: control group (n = 28), impaired glucose tolerance (IGT) group (n = 30) and GDM group (n = 30). Results: Visfatin levels were significantly higher in the GDM and IGT group than in control (p < 0.001 for GDM vs. control, and p = 0.004 for IGT vs. control). Serum visfatin was significantly associated with serum ferritin, insulin, age, gravidity, and body mass index. In a linear regression model, the covariates explained only 17% of variability of serum visfatin concentration. Body mass index (p < 0.001) contributed independently to visfatin variance. Conclusion: Serum visfatin concentration is significantly higher in GDM and is correlated with ferritin levels.

show abstract

Chronic Stretching of Amniotic Epithelial Cells Increases Pre-B Cell Colony-Enhancing Factor (PBEF/Visfatin) Expression and Protects Them from Apoptosis

Cited by 48 publications

References 41 publications

Visfatin inhibits apoptosis of pancreatic β-cell line, MIN6, via the mitogen-activated protein kinase/phosphoinositide 3-kinase pathway

Visfatin inhibits apoptosis of pancreatic β-cell line, MIN6, via the mitogen-activated protein kinase/phosphoinositide 3-kinase pathway

Stretch and inflammation-induced Pre-B cell colony-enhancing factor (PBEF/Visfatin) and Interleukin-8 in amniotic epithelial cells☆

Serum Levels of Visfatin and Possible Interaction with Iron Parameters in Gestational Diabetes Mellitus

Contact Info

Product

Resources

About