Vaspin inhibited proinflammatory cytokine induced activation of nuclear factor-kappa B and its downstream molecules in human endothelial EA.hy926 cells

Liu, Shiwei; Dong, Yanting; Wang, Tong; Zhao, S. J.; Yang, Kun; Chen, Xiaoqin; Zheng, Chao‐Hui

doi:10.1016/j.diabres.2013.12.002

Cited by 51 publications

(39 citation statements)

References 44 publications

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“…Consistently, vaspin diminishes methylglyoxal-induced apoptotic activity in ECs by inhibiting caspase-3 activation through inhibition of Nox-mediated ROS generation [323]. Taken [325,326], confirming the anti-inflammatory role of vaspin on ECs.…”

Section: Vaspinsupporting

confidence: 54%

Insights into the molecular mechanisms of diabetes-induced endothelial dysfunction: focus on oxidative stress and endothelial progenitor cells

et al. 2015

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Diabetes mellitus is a heterogeneous, multifactorial, chronic disease characterized by hyperglycemia owing to insulin insufficiency and insulin resistance (IR). Recent epidemiological studies showed that the diabetes epidemic affects 382 million people worldwide in 2013, and this figure is expected to be 600 million people by 2035. Diabetes is associated with microvascular and macrovascular complications resulting in accelerated endothelial dysfunction (ED), atherosclerosis, and cardiovascular disease (CVD). Unfortunately, the complex pathophysiology of diabetic cardiovascular damage is not fully understood. Therefore, there is a clear need to better understand the molecular pathophysiology of ED in diabetes, and consequently, better treatment options and novel efficacious therapies could be identified. In the light of recent extensive research, we re-investigate the association between diabetes-associated metabolic disturbances (IR, subclinical inflammation, dyslipidemia, hyperglycemia, dysregulated production of adipokines, defective incretin and gut hormones production/action, and oxidative stress) and ED, focusing on oxidative stress and endothelial progenitor cells (EPCs). In addition, we re-emphasize that oxidative stress is the final common pathway that transduces signals from other conditions-either directly or indirectly-leading to ED and CVD.

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Section: Vaspinsupporting

confidence: 54%

Insights into the molecular mechanisms of diabetes-induced endothelial dysfunction: focus on oxidative stress and endothelial progenitor cells

et al. 2015

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“…Subsequently, decreased vaspin levels have been reported to be linked to diabetes, metabolic syndrome, obesity, coronary artery disease, and impaired insulin sensitivity [113]. Vaspin interacts with GRP78, a cell membrane glucose-regulated protein, to induce intracellular signaling in vascular smooth muscle cells that inhibits reactive oxidative species, MAPK, PI3K/Akt, and the phosphorylation of NF- k B and PKC θ induced by TNF- α , which improves glucose and lipid metabolism and relieves metabolic dysfunction and inflammatory responses in obesity [111, 113, 114]. …”

Section: Adipokines and Their Receptorsmentioning

confidence: 99%

Adipokine Contribution to the Pathogenesis of Osteoarthritis

Azamar-Llamas

Hernández-Molina

Ramos-Ávalos

et al. 2017

Mediators of Inflammation

133

106

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Recent studies have shown that overweight and obesity play an important role in the development of osteoarthritis (OA). However, joint overload is not the only risk factor in this disease. For instance, the presence of OA in non-weight-bearing joints such as the hand suggests that metabolic factors may also contribute to its pathogenesis. Recently, white adipose tissue (WAT) has been recognized not only as an energy reservoir but also as an important secretory organ of adipokines. In this regard, adipokines have been closely associated with obesity and also play an important role in bone and cartilage homeostasis. Furthermore, drugs such as rosuvastatin or rosiglitazone have demonstrated chondroprotective and anti-inflammatory effects in cartilage explants from patients with OA. Thus, it seems that adipokines are important factors linking obesity, adiposity, and inflammation in OA. In this review, we are focused on establishing the physiological mechanisms of adipokines on cartilage homeostasis and evaluating their role in the pathophysiology of OA based on evidence derived from experimental research as well as from clinical-epidemiological studies.

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“…Studies of central vaspin administration revealed a significant reduction of food intake in rats and mice [8], [9], and, recently, a novel vaspin-mediated signaling axis between brain and liver, regulating hepatic glucose production and insulin signaling, was unraveled [10]. In vitro studies provide evidence of anti-inflammatory [11], [12], anti-atherogenic [13], [14], [15], [16], and anti-apoptotic [17], [18], [19] properties of vaspin in various endothelial cell lines (reviewed in [20]). Nonetheless, the underlying molecular mechanisms of vaspin action and signal transduction are not well understood.…”

Section: Introductionmentioning

confidence: 99%

Brown adipose tissue (BAT) specific vaspin expression is increased after obesogenic diets and cold exposure and linked to acute changes in DNA-methylation

Weiner

Rohde

Krause

et al. 2017

Molecular Metabolism

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ObjectiveSeveral studies have demonstrated anti-diabetic and anti-obesogenic properties of visceral adipose tissue-derived serine protease inhibitor (vaspin) and so evoked its potential use for treatment of obesity-related diseases. The aim of the study was to unravel physiological regulators of vaspin expression and secretion with a particular focus on its role in brown adipose tissue (BAT) biology.MethodsWe analyzed the effects of obesogenic diets and cold exposure on vaspin expression in liver and white and brown adipose tissue (AT) and plasma levels. Vaspin expression was analyzed in isolated white and brown adipocytes during adipogenesis and in response to adrenergic stimuli. DNA-methylation within the vaspin promoter was analyzed to investigate acute epigenetic changes after cold-exposure in BAT.ResultsOur results demonstrate a strong induction of vaspin mRNA and protein expression specifically in BAT of both cold-exposed and high-fat (HF) or high-sugar (HS) fed mice. While obesogenic diets also upregulated hepatic vaspin mRNA levels, cold exposure tended to increase vaspin gene expression of inguinal white adipose tissue (iWAT) depots. Concomitantly, vaspin plasma levels were decreased upon obesogenic or thermogenic triggers. Vaspin expression was increased during adipogenesis but unaffected by sympathetic activation in brown adipocytes. Analysis of vaspin promoter methylation in AT revealed lowest methylation levels in BAT, which were acutely reduced after cold exposure.ConclusionsOur data demonstrate a novel BAT-specific regulation of vaspin gene expression upon physiological stimuli in vivo with acute epigenetic changes that may contribute to cold-induced expression in BAT. We conclude that these findings indicate functional relevance and potentially beneficial effects of vaspin in BAT function.

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Vaspin inhibited proinflammatory cytokine induced activation of nuclear factor-kappa B and its downstream molecules in human endothelial EA.hy926 cells

Cited by 51 publications

References 44 publications

Insights into the molecular mechanisms of diabetes-induced endothelial dysfunction: focus on oxidative stress and endothelial progenitor cells

Insights into the molecular mechanisms of diabetes-induced endothelial dysfunction: focus on oxidative stress and endothelial progenitor cells

Adipokine Contribution to the Pathogenesis of Osteoarthritis

Brown adipose tissue (BAT) specific vaspin expression is increased after obesogenic diets and cold exposure and linked to acute changes in DNA-methylation

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