Omentin inhibits TNF-α-induced expression of adhesion molecules in endothelial cells via ERK/NF-κB pathway

Zhong, Xia; Li, Xiaonan; Liu, Fuli; Tan, Hui; Shang, Deya

doi:10.1016/j.bbrc.2012.07.110

Cited by 124 publications

(94 citation statements)

References 30 publications

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“…Additionally, TNF-α triggers signaling pathways that converge on the activation of transcription factor NF-κB. 18,24,26 More recently, others have showed that TNF-α activates NF-κB in both human umbilical vein ECs 26 and dermal microvascular ECs. 36 Thus, NF-κB is a transcription factor that regulates the pro-inflammatory responses in ECs, including ZO-1 expression as shown in lupus condition.…”

Section: Discussionmentioning

confidence: 99%

“…15,24 Importantly, it was also documented that NF-κB is a critical signaling molecule in TNF-α-induced inflammatory response. 25,26 Thus, we further investigated the role of NF-κB in METH-induced barrier dysfunction by using an inhibitor of this pathway, BAY 11-7085. 27 In more detail, BAY is an upstream inhibitor of NF-κB that prevents the activation of inhibitory κB kinase, an enzyme required for the activation of NF-κB.…”

Section: Methamphetamine Impairs the Barrier Function Of Endothelial mentioning

confidence: 99%

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The TNF-α/Nf-κB Signaling Pathway has a Key Role in Methamphetamine–Induced Blood–Brain Barrier Dysfunction

Coelho-Santos

Leitão

Cardoso

et al. 2015

J Cereb Blood Flow Metab

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Methamphetamine (METH) is a psychostimulant that causes neurologic and psychiatric abnormalities. Recent studies have suggested that its neurotoxicity may also result from its ability to compromise the blood-brain barrier (BBB). Herein, we show that METH rapidly increased the vesicular transport across endothelial cells (ECs), followed by an increase of paracellular transport. Moreover, METH triggered the release of tumor necrosis factor-alpha (TNF-α), and the blockade of this cytokine or the inhibition of nuclear factor-kappa B (NF-κB) pathway prevented endothelial dysfunction. Since astrocytes have a crucial role in modulating BBB function, we further showed that conditioned medium obtained from astrocytes previously exposed to METH had a negative impact on barrier properties also via TNF-α/NF-κB pathway. Animal studies corroborated the in vitro results. Overall, we show that METH directly interferes with EC properties or indirectly via astrocytes through the release of TNF-α and subsequent activation of NF-κB pathway culminating in barrier dysfunction.

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Section: Discussionmentioning

confidence: 99%

Section: Methamphetamine Impairs the Barrier Function Of Endothelial mentioning

confidence: 99%

The TNF-α/Nf-κB Signaling Pathway has a Key Role in Methamphetamine–Induced Blood–Brain Barrier Dysfunction

Coelho-Santos

Leitão

Cardoso

et al. 2015

J Cereb Blood Flow Metab

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show abstract

“…40 Another study showed that omentin reduces vascular cell adhesion protein-1 expression on the surface of monocytes and also reduces intercellular adhesion molecule-1 expression (via suppression of extracellular ERK/NF -κB), which results in reduced adhesion of monocytes to endothelial cells. 41 Omentin has also shown an inhibitory effect on TNF-α -induced adhesion of U937 monocytes in rat vascular smooth muscle cells. 42 Considering the aforementioned properties of omentin, many scientists conclude that it may be a good marker for evaluating vascular endothelial function when assessing ischemic complications in patients with diabetes.…”

Section: Resultsmentioning

confidence: 98%

The role of the ITLN1 gene rs2274907 polymorphism in diabetic foot patients

Mrozikiewicz-Rakowska¹,

Sobczyk-Kopcioł²,

Szymański³

et al. 2017

Polish Archives of Internal Medicine

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“…Several cross-sectional studies further reported that omentin levels are inversely associated with insulin resistance (assessed as homeostasis model assessmentestimated insulin resistance (HOMA-IR)) (7, 8,11,12,13,14) and decreased in individuals with impaired fasting glucose (IFG), impaired glucose tolerance (IGT), or type 2 diabetes (8,11,12,14,15,16). Such an inverse association may be explained by the anti-inflammatory properties of omentin that have been observed in in vitro studies on endothelial cells and smooth muscle cells (17,18,19). However, data on omentin and type 2 diabetes as well as diabetes-related traits were collected in small cross-sectional studies.…”

Section: Introductionmentioning

confidence: 94%

Adiponectin may mediate the association between omentin, circulating lipids and insulin sensitivity: results from the KORA F4 study

Herder

Ouwens

Carstensen

et al. 2015

European Journal of Endocrinology

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Objective: Reduced circulating omentin levels have been reported in obesity and type 2 diabetes, but data were mostly derived from univariate analyses in small study samples. This study aimed to investigate the relationship between omentin, abnormal glucose tolerance and related metabolic factors in a large population-based cross-sectional study. Design and methods: Serum omentin was measured by ELISA in 1092 participants of the German KORA F4 survey (2006)(2007)(2008). Associations between omentin serum levels, glucose tolerance (assessed with an oral glucose tolerance test) and diabetesrelated factors were estimated using logistic and linear regression models respectively. Results: Serum levels of omentin were not related to categories of glucose tolerance. However, serum omentin was positively associated with whole-body insulin sensitivity index (ISI (composite)) and HDL cholesterol and showed inverse associations with 2-h post-load glucose, fasting insulin, homeostasis model assessment-estimated insulin resistance, BMI and triglycerides (all P%0.03 after adjustment for age, sex and lifestyle factors). Further adjustment for BMI and/or serum lipids attenuated the associations with parameters of glucose metabolism, whereas adjustment for serum adiponectin virtually abolished all aforementioned associations. In contrast, adjustment for omentin had no effect on the positive association between adiponectin levels and ISI (composite). Conclusions: The data from this large population-based cohort show that circulating omentin levels are associated with insulin sensitivity. Our observations further suggest that omentin acts via upregulation of adiponectin, which in turn affects lipid metabolism and thereby also indirectly enhances insulin sensitivity, but mechanistic studies are required to corroborate this hypothesis.

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Omentin inhibits TNF-α-induced expression of adhesion molecules in endothelial cells via ERK/NF-κB pathway

Cited by 124 publications

References 30 publications

The TNF-α/Nf-κB Signaling Pathway has a Key Role in Methamphetamine–Induced Blood–Brain Barrier Dysfunction

The TNF-α/Nf-κB Signaling Pathway has a Key Role in Methamphetamine–Induced Blood–Brain Barrier Dysfunction

The role of the ITLN1 gene rs2274907 polymorphism in diabetic foot patients

Adiponectin may mediate the association between omentin, circulating lipids and insulin sensitivity: results from the KORA F4 study

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