The Rise of Soluble TWEAK Levels in Severely Obese Subjects After Bariatric Surgery May Affect Adipocyte-Cytokine Production Induced by TNFα

Maymó-Masip, Elsa; Fernández‐Veledo, Sonia; Garcı́a-España, Antonio; Vázquez-Carballo, Ana; Tinahones, Francisco J.; Garcı́a-Fuentes, Eduardo; Garrifo-Sanchez, Lourdes; Rodríguez, M; Vendrell, Joan; Chacón, Matilde R.

doi:10.1210/jc.2012-4177

Cited by 31 publications

(41 citation statements)

References 38 publications

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“…Our finding that lower sTWEAK concentrations were related with abdominal obesity agrees with the data obtained by Maymó-Masip et al [27], which show that sTWEAK levels in severely obese patients are lower than in controls, and that their concentration increases after weight loss. This may suggest that sTWEAK plays an anti-inflammatory role in this setting, although additional in vivo and in vitro studies are required.…”

Section: Discussionsupporting

confidence: 93%

“…Despite the moderate inflammatory capacity of the sTWEAK cytokine over the adipocyte, a competitive interfering activity with TNFα signalling in the adipocyte has been described [27,28]. An imbalance of sTWEAK forms (membrane bound mTWEAK and soluble sTWEAK) in the obese state may help potentiate the inflammatory effect of TNFα over the adipocyte.…”

Section: Discussionmentioning

confidence: 99%

“…This may suggest that sTWEAK plays an anti-inflammatory role in this setting, although additional in vivo and in vitro studies are required. Moreover, in the case of severely obese individuals they found that the main determinant of the sTWEAK circulating levels was BMI, in an inverse-dependent manner [27]. …”

Section: Discussionmentioning

confidence: 99%

“…Recently, we reported increased Fn14 expression in human adipocytes from severely obese subjects [31]. These cells also showed an increase in Fn14 expression after inflammatory stimulation, thus increasing availability for the sTWEAK ligand, which could lead to a peripheral reduction in serum sTWEAK [26,27]. An alternative hypothesis proposes the involvement of CD163, a monocyte-macrophage surface receptor which seems to act as a scavenger receptor for sTWEAK [32].…”

Section: Discussionmentioning

confidence: 99%

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Reduced circulating sTWEAK levels are associated with metabolic syndrome in elderly individuals at high cardiovascular risk

Díaz-López

Bulló

Chacón

et al. 2014

Cardiovasc Diabetol

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BackgroundThe circulating soluble TNF-like weak inducer of apoptosis (sTWEAK) is a cytokine that modulates inflammatory and atherogenic reactions related to cardiometabolic risk. We investigated the association between sTWEAK levels and metabolic syndrome (MetS) and its components in older subjects at high cardiovascular risk.MethodsCross-sectional analysis of 452 non-diabetic individuals (men and women aged 55–80 years) at high cardiovascular risk. MetS was defined by AHA/NHLBI and IDF criteria. Logistic regression analyses were used to estimate odds ratios (ORs) for MetS and its components by tertiles of serum sTWEAK concentrations measured by ELISA.ResultssTWEAK concentrations were lower in subjects with MetS than in those without. In gender- and age-adjusted analyses, subjects in the lowest sTWEAK tertile had higher ORs for overall MetS [1.71 (95% CI, 1.07-2.72)] and its components abdominal obesity [2.01 (1.15-3.52)], hyperglycemia [1.94 (1.20-3.11)], and hypertriglyceridemia [1.73 (1.05-2.82)] than those in the upper tertile. These associations persisted after controlling for family history of diabetes and premature coronary heart disease, lifestyle, kidney function and other MetS components. sTWEAK concentrations decreased as the number of MetS components increased. Individuals in the lowest vs the upper sTWEAK tertile had an increased risk of disclosing greater number of MetS features. Adjusted ORs for individuals with 2 vs ≤1, 3 vs ≤1, and ≥4 vs ≤ 1 MetS components were 2.60 (1.09-6.22), 2.83 (1.16-6.87) and 6.39 (2.42-16.85), respectively.ConclusionIn older subjects at high cardiovascular risk, reduced sTWEAK levels are associated with MetS: abdominal obesity, hypertriglyceridemia and hyperglycemia are the main contributors to this association.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Reduced circulating sTWEAK levels are associated with metabolic syndrome in elderly individuals at high cardiovascular risk

Díaz-López

Bulló

Chacón

et al. 2014

Cardiovasc Diabetol

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“…TWEAK is constitutively expressed in adipose tissue (124, 125), suggesting that it actively antagonizes the process of insulin resistance. Evidence for this is shown by a recent study demonstrating that reduced levels of TWEAK correlate with increased risk of diabetes (140), at least in part by reducing autocrine release of TNFα from adipocytes (141). Overall, these findings suggest that TWEAK can operate in a feed-forward mechanism to both promote muscle regeneration and attenuate the pathogenesis of diabetes.…”

Section: Tweak Signaling In Diabetes and Muscle Regenerationmentioning

confidence: 99%

Role of the TWEAK-Fn14-cIAP1-NF-κB Signaling Axis in the Regulation of Myogenesis and Muscle Homeostasis

et al. 2014

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Mammalian skeletal muscle maintains a robust regenerative capacity throughout life, largely due to the presence of a stem cell population known as “satellite cells” in the muscle milieu. In normal conditions, these cells remain quiescent; they are activated upon injury to become myoblasts, which proliferate extensively and eventually differentiate and fuse to form new multinucleated muscle fibers. Recent findings have identified some of the factors, including the cytokine TNFα-like weak inducer of apoptosis (TWEAK), which govern these cells’ decisions to proliferate, differentiate, or fuse. In this review, we will address the functions of TWEAK, its receptor Fn14, and the associated signal transduction molecule, the cellular inhibitor of apoptosis 1 (cIAP1), in the regulation of myogenesis. TWEAK signaling can activate the canonical NF-κB signaling pathway, which promotes myoblast proliferation and inhibits myogenesis. In addition, TWEAK activates the non-canonical NF-κB pathway, which, in contrast, promotes myogenesis by increasing myoblast fusion. Both pathways are regulated by cIAP1, which is an essential component of downstream signaling mediated by TWEAK and similar cytokines. This review will focus on the seemingly contradictory roles played by TWEAK during muscle regeneration, by highlighting the interplay between the two NF-κB pathways under physiological and pathological conditions. We will also discuss how myogenesis is negatively affected by chronic conditions, which affect homeostasis of the skeletal muscle environment.

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TWEAK promotes migration and invasion in MEFs through a mechanism dependent on ERKs activation and Fibulin 3 down‐regulation

Sequera

Vázquez-Carballo

Arechederra

et al. 2017

Journal Cellular Physiology

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TWEAK regulates multiple physio-pathological processes in fibroblasts such as fibrosis. It also induces migration and invasion in tumors and it can activate p38 MAPK in various cell types. Moreover, p38α MAPK promotes migration and invasion in several cancer cells types and in mouse embryonic fibroblasts (MEFs). However, it remains unknown if TWEAK could promote migration in fibroblasts and whether p38α MAPK might play a role. Our results reveal that TWEAK activates ERKs, Akt, and p38α/β MAPKs and reduces secreted Fibulin 3 in MEFs. TWEAK also increases migration and invasion in wt and p38α deficient MEFs, which indicates that p38α MAPK is not required to mediate these effects. In contrast, ERKs inhibition significantly decreases TWEAK-induced migration and Fibulin 3 knock-down mimics TWEAK effect. These results indicate that both ERKs activation and Fibulin 3 down-regulation would contribute to mediate TWEAK pro-migratory effect. In fact, the additional regulation of ERKs and/or p38β as a consequence of Fibulin 3 decrease might be also involved in the pro-migratory effect of TWEAK in MEFs. In conclusion, our studies uncover novel mechanisms by which TWEAK would favor tissue repair by promoting fibroblasts migration.

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The Rise of Soluble TWEAK Levels in Severely Obese Subjects After Bariatric Surgery May Affect Adipocyte-Cytokine Production Induced by TNFα

Abstract: The decrease of sTWEAK in severely obese patients may favor the proinflammatory activity elicited by TNFα.

Cited by 31 publications

References 38 publications

Reduced circulating sTWEAK levels are associated with metabolic syndrome in elderly individuals at high cardiovascular risk

Reduced circulating sTWEAK levels are associated with metabolic syndrome in elderly individuals at high cardiovascular risk

Role of the TWEAK-Fn14-cIAP1-NF-κB Signaling Axis in the Regulation of Myogenesis and Muscle Homeostasis

TWEAK promotes migration and invasion in MEFs through a mechanism dependent on ERKs activation and Fibulin 3 down‐regulation

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