Adiponectin and Its Globular Fragment Differentially Modulate the Oxidative Burst of Primary Human Phagocytes

Chedid, Pia; Hurtado-Nédelec, Margarita; Marion-Gaber, Benoit; Bournier, Odile; Hayem, Gilles; Gougerot‐Pocidalo, Marie‐Anne; Frystyk, Jan; Flyvbjerg, Alan; Benna, Jamel El; Marie, Jean‐Claude

doi:10.1016/j.ajpath.2011.10.013

Cited by 50 publications

(53 citation statements)

References 47 publications

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“…We also found quantitative and qualitative differences between articular and circulating adiponectin; namely its lower SF concentration and enrichment in the LMW at the cost of the HMW isoform, as compared with sera. Similar results have been observed by others in RA patients and healthy donors (11). In agreement with this finding, we recently reported that release of adiponectin by articular adipose tissue (AAT) and synovial membrane is not modified by pro-inflammatory factors, in contrast to leptin, which in AAT is up-regulated by numerous pro-inflammatory cytokines relevant to RA pathogenesis (9).…”

Section: Discussionsupporting

confidence: 76%

The effect of multimeric adiponectin isoforms and leptin on the function of rheumatoid fibroblast-like synoviocytes

Kontny¹,

Janicka²,

Skalska³

et al. 2015

Scandinavian Journal of Rheumatology

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Section: Discussionsupporting

confidence: 76%

The effect of multimeric adiponectin isoforms and leptin on the function of rheumatoid fibroblast-like synoviocytes

Kontny¹,

Janicka²,

Skalska³

et al. 2015

Scandinavian Journal of Rheumatology

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“…We found that VIP inhibited the phosphorylation of Ser345 residue of p47 phox subunit in response to fMLF and this is likely to be due to the identified downstream inhibition of kinase activation (ERK/p38MAPK) in agreement with the anti-inflammatory mechanism exerted by IL-10 and adiponectin. 11,12 Further, the availability of VIP to act on the VPAC1 receptors is likely as neurons, immune cells, and multiple tissues are able to increase VIP levels in response to inflammation after LPS challenge. 13,29 Also, VPAC1 receptor upregulation in macrophages and monocytes is a common response to acute and chronic pro-inflammatory stimuli.…”

Section: Discussionmentioning

confidence: 99%

“…Monocytes were purified by using anti-CD14-labeled microbeads from Miltenyi (Paris, France). 12 Cell counting and purity were determined by Turk's staining and flow cytometry analysis, respectively.…”

Section: Methodsmentioning

confidence: 99%

“…Among the different serine residues, the phosphorylation of Ser 345 residue of p47 phox is inhibited by either IL-10 or adiponectin, resulting in a diminished ROS production by phagocytes in response to fMLF. 11,12 Regulation of Ser345 phosphorylation status is crucial in inhibiting or even potentiating subsequent fMLF effect on phagocyte ROS production and this pathway could have a role in VIP antiinflammatory effects.…”

Section: Introductionmentioning

confidence: 99%

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Vasoactive intestinal peptide dampens formyl-peptide-induced ROS production and inflammation by targeting a MAPK-p47phox phosphorylation pathway in monocytes

et al. 2017

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Reactive oxygen species (ROS) produced by the phagocyte NADPH oxidase (NOX2) are required for microbial clearance; however, when produced in excess they exacerbate inflammatory response and injure surrounding tissues. NOX2 is a multicomponent enzyme composed of membrane-associated cytochrome b588 and cytosolic components p47, p67, p40, and rac1/2. We investigated whether vasoactive intestinal peptide (VIP), an endogenous immune-modulatory peptide, could affect ROS production by NOX2 in primary human phagocytes. VIP did not modulate basal ROS production by phagocytes, but it inhibited monocyte and not neutrophil ROS production in response to the bacterial peptide N-formyl-methionyl-leucyl-phenylalanine (fMLF). The action of VIP was essentially mediated by high-affinity G-protein coupled receptors VPAC1 as its specific agonist, [ALA]VIP, mimicked VIP-inhibitory effect, whereas the specific VPAC1 antagonist, PG97-269, blunted VIP action. Further, we showed that VIP inhibited fMLF-induced phosphorylation of ERK1/2 (extracellular signal-regulated kinase 1/2), p38MAPK (p38 mitogen-activated protein kinase) pathways, and phosphorylation of p47 on Ser345 residue. Also, VIP exerted an anti-inflammatory effect in a model of carrageenan-induced inflammation in rats. We thus found that VIP exerts anti-inflammatory effects by inhibiting the "MAPK-p47 phosphorylation-NOX2 activation" axis. These data suggest that VIP acts as a natural anti-inflammatory agent of the mucosal system and its analogs could be novel anti-inflammatory molecules.

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“…Considering the dearth of data on the relationship between gAd and breast cancer outcomes, it is instructive that recent study of gAd in rheumatoid arthritis reported considerably elevated gAd levels in patient synovial fluid versus circulating blood [51]. This suggests that gAd may be localized in areas of inflammation and repair, typical of tumor microenvironments.…”

Section: Globular Adiponectin and Breast Cancer Metastasismentioning

confidence: 99%

Linking adiponectin and autophagy in the regulation of breast cancer metastasis

et al. 2014

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Adipokines within the tumor microenvironment may play important roles in regulating the early steps of breast cancer metastasis. Adiponectin (AdipoQ) is the most abundant adipokine and exists in multiple forms: full-length multimers (fAd) and a cleaved, globular isoform (gAd). While these isoforms are observed as having distinct biological properties, nearly all investigation into AdipoQ in breast cancer has focused on the anti-tumor roles of fAd, while mostly ignoring gAd. However, evidence from other disease settings suggests that gAd is linked to processes known to promote metastasis. Here we discuss key areas in which knowledge about AdipoQ in breast cancer is lacking, expressly focusing on data suggesting that gAd is elevated in the microenvironment and may act directly on invasive breast cancer cells to support their initial metastatic progression. We discuss autophagy as a potential mechanism of action for this effect. Overall, given that AdipoQ and AdipoQ receptor agonists have been proposed as therapeutic strategies, it is necessary to better understand the various functions of these regulatory molecules in metastatic breast cancer. Doing so will help ensure the most effective approaches to treating this disease, for which there remain no curative options.

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Adiponectin and Its Globular Fragment Differentially Modulate the Oxidative Burst of Primary Human Phagocytes

Cited by 50 publications

References 47 publications

The effect of multimeric adiponectin isoforms and leptin on the function of rheumatoid fibroblast-like synoviocytes

The effect of multimeric adiponectin isoforms and leptin on the function of rheumatoid fibroblast-like synoviocytes

Vasoactive intestinal peptide dampens formyl-peptide-induced ROS production and inflammation by targeting a MAPK-p47phox phosphorylation pathway in monocytes

Linking adiponectin and autophagy in the regulation of breast cancer metastasis

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