Atrial natriuretic peptide inhibits the production of adipokines and cytokines linked to inflammation and insulin resistance in human subcutaneous adipose tissue

Moro, Cédric; Klimčáková, Eva; Lolmède, Karine; Berlan, Michel; Lafontan, Max; Štich, Vladimír; Bouloumié, Anne; Galitzky, Jean; Arner, Peter; Langin, Dominique

doi:10.1007/s00125-007-0614-3

Cited by 111 publications

(80 citation statements)

References 56 publications

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“…However, the effects of rhBNP on HFL-1 cells in terms of inflammation have not yet been described. rhBNP is known to exert its anti-inflammatory activity in various organs (18)(19)(20)(21). Therefore, further investigation of the mechanism by which rhBNP influences LPS-induced human lung fibroblasts has important clinical implications.…”

Section: Discussionmentioning

confidence: 99%

Recombinant human brain natriuretic peptide attenuates LPS-induced cellular injury in human fetal lung fibroblasts via inhibiting MAPK and NF-κB pathway activation

Song

Zhao

Liu

et al. 2016

Molecular Medicine Reports

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Abstract. Inflammatory responses are vital in lung injury diseases, particularly acute respiratory distress syndrome (ARDS). Recombinant human brain natriuretic peptide (rhBNP) has been shown to exhibit anti-inflammatory effects in vivo in our previous studies. The present study aimed to investigate the mechanisms underlying the anti-inflammatory effects of rhBNP on lipopolysaccharide (LPS)-induced human fetal lung fibroblasts (HFL-1). The results showed that LPS induced a significant increase in the leakage of lactate dehydrogenase and the secretion of interleukin (IL)-1β. Activation of p38, extracellular-signal regulated kinase (ERK) 1/2, c-Jun NH2-terminal kinase (JNK) mitogen-activated protein kinases (MAPK)s, and nuclear factor (NF)-κB in HFL-1 cells was also observed following treatment with LPS. Treatment with rhBNP (0.1 µM) reduced the production of IL-1β at the protein and mRNA levels. Moreover, rhBNP decreased the phosphorylation of p38, ERK1/2 and JNK induced by LPS. However, the JNK inhibitor, SP600125, significantly inhibited LPS-induced IL-1β production. These results indicate that the inhibition of IL-1β by may dependent upon the JNK signaling pathway. The LPS-induced NF-κB activation was also suppressed by rhBNP, and IL-1β production was inhibited by the NF-κB inhibitor. Furthermore, NF-κB activation was attenuated by the JNK inhibitor, indicating that NF-κB activation was dependent on the JNK signaling pathway. The present study suggests that rhBNP exhibits an anti-inflammatory effect on LPS-induced HFL-1 cell injury via the inhibition of MAPK and NF-κB signaling pathways and may exhibit therapeutic potential for acute lung injury and ARDS.

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Section: Discussionmentioning

confidence: 99%

Recombinant human brain natriuretic peptide attenuates LPS-induced cellular injury in human fetal lung fibroblasts via inhibiting MAPK and NF-κB pathway activation

Song

Zhao

Liu

et al. 2016

Molecular Medicine Reports

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“…Human adipose tissue explants. Cultures of human subcutaneous adipose tissue explants were performed as described previously (14). After 24 h of treatment with rosiglitazone (1 mol/l) or vehicle (DMSO), tissue pieces were collected for mRNA analysis.…”

Section: Methodsmentioning

confidence: 99%

The Transcriptional Coactivator Peroxisome Proliferator–Activated Receptor (PPAR)γ Coactivator-1α and the Nuclear Receptor PPARα Control the Expression of Glycerol Kinase and Metabolism Genes Independently of PPARγ Activation in Human White Adipocytes

et al. 2007

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OBJECTIVE—The purpose of this work was to determine the pattern of genes regulated by peroxisome proliferator–activated receptor (PPAR) γ coactivator 1α (PGC-1α) in human adipocytes and the involvement of PPARα and PPARγ in PGC-1α transcriptional action. RESEARCH DESIGN AND METHODS—Primary cultures of human adipocytes were transduced with a PGC-1α adenovirus and treated with PPARγ and PPARα agonists. Variation in gene expression was assessed using pangenomic microarrays and quantitative RT-PCR. To investigate glycerol kinase (GyK), a target of PGC-1α, we measured enzymatic activity and glycerol incorporation into triglycerides. In vivo studies were performed on wild-type and PPARα−/− mice. The GyK promoter was studied using chromatin immunoprecipitation and promoter reporter gene assays. RESULTS—Among the large number of genes regulated by PGC-1α independently of PPARγ, new targets involved in metabolism included the gene encoding GyK. The induction of GyK by PGC-1α was observed at the levels of mRNA, enzymatic activity, and glycerol incorporation into triglycerides. PPARα was also upregulated by PGC-1α. Its activation led to an increase in GyK expression and activity. PPARα was shown to bind and activate the GyK promoter. Experiments in mice confirmed the role of PGC-1α and PPARα in the regulation of GyK in vivo. CONCLUSIONS—This work uncovers novel pathways regulated by PGC-1α and reveals that PPARα controls gene expression in human white adipocytes. The induction of GyK by PGC-1α and PPARα may promote a futile cycle of triglyceride hydrolysis and fatty acid reesterification.

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“…In human adipocytes, RBP4 production is downregulated by the proinflammatory cytokine TNF-a, which is clearly linked to adipocyte insulin resistance [8]. In a very recent study, secretion of RBP4 and other pro-inflammatory cytokines was downregulated by atrial natriuretic peptide (ANP) [9]. ANP stimulates lipolysis in adipocytes and in humans [10], an effect that can also be attributed to TNF-a.…”

mentioning

confidence: 99%

Regulation of retinol binding protein 4 production in primary human adipocytes by adiponectin, troglitazone and TNF-α

Sell

Eckel

2007

Diabetologia

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Atrial natriuretic peptide inhibits the production of adipokines and cytokines linked to inflammation and insulin resistance in human subcutaneous adipose tissue

Abstract: We suggest that ANP, either by direct action on adipocytes and macrophages or through activation of adipocyte hormone-sensitive lipase, inhibits the secretion of factors involved in inflammation and insulin resistance.

Cited by 111 publications

References 56 publications

Recombinant human brain natriuretic peptide attenuates LPS-induced cellular injury in human fetal lung fibroblasts via inhibiting MAPK and NF-κB pathway activation

Recombinant human brain natriuretic peptide attenuates LPS-induced cellular injury in human fetal lung fibroblasts via inhibiting MAPK and NF-κB pathway activation

The Transcriptional Coactivator Peroxisome Proliferator–Activated Receptor (PPAR)γ Coactivator-1α and the Nuclear Receptor PPARα Control the Expression of Glycerol Kinase and Metabolism Genes Independently of PPARγ Activation in Human White Adipocytes

Regulation of retinol binding protein 4 production in primary human adipocytes by adiponectin, troglitazone and TNF-α

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