Molecular and cellular biochemistry, 2020-01, Vol.463 (1-2), p.45-55
2020
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- Autor(en) / Beteiligte
- Titel
- Beneficial effect of ER stress preconditioning in protection against FFA-induced adipocyte inflammation via XBP1 in 3T3-L1 adipocytes
- Ist Teil von
- Molecular and cellular biochemistry, 2020-01, Vol.463 (1-2), p.45-55
- Ort / Verlag
- New York: Springer US
- Erscheinungsjahr
- 2020
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- Adipose tissue inflammation is closely associated with the development of obesity and insulin resistance. Free fatty acids (FFAs) are a major inducer of obesity-related insulin resistance. Previously, we reported that endoplasmic reticulum (ER) stress potentially mediated retinal inflammation in diabetic retinopathy. The unfolded protein response (UPR) protects cells against damage induced by oxidative stress. X-box binding protein 1 (XBP1) plays a major role in protecting cells by modulating the UPR. However, the link between ER stress and adipocyte inflammation has been poorly investigated. In the present study, we found that pretreatment of 3T3-L1 adipocytes with a low dose of ER stress inducer tunicamycin inhibited FFA-induced upregulated expression of inflammatory cytokines. In addition, FFAs induced phosphorylation of the p65 subunit of NF-κB was largely inhibited by pretreatment with tunicamycin in 3T3-L1 adipocytes. Knockdown of XBP1 by siRNA markedly mitigated the protective effects of preconditioning against inflammation. Conversely, overexpression of XBP1 alleviated FFA-induced phosphorylation of IκB-α, IKKα/β, and NF-κB, which was accompanied by decreased inflammatory cytokine expression. Collectively, these results imply a beneficial role of ER stress preconditioning in protecting against FFA-induced 3T3-L1 adipocyte inflammation, which is likely mediated through inhibition of the IKK/NF-κB pathway via XBP1.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 0300-8177eISSN: 1573-4919DOI: 10.1007/s11010-019-03627-3Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6946732
- Format
- –
- Schlagworte
- 3T3-L1 Cells, Acid resistance, Activating transcription factor 1, Adipocytes, Adipocytes - metabolism, Adipocytes - pathology, Adipose tissue, Adipose tissues, Animals, Biochemistry, Biomedical and Life Sciences, Cardiology, Cytokines, Cytokines - metabolism, Diabetes mellitus, Diabetic retinopathy, Endoplasmic reticulum, Endoplasmic Reticulum Stress - drug effects, Fatty acids, Fatty Acids - adverse effects, Fatty Acids - pharmacology, Inflammation, Inflammation - chemically induced, Inflammation - metabolism, Inflammation - pathology, Insulin, Insulin resistance, Life Sciences, Medical Biochemistry, Mice, NF-κB protein, Obesity, Oncology, Oxidative stress, Phosphorylation, Preconditioning, Pretreatment, Protein binding, Protein folding, Proteins, RAW 264.7 Cells, Retina, Retinopathy, Signal Transduction - drug effects, siRNA, Tunicamycin, Tunicamycin - pharmacology, X-Box Binding Protein 1 - metabolism