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Reduced Endoplasmic Reticulum Stress-Mediated Autophagy Is Required for Leptin Alleviating Inflammation in Adipose Tissue.

Frontiers in immunology (2017-12-19)
Lu Gan, Zhenjiang Liu, Dan Luo, Qian Ren, Hua Wu, Changxing Li, Chao Sun
RÉSUMÉ

Leptin is an adipocyte-derived hormone and maintains adipose function under challenged conditions. Autophagy is also essential to maintain cellular homeostasis and regulate characteristics of adipose tissue. However, the effects of leptin on autophagy of adipocyte remain elusive. Here, we demonstrated endoplasmic reticulum (ER) stress and leptin were correlated with autophagy and inflammation by transcriptome sequencing of adipose tissue. Leptin-mediated inhibition of autophagy was involved in upstream reduction of ER stress proteins such as Chop, GRP78, and Atf4, since blockage of autophagy using pharmacological approach had no effect on tunicamycin-induced ER stress. Moreover, we determined

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Tunicamycine from Streptomyces sp.
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Thapsigargine, ≥98% (HPLC), solid film
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3-Methyladenine, autophagy inhibitor
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4-Phenylbutyric acid, 99%
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Durcupan ACM, single component A, M epoxy resin
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Dansylcadaverine, suitable for fluorescence, BioReagent, ≥99.0% (HPLC)