Skip to Content
Merck
  • Reduced Endoplasmic Reticulum Stress-Mediated Autophagy Is Required for Leptin Alleviating Inflammation in Adipose Tissue.

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
ABSTRACT

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

MATERIALS
Product Number
Brand
Product Description

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