Differential Activation of ER Stress Signal Pathway s Contributes to Palmitate-Induced Hepatocyte Lipoapoptosis

Cell Biology 4 (1):128 (2016)
Download Edit this record How to cite View on PhilPapers
Abstract
Saturated free fatty acids-induced hepatocyte lipoapoptosis plays a pivotal role in non-alcoholic steatohepatitis. Theactivation of endoplasmic reticulum (ER) stress isinvolved in hepatocyte lipoapoptosis induced by thesaturated free fatty acidpalmitate (PA). However, the underlying mechanismsof the role of ER stress in hepatocyte lipoapoptosis remain largely unclear.In this study, we showed that PA and tunicamycin (Tun), a classic ER stress inducer, resulted in differential activation of ERstress pathways. Our data revealed that PA inducedchronic and persistent ER stress response, but Tuninduced acute and transientER stress response. Compared with Tun treatment, PAinduced much lower glucose-regulated protein 78 (GRP78), a centralregulator of ER homeostasis, accumulation. It is noteworthy that GRP78 over-expression not only inhibited PA-induced ERstress but also decreased PA-induced apoptosis. Taken together, our data suggest that the differentialactivation of ER stresssignal plays an important role in PA-induced hepatocyte lipoapoptosis. More detailed studies on the mechanisms of PA inrepressing the accumulation of GRP78 will contribute to the understanding of molecular mechanisms of lipoapoptosis.
Keywords
Categories
No categories specified
(categorize this paper)
PhilPapers/Archive ID
ZHADAO-3
Upload history
Archival date: 2016-06-15
View other versions
Added to PP index
2016-06-15

Total views
167 ( #34,047 of 2,448,705 )

Recent downloads (6 months)
16 ( #36,591 of 2,448,705 )

How can I increase my downloads?

Downloads since first upload
This graph includes both downloads from PhilArchive and clicks on external links on PhilPapers.