期刊
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS
卷 1841, 期 12, 页码 1648-1655出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbalip.2014.09.012
关键词
ER stress; Heart; Lipid; PPAR; ACSL1; Triglycerides
资金
- National Heart, Lung, and Blood Institute (NHLBI) [HL45095, HL73029, HL112853]
- Dr. E. Dekker Student Fellowship of the Netherlands Heart Foundation
We used human cardiomyocyte-derived cells to create an in vitro model to study lipid metabolism and explored the effects of PPAR gamma, ACSL1 and ATGL on fatty acid-induced ER stress. Compared to oleate, palmitate treatment resulted in less intracellular accumulation of lipid droplets and more ER stress, as measured by upregulation of CHOP, ATF6 and GRP78 gene expression and phosphorylation of eukaryotic initiation factor 2a (ElF2a). Both ACSL1 and PPAR gamma adenovirus-mediated expression augmented neutral lipid accumulation and reduced palmitate-induced upregulation of ER stress markers to levels similar to those in the oleate and control treatment groups. This suggests that increased channeling of non-esterffied free fatty acids (NEFA) towards storage in the form of neutral lipids in lipid droplets protects against palmitate-induced ER stress. Overexpression of ATGL in cells incubated with oleate-containing medium increased NEFA release and stimulated expression of ER stress markers. Thus, inefficient creation of lipid droplets as well greater release of stored lipids induces ER stress. (C) 2014 Elsevier B.V. All rights reserved.
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