Adiponectin inhibits palmitate-induced apoptosis through suppression of reactive oxygen species in endothelial cells: involvement of cAMP/protein kinase A and AMP-activated protein kinase

Title
Adiponectin inhibits palmitate-induced apoptosis through suppression of reactive oxygen species in endothelial cells: involvement of cAMP/protein kinase A and AMP-activated protein kinase
Author(s)
박소영김지은송승은김용운김종연박성철박윤기백석환이인규[이인규]
Keywords
NECROSIS-FACTOR-ALPHA; INDUCED INSULIN-RESISTANCE; SMOOTH-MUSCLE-CELL; FREE FATTY-ACIDS; PLASMA-PROTEIN; HIGH-GLUCOSE; SIGNAL-TRANSDUCTION; VASCULAR-DISEASE; OXIDATIVE STRESS; STEARIC-ACID
Issue Date
201010
Publisher
BIOSCIENTIFICA LTD
Citation
JOURNAL OF ENDOCRINOLOGY, v.207, no.1, pp.35 - 44
Abstract
The present study examined whether adiponectin can inhibit palmitate-induced apoptosis, and also the associated mechanisms and signal transduction pathways in human umbilical vein endothelial cells. Cells treated with 500 mu M palmitate for 48 h increased reactive oxygen species (ROS) generation and induced apoptosis. Treatment with antioxidant N-acetyl-L-cysteine (1 mM) and globular adiponectin (5 mu g/ml) inhibited palmitate-induced ROS generation and apoptosis. The AMP-activated protein kinase (AMPK) activator 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR; 1 mM), and cAMP activators forskolin (10 mu M) and cholera toxin (200 ng/ml) also displayed the same effects. The inhibitory effects of adiponectin on ROS generation and apoptosis were reversed by the AMPK inhibitor compound C (40 mu M), cAMP inhibitor SQ22536 (50 mu M), and protein kinase A (PKA) inhibitor H-89 (10 mu M). The inhibitory effect of forskolin on palmitate-induced apoptosis was reversed by compound C, whereas the inhibitory effect of AICAR was not reversed by SQ22536 and H-89. AICAR and forskolin could not inhibit palmitate-induced apoptosis in cells treated with dominant-negative AMPK. Forskolin increased phosphorylated AMPK at both Thr-172 and Ser-485/491. These results suggest that adiponectin inhibits palmitate-induced apoptosis by suppression of ROS generation via both the cAMP/PKA and AMPK pathways. Interaction between cAMP/PKA and AMPK pathways may be involved. Journal of Endocrinology (2010) 207, 35-44
URI
http://hdl.handle.net/YU.REPOSITORY/23525http://dx.doi.org/10.1677/JOE-10-0093
ISSN
0022-0795
Appears in Collections:
의과대학 > 생리학교실 > Articles
의과대학 > 영상의학과학교실 > Articles
의과대학 > 산부인과학교실 > Articles
의과대학 > 생화학.분자생물학교실 > Articles
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