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Acta Pharmacologica Sinica 2006 September; 27 (9): 1146-1152; doi: 10.1111/j.1745-7254.2006.00359.x |
| Original Article | [ Full text ] |
PPARg phosphorylation mediated by JNK MAPK: a potential role in macrophage-derived foam cell formation1 |
| Ran YIN2, Yu-gang DONG2,4, Hong-liang LI3
2Department of Cardiology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, China; 3Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing 100005, China |
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Aim: To investigate whether oxidized low-density lipoprotein (ox-LDL) modulates peroxisome proliferator-activated receptor g (PPARg) activity through phosphorylation in macrophages, and the effect of PPARg phosphorylation on macrophages-derived foam cell formation.
Methods: After exposing the cultured THP-1 cells to ox-LDL in the presence or absence of different mitogen-activated protein kinase (MAPK) inhibitors, PPARg and phosphorylated PPARg protein levels were detected by Western blot. MAPK activity was analyzed using MAP Kinase Assay Kit. Intracellular cholesterol accumulation was assessed by Oil red O staining and cholesterol oxidase enzymatic method. The mRNA level of PPARg target gene was determined by reverse transcription-polymerase chain reaction (RT-PCR).
Results: ox-LDL evaluated PPARg phosphorylation status and subsequently decreased PPARg target gene expression in a dose-dependent manner. ox-LDL also induced MAPK activation. Treatment of THP-1 cells with c-Jun N-terminal kinase-, but not p38- or extracellular signal-regulated kinase-MAPK inhibitor, significantly suppressed PPARg phosphorylation induced by ox-LDL, which in turn inhibited foam cell formation.
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Keywords: peroxisome proliferator-activated receptor g; phosphorylation; macrophages; LDL lipoprotein |
| 1 Project supported by the Natural Science Foundation of Guangdong Province, China (2003). |
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