@article{oai:soar-ir.repo.nii.ac.jp:00021726,
 author = {Tsukahara, Ryoko and Haniu, Hisao and Matsuda, Yoshikazu and Tsukahara, Tamotsu},
 journal = {MOLECULAR AND CELLULAR ENDOCRINOLOGY},
 month = {Sep},
 note = {Alkyl-glycerophosphate (AGP) accumulates in atherogenic oxidized-LDL and human atherosclerotic plaques and is a potent agonist of peroxisome-proliferator-activated receptor-gamma (PPAR gamma). Recent studies suggest a potential regulatory role for PPAR gamma in endothelial nitric oxide synthase (eNOS) expression/activation and nitrogen oxide (NO) generation in the vascular endothelium. Importantly, eNOS-induced NO and advanced glycation end-products (AGEs) are involved in blood-vessel damage, and diabetic patients exhibit high serum NO and AGE levels; however, the effect of AGP on NO- and AGE-mediated endothelium dysfunction remains unknown. Investigation of the AGP-specific effects on NO- and AGE-mediated dysfunction and the underlying molecular mechanisms revealed that AGP upregulated eNOS expression and NO production, and that eNOS silencing and gamma antagonism inhibited AGP-mediated eNOS upregulation and NO production. Moreover, AGP-PPAR gamma-axis-mediated NO production promoted the generation of reactive oxygen species and AGE formation. These results suggested that AGP plays a significant role in the initiation/progression of diabetes-related atherosclerosis through PPAR gamma activation. (C) 2018 Elsevier B.V. All rights reserved., Article, MOLECULAR AND CELLULAR ENDOCRINOLOGY. 473:100-113 (2018)},
 pages = {100--113},
 title = {The AGP-PPAR gamma axis promotes oxidative stress and diabetic endothelial cell dysfunction},
 volume = {473},
 year = {2018}
}