Microglial peroxiredoxin V acts as an inducible anti‐inflammatory antioxidant through cooperation with redox signaling cascades

• DOI: 10.1111/j.1471-4159.2010.06691.x
• Publication Date: 2010-03-21T00:47:35Z
• Authors: Hu‐Nan Sun; Sun‐Uk Kim; Song Mei Huang; Jin‐Man Kim; Young‐Ho Park; Seok‐Ho Kim; Hee‐Young Yang; Kyoung‐Jin Chung; Tae‐Hoon Lee; Hoon Sung Choi; Ju Sik Min; Moon‐Ki Park; Sang‐Keun Kim; Sang‐Rae Lee; Kyu‐Tae Chang; Sang‐Ho Lee; Dae‐Yeul Yu; Dong‐Seok Lee
• Keywords: Peroxiredoxin; Mitochondrial ROS; Apocynin

Reactive oxygen species (ROS) actively participate in microglia-mediated pathogenesis as pro-inflammatory molecules. However, little is known about the involvement of specific antioxidants maintaining microglial oxidative balance. We demonstrate that peroxiredoxin (Prx) 5 expression up-regulated by lipopolysaccharide (LPS) through activation ROS-sensitive signaling pathway and involved attenuation both nitric oxide (NO) generation. Unlike stimulation insults with paraquat hydrogen peroxide, Prx V highly sensitive to LPS-stimulation microglia. Reduction ROS level treatment either NADPH oxidase inhibitor or antioxidant ablates LPS-mediated up-regulation BV-2 cells closely associated c-jun N-terminal kinase (JNK) pathway. This suggests ROS/JNK induction. Furthermore, NO induces ablated addition inducible synthase deleted mutation LPS-stimulated Therefore, these results suggest induced cooperative action among ROS, RNS, JNK cascades. Interestingly, knockdown causes acceleration microglia activation, including augmented generation JNK-dependent production. In summary, we plays a key role process modulation balance between ROS/NO corresponding cascade activation.