Noviherbaspirillum galbum sp. nov., a bacterium isolated from soil.

A Gram-stain-negative, aerobic, non-motile and yellow-colored bacterium, strain 17J57-3 T, was isolated from soil collected in Pyeongchang city, Korea. Phylogenetic analyses based on 16S rRNA gene sequences revealed that strain 17J57-3 T formed a distinct lineage within the family Oxalobacteraceae (order Burkholderiales, class Betaproteobacteria). Strain 17J57-3 T was the most closely related to Noviherbaspirillum humi U15T (96.4% 16S rRNA gene sequence similarity) and Noviherbaspirillum massiliense JC206T (96.2%). The draft genome size of strain 17J57-3 T was 6,117,206 bp. Optimal growth occurred at 30 °C, pH 7.0 without NaCl. The predominant cellular fatty acids were summed feature 3 (C16:1 ω6c/C16:1 ω7c) and C16:0. The major respiratory quinone was Q-8. The major polar lipids were diphosphatidylglycerol, phosphatidylglycerol and phosphatidylethanolamine. Biochemical, chemotaxonomic and phylogenetic analyses indicated that strain 17J57-3 T represents a novel bacterial species within the genus Noviherbaspirillum, for which the name Noviherbaspirillum galbum is proposed. The type strain of Noviherbaspirillum galbum is 17J57-3 T (= KCTC 62213 T = NBRC 114384 T).

Transduced Tat-aldose Reductase Protects Hippocampal Neuronal Cells against Oxidative Stress-induced Damage.

Aldose reductase (AR) protein, a member of the NADPH-dependent aldo-keto reductase family, reduces a wide range of aldehydes and enhances cell survival by inhibition of oxidative stress. Oxidative stress is known as one of the major pathological factor in ischemia. Since the precise function of AR protein in ischemic injury is fully unclear, we examined the function of AR protein in hippocampal neuronal (HT-22) cells and in an animal model of ischemia in this study. Cell permeable Tat-AR protein was produced by fusion of protein transduction domain in Tat for delivery into the cells. Tat-AR protein transduced into HT-22 cells and significantly inhibited cell death and regulated the mitogen-activate protein kinases (MAPKs), Bcl-2, Bax, and Caspase-3 under oxidative stress condition. In an ischemic animal model, Tat-AR protein transduced into the brain tissues through the blood-brain barrier (BBB) and drastically decreased neuronal cell death in hippocampal CA1 region. These results indicate that transduced Tat-AR protein has protective effects against oxidative stress-induced neuronal cell death in vitro and in vivo, suggesting that Tat-AR protein could be used as potential therapeutic agent in ischemic injury.