Rabbit Anti-Human ATPB Polyclonal antibody

Telmisartan provides renal benefit at all stages of the renal continuum in patients with type 2 diabetes mellitus. This research is to investigate the effect of telmisartan on kidney function in diabetic rats and to identify the underlying molecular mechanisms. Diabetic rats were divided into vehicle group, low dosage (TeL) group, and high dosage of telmisartan (TeH) group. We performed Illumina RatRef-12 Expression BeadChip gene array experiments. We found 3-months of treatment with telmisartan significantly decreased 24-h urinary albumin, serum creatinine, blood urea nitrogen, and increased creatinine clearance rate. Kidney hypertrophy and glomerular mesangial matrix expansion were ameliorated. The glomeruli from the TeH group had 1541 genes with significantly changed expression (554 increased, 987 decreased). DAVID (Database for annotation, visualization and Integrated discovery) analyses showed that the most enriched term was 'mitochondrion' (Gene Ontology (GO: 0005739)) in all 67 GO functional categories. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses indicated that all differentially expressed genes included seven KEGG pathways. Of those pathways, four are closely related to the oxidative phosphorylation pathway. Quantitative real-time PCR verified that the H+ transporting mitochondrial F1 complex, beta subunit (Atp5b), cytochrome c oxidase subunit VIc (Cox6c), and NADH dehydrogenase (ubiquinone) Fe-S protein 3 (Ndufs3) were significantly downregulated both in TeL and TeH groups, while nephrosis 1 homolog (Nphs1) and nephrosis 2 homolog (Nphs2) were significantly upregulated. The increased expression of malonaldehyde and NDUFS3 in the glomeruli of diabetic rats was attenuated by telmisartan. The other significantly changed pathway we found was the peroxisome proliferator-activated receptor (PPAR) signaling pathway. Our data suggest that telmisartan can improve kidney function in diabetic rats. The mechanism may be involved in mitochondrion oxidative phosphorylation, the PPAR-gamma pathway, and the slit diaphragm. Journal of Molecular Endocrinology (2012) 49, 35-46

Alzheimer's disease (AD) is an age-related neurodegenerative disorder that is characterized by the extracellular deposition of beta-amyloid and intracellular hyperphosphorylation of tau in the cortex and hippocampus of the brain. These characterizations are caused by abnormal expression, modification and deposition of certain proteins. Post-translational modifications of proteins including oxidation and nitration might be involved in the pathogenesis of AD. In this study, AD-related proteins were identified in the cortex of Tg2576 mice used as a model for studying AD. Tg2576 mice express high levels of the Swedish mutated form of human beta-amyloid precursor protein (APP) and generated high levels of beta-amyloid in the brains. Using Western blofting and two-dimensional electrophoresis, proteins with differences in expression, oxidation and nitration in the cortex of Tg2576 mice brains were compared to littermate mice brains used as a control. The proteins with different expression levels were identified using matrix-assisted laser desorption/ionization-time of flight and liquid chromatographytandem mass spectrometry analyses. As a result, 12 proteins were identified among 37 different proteins using the PDQuest program. Furthermore, two proteins, laminin receptor and alpha-enolase, were more susceptible to oxidative modification in the brains of Tg2576 mice compared to those of littermates. Similarly, alpha-enolase, calpain 12, and Atp5b were more modified by nitration in brains of Tg2576 mice than those of littermates. Taken together, these proteins and their modifications may play an important role in the plaque deposition of Tg2576 mice brains.