Methionine-induced hyperhomocysteinemia and bleomycin hydrolase deficiency alter the expression of mouse kidney proteins involved in renal disease.

摘要: Abstract Scope Hyperhomocysteinemia (HHcy) induced by dietary or genetic factors is linked to kidney disease. Bleomycin hydrolase (Blmh) metabolizes Hcy-thiolactone Hcy. We aimed explain the role of HHcy in Methods and results examined proteome Blmh-knockout mouse models using 2D IEF/SDS-PAGE gel electrophoresis MALDI-TOF mass spectrometry. found that was altered Blmh −/− genotype. Proteins involved metabolism lipoprotein (ApoA1), amino acid protein (Acy1, Hspd1), carbohydrate (Pdhb, Fbp1-isoform 1, Eno1), energy (Ndufs8, Ldhd) were down-regulated. (Fbp1-isoform 2), oxidative stress response (Prdx2), detoxification (Glod4) up-regulated. The genotype down-regulated Glod4 isoform 3 mRNA but did not affect 1 expression kidneys, suggesting post-transcriptional regulation +/+ Responses ApoA1, Acy1, Hspd1, Ndufs8, Fbp1, Eno1, Prdx2 and/or deficiency mimic their responses renal Conclusion Our findings indicate interacts with diverse cellular processes – lipoprotein, protein, carbohydrate, metabolisms, detoxification, antioxidant defenses are essential for normal homeostasis deregulation these can account involvement