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Renal NOS isoforms and splicing in 13 week obese female Zucker rats on antioxidant vs regular diet
Author(s) -
Inman Sharon R,
Slyvka Yuriy,
Feldman Yelena,
Nowak Felicia V
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.971.2
Subject(s) - enos , endocrinology , medicine , endothelial nos , gene isoform , medulla , kidney , nitric oxide synthase , renal cortex , western blot , alternative splicing , cortex (anatomy) , diabetic nephropathy , biology , chemistry , nitric oxide , biochemistry , gene , neuroscience
NO and NOS activity are important for development of diabetic nephropathy and an antioxidant fortified (AO) diet may protect the kidney in the case of diabetes. Female obese Zucker rats (fa/fa) were studied at 13 weeks of age on regular (REG) and AO diets. AO diet was started at 4 weeks. NOS isoforms (n‐neuronal, e‐endothelial and i‐inducible) and their splice forms were tested with Western blot. The AO diet resulted in lower levels of all NOS isoforms both in kidney cortex and medulla compared to the REG diet. There was no significant difference in NOS expression between cortex and medulla in either group. The following splice forms were present in rat kidneys on AO diet: iNOS (122‐124, 77‐83, 72‐75 kDa), nNOS (110‐113, 76‐77, 68‐70 kDa), eNOS (110‐116, 73‐77, 66‐68 kDa). Animals on the REG diet had the following splice forms: iNOS (114‐118, 76‐79, 70‐72 kDa), nNOS (110‐114, 74‐79, 68‐72 kDa), eNOS (102‐103, 70‐72, 64‐66, 38 kDa). The difference between content of NOS isoforms is the result of an increase in the largest and smallest splice forms of eNOS and iNOS in kidney cortex. In medulla the difference is the result of increase of all splice forms for iNOS and nNOS, but for eNOS only the largest and smallest splice form increased and a new smaller additional 38 kDa form was seen in rats on the REG diet. Conclusion AO diet decreased the expression of NOS isoforms in kidneys in obese Zucker rats. Supported by NIH R15 DK073066 to SRI and FVN.