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Regulation of NOS enzymes by splice variants
Author(s) -
Hill Melanie L.,
Perkins Andrew,
Memili Erdogan,
Alexander Barbara T.,
Hennington Bettye Sue
Publication year - 2011
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.25.1_supplement.1029.9
Subject(s) - splice , alternative splicing , enos , rna splicing , biology , gene isoform , messenger rna , gene , nitric oxide synthase , genetics , medicine , endocrinology , microbiology and biotechnology , nitric oxide , rna
Low birth weight (LBW) is a risk factor for cardiovascular disease (CVD). Our lab utilizes a rat model of LBW induced by placental insufficiency in which male LBW rats develop hypertension in adulthood that is associated with differential expression of renal endothelial nitric oxide synthase (eNOS) mRNA and protein. Splice variants result from alternative splicing of primary mRNA; and NOS splice variants are abnormal in CVD. Thus, we tested the hypothesis that splice variants for NOS isoforms may alter NOS expression and thus, contribute to LBW hypertension. Data obtained from the National Center for Biotechnology Information (NCBI) databases of Pub Med, Nucleotide, Gene, Protein and Genome indicate splice variants for rat kidney neuronal or nNOS, eNOS, and inducible or iNOS. Utilizing PCR and primers specific to the 5′ or 3′ end of each NOS we found single bands only for each NOS. We would have expected multiple bands if splice variants existed. Thus, these results may shed light on molecular mechanisms critical in the regulation of blood pressure in LBW.