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Effect of ozone on nitric oxide synthases gene expression in endothelial cells
Author(s) -
Castillo Carmen,
Villanueva Cleva,
MedinaSantillan Roberto,
Floriano Esau,
Mera Elvia,
CastilloHenkel Carlos
Publication year - 2008
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.22.1_supplement.964.39
Subject(s) - nitric oxide , gene expression , ozone , chemistry , nitric oxide synthase , basal (medicine) , gene isoform , medicine , microbiology and biotechnology , endocrinology , andrology , gene , biochemistry , biology , organic chemistry , insulin
The goal was to explore the effects of ozone (O3) on gene expression of nitric oxide synthases (NOSs) in endothelial cells (EC) isolated from rat aorta. EC grew until confluence and then they were exposed (1h) to 1ppm of O3 or to 0.05 ppm of O3 (to assess the effect of separating the cells from the culture environment) under sterile conditions. After O3 exposure EC were incubated within normal culture environment during 3, 6 or 9 hs. mRNA was determined by means of real time RT‐PCR. O3 at 0.05 ppm significantly decreased the expression of NOSs after 6 h (p<0.05, compared to basal expression) with a partial recovery after 9 h. O3 exposure at 1ppm also decreased NOSs expression but it happened earlier (3 h, p<0.001 compared to basal), was more significant at 6 h (p<0.001) and greater than the effect produced by 0.05 ppm of O3 (p<0.01), and it had also a partial recovery after 9 h. It is concluded that O3 inhibits NOSs gene expression in isolated EC, which is different from the effect on the whole animal where O3 decreases the vascular endothelial and neuronal NOS while increases the inducible isoform, probably because of the systemic induction of inflammatory mediators by O3