The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Transforming growth factor-beta 1, but not dexamethasone, down-regulates nitric-oxide synthase mRNA after its induction by interleukin-1 beta in rat smooth muscle cells.
Open accessAbstract
Nitric oxide (NO), which accounts for the biologic properties of endothelium-derived relaxing factor, is synthesized from L-arginine by nitric-oxide synthase (NOS). Two classes of NOS have been identified: a constitutive, calcium-dependent isozyme (cNOS) and an inducible, calcium-independent isozyme (iNOS). NO is generated after the induction of iNOS by cytokines such as interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha. As a potent vasodilator, NO may have an important role in the severe hypotension of septic shock. We investigated whether dexamethasone and transforming growth factor-beta 1 (TGF-beta 1) suppress iNOS mRNA after its induction by IL-1 beta. We found that IL-1 beta induced iNOS mRNA in rat aortic smooth muscle cells (RASMC) in a dose- and time-dependent fashion. IL-1 beta promoted a dramatic and prolonged induction of RASMC iNOS mRNA that peaked at 48 h. Dexamethasone prevented this induction of iNOS mRNA only when given before the addition of IL-1 beta. In contrast, TGF-beta 1 inhibited the induction of iNOS mRNA and NO production in RASMC both before and after the addition of IL-1 beta. After 24 h of IL-1 beta stimulation, TGF-beta 1 down-regulated the iNOS mRNA that had been induced during this initial time period. In nuclear run-on experiments, we found that the down-regulation of iNOS mRNA by TGF-beta 1 in RASMC occurred at the transcriptional level. Our observation that TGF-beta 1 mediates inhibition of RASMC iNOS mRNA after its induction by cytokines may be an important insight into the treatment of septic shock.
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Cites
Biochemistry of nitric oxide and its redox-activated forms
Stamler, J. S., Singel, D. J., & Loscalzo, J. (1992) · Science · doi:10.1126/science.1281928 · Cited by 2,744
Pathogenetic Mechanisms of Septic Shock
Epstein, F. H., & Parrillo, J. E. (1993) · New England Journal of Medicine · doi:10.1056/nejm199305203282008 · Cited by 1,548
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Nitric Oxide Synthases and Cardiac Muscle: Autocrine and Paracrine Influences
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Leiro, J. M., Álvarez, E., Arranz, J. A., Siso, I. G., & Orallo, F. (2003) · Biochemical Pharmacology · doi:10.1016/s0006-2952(03)00041-8 · Cited by 154
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Metadata
- Authors
- Perrella, M. A., Yoshizumi, M., Fen, Z., Tsai, J. C., Hsieh, C. M., Kourembanas, S., & Lee, M. E.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 1994-05
- Volume
- 269
- Issue
- 20
- Pages
- 14595-14600
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W1565444604
- Cited by
- 165
- References
- 2
- FWCI
- 14.09
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- The paper
- Perrella, M. A., Yoshizumi, M., Fen, Z., Tsai, J. C., Hsieh, C. M., Kourembanas, S., & Lee, M. E. (1994). Transforming growth factor-beta 1, but not dexamethasone, down-regulates nitric-oxide synthase mRNA after its induction by interleukin-1 beta in rat smooth muscle cells. Journal of Biological Chemistry. https://doi.org/10.1016/s0021-9258(17)36665-6
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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