ArticleThe Journal of clinical investigation1998
Retinoic acid uses divergent mechanisms to activate or suppress mitogenesis in rat aortic smooth muscle cells.
Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 67 citations in OpenAlex.
- The Effect of Retinoids in Vascular Smooth Muscle Cells: From Phenotyping Switching to Proliferation and Migration.International journal of molecular sciences · 2024Review
- Potential Therapeutic Effect of All-Trans Retinoic Acid on Atherosclerosis.Biomolecules · 2022Review
- The role of β-carotene and vitamin A in atherogenesis: Evidences from preclinical and clinical studies.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020Review
- The membrane receptor for plasma retinol-binding protein, a new type of cell-surface receptor.International review of cell and molecular biology · 2011Review
- A role for the cell cycle phosphatase Cdc25a in vitamin D-dependent inhibition of adult rat vascular smooth muscle cell proliferation.The Journal of steroid biochemistry and molecular biology · 2010Article
- Vitamin D-dependent suppression of endothelin-induced vascular smooth muscle cell proliferation through inhibition of CDK2 activity.The Journal of steroid biochemistry and molecular biology · 2010Article
- Expression of the vitamin d receptor is increased in the hypertrophic heart.Hypertension (Dallas, Tex. : 1979) · 2008Article
- The early- and late stages in phenotypic modulation of vascular smooth muscle cells: differential roles for lysophosphatidic acid.Biochimica et biophysica acta · 2008Article
- Regulation and characteristics of vascular smooth muscle cell phenotypic diversity.Netherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation · 2007Article
- Retinoic acid inhibits airway smooth muscle cell migration.American journal of respiratory cell and molecular biology · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In different experimental models, retinoid has been shown to stimulate or suppress mitogenesis in cultured cells. The mechanisms underlying this seemingly paradoxical activity remain only partially understood. We have examined the ability of all-trans retinoic acid (ATRA), as well as a number of synthetic retinoids, either alone or in the presence of a mitogenic stimulus (i.e., endothelin), to regulate DNA synthesis and cell replication in cultured rat aortic smooth muscle cells. ATRA alone stimulates [3H]thymidine incorporation (approximately twofold) and increases cell number (approximately twofold) in these cultures but suppresses [3H]thymidine incorporation and reduces cell number in cultures treated with endothelin. The reduction in endothelin-stimulated DNA synthesis correlates closely with the ability of ATRA to inhibit endothelin-stimulated extracellular signal-regulated kinase but not c-Jun NH2-terminal kinase activity. Activation of mitogenesis, seen in the presence of ATRA alone, was independent of extracellular signal-regulated kinase activation but correlated well with increased expression of cyclin D1 mRNA and protein. Concomitant activation of the cdk inhibitor p21 led to truncation of ATRA's mitogenic activity at higher doses of ligand. Collectively, these data indicate that the role of retinoids in the regulation of mitogenesis in vascular smooth muscle is complex. Under quiescent conditions they activate mitogenesis, while in the presence of growth stimulation, as is frequently seen with vasculopathic conditions, they suppress mitogenesis. It appears that independent circuitry is involved in signaling each of these effects.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.