ArticleThe Journal of clinical investigation1996
G-protein coupled and tyrosine kinase receptors: evidence that activation of the insulin-like growth factor I receptor is required for thrombin-induced mitogenesis of rat aortic smooth muscle cells.
Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 73 citations in OpenAlex.
- The expression profile analysis of atrial mRNA in rats with atrial fibrillation: the role of IGF1 in atrial fibrosis.BMC cardiovascular disorders · 2019Article
- Proteinase-activated receptors (PARs) - focus on receptor-receptor-interactions and their physiological and pathophysiological impact.Cell communication and signaling : CCS · 2013Review
- Characterization of PAR1 and FGFR1 expression in invasive breast carcinomas: Prognostic significance.Oncology letters · 2012Article
- IGF-1 has plaque-stabilizing effects in atherosclerosis by altering vascular smooth muscle cell phenotype.The American journal of pathology · 2011Article
- Evidence for prostacyclin and cAMP upregulation by bradykinin and insulin-like growth factor 1 in vascular smooth muscle cells.Journal of receptor and signal transduction research · 2010Article
- Secretion without Golgi.Journal of cellular biochemistry · 2008Review
- Epiregulin is a potent vascular smooth muscle cell-derived mitogen induced by angiotensin II, endothelin-1, and thrombin.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- Blocking ligand occupancy of the alphaVbeta3 integrin inhibits insulin-like growth factor I signaling in vascular smooth muscle cells.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Protease-resistant form of insulin-like growth factor-binding protein 5 is an inhibitor of insulin-like growth factor-I actions on porcine smooth muscle cells in culture.The Journal of clinical investigation · 1997Article
- Stimulation of activin A expression in rat aortic smooth muscle cells by thrombin and angiotensin II correlates with neointimal formation in vivo.The Journal of clinical investigation · 1997Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
IGF I is an ubiquitous peptide that activates a membrane tyrosine kinase receptor and has autocrine/paracrine effects on vascular smooth muscle cells. Thrombin activates a G-protein coupled receptor and is also a mitogen for vascular smooth muscle cells. To assess the potential role of IGF I as a mediator of thrombin's effects, we characterized expression of IGF I and of its receptor on vascular smooth muscle cells exposed to thrombin. Thrombin dose-dependently decreased IGF I mRNA levels and caused a delayed decrease in IGF I secretion from vascular smooth muscle cells. This effect was mimicked by the hexapeptide SF-FLRN (that functions as a tethered ligand) and was inhibited by hirudin. In contrast, thrombin doubled IGF I receptor density on vascular smooth muscle cells, without altering binding affinity (Kd). An anti-IGF I antiserum markedly reduced thrombin-induced DNA synthesis, whereas nonimmune serum and an anti-fibroblast growth factor antibody were without effect. Cell counts confirmed these results. Downregulation of IGF I receptors by antisense phosphorothioate oligonucleotides likewise markedly inhibited thrombin-induced DNA synthesis. These data demonstrate that a functional IGF I-IGF I receptor pathway is essential for thrombin-induced mitogenic signaling and support the concept of cross talk between G-protein coupled and tyrosine kinase receptors.
Indexed as
Identifiers
What OpenQuestion holds
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.