ArticlePLoS computational biology2017
Transcriptional and Post-Transcriptional Regulation of Thrombospondin-1 Expression: A Computational Model.
Article in PLoS computational biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- A mechanistic computational model of HGF-VEGF-mediated endothelial cell proliferation and vascular permeability.iScience · 2025Article
- Endothelial cells signaling and patterning under hypoxia: a mechanistic integrative computational model including the Notch-Dll4 pathway.Frontiers in physiology · 2024Article
- Systems biology of angiogenesis signaling: Computational models and omics.WIREs mechanisms of disease · 2022Review
- A mechanistic integrative computational model of macrophage polarization: Implications in human pathophysiology.PLoS computational biology · 2019Article
- Extensive transcriptional responses are co-ordinated by microRNAs as revealed by Exon-Intron Split Analysis (EISA).Nucleic acids research · 2019Article
- Discovery of Biomarker Panels for Neural Dysfunction in Inborn Errors of Amino Acid Metabolism.Scientific reports · 2019Article
- Protein ensembles link genotype to phenotype.PLoS computational biology · 2019Review
- TSP-1 is downregulated and inversely correlates with miR-449c expression in Cushing's disease.Journal of cellular and molecular medicine · 2019Article
- Deciphering the complex role of thrombospondin-1 in glioblastoma development.Nature communications · 2019Article
- Mechanistic Computational Models of MicroRNA-Mediated Signaling Networks in Human Diseases.International journal of molecular sciences · 2019Review
- Human expression patterns: qualitative and quantitative analysis of thrombospondin-1 under physiological and pathological conditions.Journal of cellular and molecular medicine · 2018Review
- Computer Simulation of TSP1 Inhibition of VEGF-Akt-eNOS: An Angiogenesis Triple Threat.Frontiers in physiology · 2018Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Hypoxia is an important physiological stress signal that drives angiogenesis, the formation of new blood vessels. Besides an increase in the production of pro-angiogenic signals such as vascular endothelial growth factor (VEGF), hypoxia also stimulates the production of anti-angiogenic signals. Thrombospondin-1 (TSP-1) is one of the anti-angiogenic factors whose synthesis is driven by hypoxia. Cellular synthesis of TSP-1 is tightly regulated by different intermediate biomolecules including proteins that interact with hypoxia-inducible factors (HIFs), transcription factors that are activated by receptor and intracellular signaling, and microRNAs which are small non-coding RNA molecules that function in post-transcriptional modification of gene expression. Here we present a computational model that describes the mechanistic interactions between intracellular biomolecules and cooperation between signaling pathways that together make up the complex network of TSP-1 regulation both at the transcriptional and post-transcriptional level. Assisted by the model, we conduct in silico experiments to compare the efficacy of different therapeutic strategies designed to modulate TSP-1 synthesis in conditions that simulate tumor and peripheral arterial disease microenvironment. We conclude that TSP-1 production in endothelial cells depends on not only the availability of certain growth factors but also the fine-tuned signaling cascades that are initiated by hypoxia.
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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.