ArticleScientific reports2020
Cleavage of proteoglycans, plasma proteins and the platelet-derived growth factor receptor in the hemorrhagic process induced by snake venom metalloproteinases.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
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- Snake Toxins Affecting Blood Vessel Walls: Mode of Action and Biological Significance.International journal of molecular sciences · 2025Review
- Thromboinflammatory complications ofFrontiers in immunology · 2025Review
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- A single nuclear transcriptomic characterisation of mechanisms responsible for impaired angiogenesis and blood-brain barrier function in Alzheimer's disease.Nature communications · 2024Article
- Mouse skin peptidomic analysis of the hemorrhage induced by a snake venom metalloprotease.Amino acids · 2023Article
- Pictolysin-III, a Hemorrhagic Type-III Metalloproteinase Isolated fromPharmaceutics · 2023Article
- Biochemical and hemostatic description of a thrombin-like enzyme TLBro fromFrontiers in chemistry · 2023Article
- Snakebite drug discovery: high-throughput screening to identify novel snake venom metalloproteinase toxin inhibitors.Frontiers in pharmacology · 2023Article
- The Middle Eastern Cousin: Comparative Venomics ofToxins · 2022Article
- Leptolysin, aFrontiers in cellular and infection microbiology · 2022Article
- Terrestrial venomous animals, the envenomings they cause, and treatment perspectives in the Middle East and North Africa.PLoS neglected tropical diseases · 2021Review
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- Bleeding and Thrombosis: Insights into Pathophysiology ofInternational journal of molecular sciences · 2021Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Envenoming by viperid snakes results in a complex pattern of tissue damage, including hemorrhage, which in severe cases may lead to permanent sequelae. Snake venom metalloproteinases (SVMPs) are main players in this pathogenesis, acting synergistically upon different mammalian proteomes. Hemorrhagic Factor 3 (HF3), a P-III class SVMP from Bothrops jararaca, induces severe local hemorrhage at pmol doses in a murine model. Our hypothesis is that in a complex scenario of tissue damage, HF3 triggers proteolytic cascades by acting on a partially known substrate repertoire. Here, we focused on the hypothesis that different proteoglycans, plasma proteins, and the platelet derived growth factor receptor (PDGFR) could be involved in the HF3-induced hemorrhagic process. In surface plasmon resonance assays, various proteoglycans were demonstrated to interact with HF3, and their incubation with HF3 showed degradation or limited proteolysis. Likewise, Western blot analysis showed in vivo degradation of biglycan, decorin, glypican, lumican and syndecan in the HF3-induced hemorrhagic process. Moreover, antithrombin III, complement components C3 and C4, factor II and plasminogen were cleaved in vitro by HF3. Notably, HF3 cleaved PDGFR (alpha and beta) and PDGF in vitro, while both receptor forms were detected as cleaved in vivo in the hemorrhagic process induced by HF3. These findings outline the multifactorial character of SVMP-induced tissue damage, including the transient activation of tissue proteinases, and underscore for the first time that endothelial glycocalyx proteoglycans and PDGFR are targets of SVMPs in the disruption of microvasculature integrity and generation of hemorrhage.
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