ArticleInfection and immunity2014
Protection of human podocytes from shiga toxin 2-induced phosphorylation of mitogen-activated protein kinases and apoptosis by human serum amyloid P component.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- The Role of the Complement System in the Pathogenesis of Infectious Forms of Hemolytic Uremic Syndrome.Biomolecules · 2023Review
- Article
- The Shiga Toxin Receptor Globotriaosylceramide as Therapeutic Target in Shiga ToxinMicroorganisms · 2021Article
- Podocytes Produce and Secrete Functional Complement C3 and Complement Factor H.Frontiers in immunology · 2020Article
- Shiga toxin triggers endothelial and podocyte injury: the role of complement activation.Pediatric nephrology (Berlin, Germany) · 2019Review
- Complement Activation Contributes to the Pathophysiology of Shiga Toxin-Associated Hemolytic Uremic Syndrome.Microorganisms · 2019Review
- CRISPR Screen Reveals that EHEC's T3SS and Shiga Toxin Rely on Shared Host Factors for Infection.mBio · 2018Article
- Differentiation of human iPSCs into functional podocytes.PloS one · 2018Article
- Diagnostic Accuracy of Serum and Urine S100A8/A9 and Serum Amyloid A in Probable Acute Abdominal Pain at Emergency Department.Disease markers · 2018Article
- The Pentraxins 1975-2018: Serendipity, Diagnostics and Drugs.Frontiers in immunology · 2018Review
- Shiga Toxin Mediated Neurologic Changes in Murine Model of Disease.Frontiers in cellular and infection microbiology · 2016Article
- Infection-Related Focal Segmental Glomerulosclerosis in Children.BioMed research international · 2016Review
- Shiga toxin type-2 (Stx2) induces glutamate release via phosphoinositide 3-kinase (PI3K) pathway in murine neurons.Frontiers in molecular neuroscience · 2015Article
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Authors and funding
14 authors at 7 institutions in 3 countries.
Funding
Abstract
Hemolytic uremic syndrome (HUS) is mainly induced by Shiga toxin 2 (Stx2)-producing Escherichia coli. Proteinuria can occur in the early phase of the disease, and its persistence determines the renal prognosis. Stx2 may injure podocytes and induce proteinuria. Human serum amyloid P component (SAP), a member of the pentraxin family, has been shown to protect against Stx2-induced lethality in mice in vivo, presumably by specific binding to the toxin. We therefore tested the hypothesis that SAP can protect against Stx2-induced injury of human podocytes. To elucidate the mechanisms underlying podocyte injury in HUS-associated proteinuria, we assessed Stx2-induced activation of mitogen-activated protein kinases (MAPKs) and apoptosis in immortalized human podocytes and evaluated the impact of SAP on Stx2-induced damage. Human podocytes express Stx2-binding globotriaosylceramide 3. Stx2 applied to cultured podocytes was internalized and then activated p38α MAPK and c-Jun N-terminal kinase (JNK), important signaling steps in cell differentiation and apoptosis. Stx2 also activated caspase 3, resulting in an increased level of apoptosis. Coincubation of podocytes with SAP and Stx2 mitigated the effects of Stx2 and induced upregulation of antiapoptotic Bcl2. These data suggest that podocytes are a target of Stx2 and that SAP protects podocytes against Stx2-induced injury. SAP may therefore be a useful therapeutic option.
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