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Articles by André Samson
Impact of BECLIN1 haploinsufficiency on goblet cell function and susceptibility to colitis
Abstract BECLIN1 is a central regulator of autophagy and endocytic trafficking essential for epithelial homoeostasis. While complete intestinal epithelial loss of BECLIN1 causes fatal enteritis originating in the small intestine, the consequences of its partial loss in the gut remain unclear. Given that BECLIN1 expression can vary in human disease, we investigated whether reduced BECLIN1 is sufficient to impair gut barrier function.
The kinase domain of RIPK3 tunes its scaffolding functions - Cell Death & Differentiation
Abstract The pro-inflammatory programmed cell death pathway, necroptosis, relies on phosphorylation of the terminal effector, MLKL, by RIPK3. RIPK3-deficient mice or those harboring the kinase-inactivating mutation, RIPK3K51A, are ostensibly normal in the absence of challenge, indicating that RIPK3 and its kinase activity are dispensable for development. However, another kinase-inactivating mutation, RIPK3D161N, results in embryonic lethality in mice due to widespread apoptosis.
Non-apoptotic caspase-8 is critical for orchestrating exaggerated inflammation during severe SARS-CoV-2 infection - Nature Communications
Abstract Inflammation and excess cytokine release are hallmarks of severe COVID-19. While programmed cell death is known to drive inflammation, its role in SARS-CoV-2 pathogenesis remains unclear. Using gene-targeted murine COVID-19 models, we here find that caspase-8 is critical for cytokine release and inflammation. Loss of caspase-8 reduces disease severity and viral load in mice, and this occurs independently of its apoptotic function.
Author Correction: In situ visualization of endothelial cell-derived extracellular vesicle formation in steady state and malignant conditions - Nature Communications
Correction to: Nature Communications https://doi.org/10.1038/s41467-024-52867-5, published online 22 October 2024 In the version of the article initially published, the flow cytometry shown in the second panel of Fig. 6a for “EμMyc” was an inadvertent duplicate of the first panel “Steady state.” The legend for Fig. 6c has been amended to include the text “Steady state control data also shown in Fig. 4a.” The figure and legend are amended in the HTML and PDF versions of the article.
Ischaemic endothelial necroptosis induces haemolysis and COVID-19 angiopathy - Nature
Abstract Microangiopathy is a major complication of SARS-CoV-2 infection and contributes to the acute and chronic complications of the disease1. Endotheliopathy and dysregulated blood coagulation are prominent in COVID-19 and are considered to be major causes of microvascular obstruction1,2. Here we demonstrate extensive endothelial cell (EC) death in the microvasculature of COVID-19 organs.
MLKL deficiency elevates testosterone production in male mice independently of necroptotic functions - Cell Death & Disease
Abstract Mixed lineage kinase domain-like (MLKL) is a pseudokinase, best known for its role as the terminal effector of the necroptotic cell death pathway. MLKL-mediated necroptosis has long been linked to various age-related pathologies including neurodegeneration, atherosclerosis and male reproductive decline, however many of these attributions remain controversial.
In situ visualization of endothelial cell-derived extracellular vesicle formation in steady state and malignant conditions - Nature Communications
Abstract Endothelial cells are integral components of all vasculature within complex organisms. As they line the blood vessel wall, endothelial cells are constantly exposed to a variety of molecular factors and shear force that can induce cellular damage and stress. However, how endothelial cells are removed or eliminate unwanted cellular contents, remains unclear.
Mapping where and when necroptotic cell death occurs in disease - Cell Death & Differentiation
A series of recent studies have established where the necroptosis machinery — RIPK1, RIPK3, MLKL, ZBP1 and Caspase-8 — occur and are activated in mouse and human tissues, and how ZBP1 splicing might regulate necroptosis. These studies highlight the importance of mapping necroptosis spatially to understand how pathway dysregulation can lead to disease.
A common human MLKL polymorphism confers resistance to negative regulation by phosphorylation - Nature Communications
Abstract Across the globe, 2-3% of humans carry the p.Ser132Pro single nucleotide polymorphism in MLKL, the terminal effector protein of the inflammatory form of programmed cell death, necroptosis. Here we show that this substitution confers a gain in necroptotic function in human cells, with more rapid accumulation of activated MLKLS132P in biological membranes and MLKLS132P overriding pharmacological and endogenous inhibition of MLKL.
MLKL deficiency protects against low-grade, sterile inflammation in aged mice - Cell Death & Differentiation
Abstract MLKL and RIPK3 are the core signaling proteins of the inflammatory cell death pathway, necroptosis, which is a known mediator and modifier of human disease. Necroptosis has been implicated in the progression of disease in almost every physiological system and recent reports suggest a role for necroptosis in aging.
MLKL trafficking and accumulation at the plasma membrane control the kinetics and threshold for necroptosis
Abstract Mixed lineage kinase domain-like (MLKL) is the terminal protein in the pro-inflammatory necroptotic cell death program. RIPK3-mediated phosphorylation is thought to initiate MLKL oligomerization, membrane translocation and membrane disruption, although the precise choreography of events is incompletely understood. Here, we use single-cell imaging approaches to map the chronology of endogenous human MLKL activation during necroptosis.
Developing a Physician Engagement Agreement at The Ottawa Hospital: A Collaborative Approach
HR Resources Database October 2012 Health Human Resources Developing a Physician Engagement Agreement at The Ottawa Hospital: A Collaborative Approach Chris G. Scott, Anne Thériault, Shaun McGuire, André Samson, Christine Clement and Jim R. Worthington Tweet Abstract [This article was originally published in Healthcare Quarterly 15.3] The Ottawa Hospital (TOH) is focused on providing safe, high-quality care to its patients.
Developing a Physician Engagement Agreement at The Ottawa Hospital: A Collaborative Approach
Healthcare Quarterly, 15(3) July 2012: 50-56.doi:10.12927/hcq.2013.23020 Health Human Resources Developing a Physician Engagement Agreement at The Ottawa Hospital: A Collaborative Approach Chris G. Scott, Anne Thériault, Shaun McGuire, André Samson, Christine Clement and Jim R. Worthington Tweet Abstract The Ottawa Hospital (TOH) is focused on providing safe, high-quality care to its patients.
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