Lydie Crescence

Aix-Marseille Université

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Laurence Panicot‐Dubois

Aix-Marseille Université

Christophe Dubois

Aix-Marseille Université

Lorenzo Archetti

Antoine Briantais

Hôpital de la Timone

Carla E. Cano

HiFiBiO Therapeutics (France)

Nicolas Boucherit

Centre de Recherche en Cancérologie de Marseille

Florence Orlanducci

Inserm

Daniel Olive

Centre de Recherche en Cancérologie de Marseille

Caroline Imbert

Centre de Recherche en Cancérologie de Marseille

Laurent Gorvel

Inserm

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Inserm

118

Aix-Marseille Université

Centre National de la Recherche Scientifique

Unité de recherche sur les maladies cardiovasculaires et métaboliques

Centre de Recherche en Cancérologie de Marseille

Institut National de Recherche pour l'Agriculture, l'Alimentation et l'Environnement

Assistance Publique Hôpitaux de Marseille

Hôpital de la Timone

Institut Paoli-Calmettes

Institut de Neurobiologie de la Méditerranée

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Cellular and Molecular Mechanisms Leading to Air Travel-Induced Thrombosis

Circulation Research (2025)

Julie Tourn Lydie Crescence Laurie Bruzzese Laurence Panicot‐Dubois Christophe Dubois

Venous thromboembolism, characterized by deep vein thrombosis and pulmonary embolism, is the third cardiovascular disease in the world. Deep vein thrombosis occurs when a blood clot forms in areas of impaired blood flow, and it is significantly affected by environmental factors. Local hypoxia, caused by venous stasis, plays a critical role in deep vein thrombosis under normal conditions, and this effect is intensified when the P o 2 decreases, such as during air travel or high-altitude exposure. The lower oxygen levels and reduced pressure at high altitudes further contribute to deep vein thrombosis development. These conditions increase the pro-coagulant activity of neutrophils, platelets, and red blood cells, which interact on the surface of activated endothelial cells, promoting clot formation. Understanding the mechanisms involved in thrombus formation when P o 2 is reduced, with or without pressure reduction, is crucial for preventing the development of venous thromboembolisms in such conditions and identifying innovative therapeutic targets. This literature review explores the mechanisms involved in thrombus formation related to high-altitude conditions and discusses the pro-coagulant consequences induced by environmental disturbances.

Blood stasis

Venous stasis

Hypoxia

10.1161/circresaha.124.325208

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Increased levels of the megakaryocyte and platelet expressed cysteine proteases stefin A and cystatin A prevent thrombosis

Scientific Reports (2019)

Anna Mezzapesa Delphine Bastelica Lydie Crescence Marjorie Poggi Michel Grino

10.1038/s41598-019-45805-9

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Citations (11)

A thrombus is formed by a gradient of platelet activation and procoagulant endothelium

Research and Practice in Thrombosis and Haemostasis (2023)

Estelle Carminita Julie Tourn Lydie Crescence Nicolas Brouilly Glenn Merrill‐Skoloff

Platelet adhesiveness

10.1016/j.rpth.2023.102209

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Citations (2)

The P2Y12 Receptor Antagonist Selatogrel Dissolves Preformed Platelet Thrombi In Vivo

Journal of Clinical Medicine (2021)

Lydie Crescence Markus Kramberg Martine Baumann Markus Rey Sébastiên Roux

Selatogrel, a potent and reversible antagonist of the P2Y12 receptor, inhibited FeCl3-induced thrombosis in rats. Here, we report the anti-thrombotic effect of selatogrel after subcutaneous applications in guinea pigs and mice. Selatogrel inhibited platelet function only 10 min after subcutaneous application in mice. In addition, in a modified Folts thrombosis model in guinea pigs, selatogrel prevented a decrease in blood-flow, indicative of the inhibition of ongoing thrombosis, approximately 10 min after subcutaneous injection. Selatogrel fully normalised blood flow; therefore, we speculate that it may not only prevent, but also dissolve, platelet thrombi. Thrombus dissolution was investigated using real-time intravital microscopy in mice. The infusion of selatogrel during ongoing platelet thrombus formation stopped growth and induced the dissolution of the preformed platelet thrombus. In addition, platelet-rich thrombi were given 30 min to consolidate in vivo. The infusion of selatogrel dissolved the preformed and consolidated platelet thrombi. Dissolution was limited to the disintegration of the occluding part of the platelet thrombi, leaving small mural platelet aggregates to seal the blood vessel. Therefore, our experiments uncovered a novel advantage of selatogrel: the dissolution of pre-formed thrombi without the disintegration of haemostatic seals, suggesting a bipartite benefit of the early application of selatogrel in patients with acute thrombosis.

Bleeding time

Ex vivo

10.3390/jcm10225349

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Citations (7)

Figure S2 from Targeting BTN2A1 Enhances Vγ9Vδ2 T-Cell Effector Functions and Triggers Tumor Cell Pyroptosis

Anne-Charlotte Le Floch Caroline Imbert Nicolas Boucherit Laurent Gorvel Stéphane Fattori

<p>Supplementary Figure S2. BTN2A1 is broadly expressed in normal and tumor cells.</p>

Pyroptosis

10.1158/2326-6066.27950815

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Figure S6 from Targeting BTN2A1 Enhances Vγ9Vδ2 T-Cell Effector Functions and Triggers Tumor Cell Pyroptosis

Anne-Charlotte Le Floch Caroline Imbert Nicolas Boucherit Laurent Gorvel Stéphane Fattori

<p>Supplementary Figure S6. Anti-BTN2A1 107G3B5 increases Vɣ9Vδ2 T cell effectors functions against hematological cell lines.</p>

Pyroptosis

10.1158/2326-6066.27950803

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An OMA1 redox site controls mitochondrial homeostasis, sarcoma growth, and immunogenicity

Life Science Alliance (2023)

Richard MIALLOT Virginie Millet Yann Groult A. Modelska Lydie Crescence

Aggressive tumors often display mitochondrial dysfunction. Upon oxidative stress, mitochondria undergo fission through OMA1-mediated cleavage of the fusion effector OPA1. In yeast, a redox-sensing switch participates in OMA1 activation. 3D modeling of OMA1 comforted the notion that cysteine 403 might participate in a similar sensor in mammalian cells. Using prime editing, we developed a mouse sarcoma cell line in which OMA1 cysteine 403 was mutated in alanine. Mutant cells showed impaired mitochondrial responses to stress including ATP production, reduced fission, resistance to apoptosis, and enhanced mitochondrial DNA release. This mutation prevented tumor development in immunocompetent, but not nude or cDC1 dendritic cell–deficient, mice. These cells prime CD8 + lymphocytes that accumulate in mutant tumors, whereas their depletion delays tumor control. Thus, OMA1 inactivation increased the development of anti-tumor immunity. Patients with complex genomic soft tissue sarcoma showed variations in the level of OMA1 and OPA1 transcripts. High expression of OPA1 in primary tumors was associated with shorter metastasis-free survival after surgery, and low expression of OPA1, with anti-tumor immune signatures. Targeting OMA1 activity may enhance sarcoma immunogenicity.

10.26508/lsa.202201767

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Assessment of Thrombotic and Bleeding Tendency in Two Mouse Models of Chronic Kidney Disease: Adenine-Diet and 5/6th Nephrectomy

TH Open (2020)

Camélia Makhloufi Lydie Crescence Roxane Darbousset Nathalie McKay Ziad A. Massy

Abstract The coexistence of bleeding and thrombosis in patients with chronic kidney disease (CKD) is frequent and poorly understood. Mouse models are essential to understand complications of CKD and to develop new therapeutic approaches improving the health of patients. We evaluated the hemostasis in two models of renal insufficiency: adenine-diet and 5/6th nephrectomy (5/6Nx). Compared with 5/6Nx mice, mice fed with 0.25% adenine had more severe renal insufficiency and so higher levels of prothrombotic uremic toxins like indoxyl sulfate. More severe renal inflammation and fibrosis were observed in the adenine group, as demonstrated by histological and reverse transcription quantitative polymerase chain reaction experiments. Liver fibrinogen γ chain expression and level of plasma fibrinogen were increased only in adenine mice. In both CKD mouse models, tissue factor (TF) expression was increased in kidney and aorta extracts. Immunochemistry analysis of kidney sections showed that TF is localized in the vascular walls. Thrombin–antithrombin complexes were significantly increased in plasma from both adenine and 5/6Nx mice. Tail bleeding time increased significantly only in adenine mice, whereas platelet count was not significant altered. Finally, results obtained by intravital microscopy after laser-induced endothelial injury showed impaired platelet function in adenine mice and an increase in fibrin generation in 5/6Nx mice. To summarize, adenine diet causes a more severe renal insufficiency compared with 5/6Nx. The TF upregulation and the hypercoagulable state were observed in both CKD models. Bleeding tendency was observed only in the adenine model of CKD that recapitulates the whole spectrum of hemostasis abnormalities observed in advanced human CKD.

10.1055/s-0040-1705138

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Citations (11)

Targeting BTN2A1 enhances Vγ9Vδ2 T cell effector functions and triggers tumor cells pyroptosis

bioRxiv (Cold Spring Harbor Laboratory) (2023)

Anne Floch Caroline Imbert Nicolas Boucherit Laurent Gorvel Stéphane Fattori

Abstract Vγ9Vδ2 T cells are potent but elusive cytotoxic effectors. Means to stimulate their function could lead to powerful new cancer immunotherapies. BTN2A1, a surface protein has recently been shown to bind the Vγ9 chain of the γδ TCR but its precise role in modulating Vγ9Vδ2 T cells functions remains unknown. Here we show that 107G3B5, a monoclonal anti-BTN2A1 agonist antibody, significantly enhances Vγ9Vδ2 T cell functions against hematological or solid cell lines and against primary cells from adult acute lymphoblastic leukemia patients. New computer vision strategies applied to holotomographic microscopy videos show that 107G3B5 enhances the interaction between Vγ9Vδ2 T cells and target cells in a quantitative and qualitative manner. In addition, we provide evidence that Vγ9Vδ2 T cells activated by 107G3B5 induce caspase 3/7 activation in tumor cells, thereby triggering their death by pyroptosis. We thus demonstrate that targeting BTN2A1 with 107G3B5 enhances the Vγ9Vδ2 T cell antitumor response by triggering the pyroptosis-induced immunogenic cell death.

Pyroptosis

10.1101/2023.06.15.545049

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TH Open (2020)

Camélia Makhloufi Lydie Crescence Roxane Darbousset Nathalie McKay Ziad A. Massy

The coexistence of bleeding and thrombosis in patients with chronic kidney disease (CKD) is frequent and poorly understood.Mouse models are essential to understand complications of CKD and to develop new therapeutic approaches improving the health of patients.We evaluated the hemostasis in two models of renal insufficiency: adenine-diet and 5/6th nephrectomy (5/6Nx).Compared with 5/6Nx mice, mice fed with 0.25% adenine had more severe renal insufficiency and so higher levels of prothrombotic uremic toxins like indoxyl sulfate.More severe renal inflammation and fibrosis were observed in the adenine group, as demonstrated by histological and reverse transcription quantitative polymerase chain reaction experiments.Liver fibrinogen γ chain expression and level of plasma fibrinogen were increased only in adenine mice.In both CKD mouse models, tissue factor (TF) expression was increased in kidney and aorta extracts.Immunochemistry analysis of kidney sections showed that TF is localized in the vascular walls.Thrombin-antithrombin complexes were significantly increased in plasma from both adenine and 5/6Nx mice.Tail bleeding time increased significantly only in adenine mice, whereas platelet count was not significant altered.Finally, results obtained by intravital microscopy after laser-induced endothelial injury showed impaired platelet function in adenine mice and an increase in fibrin generation in 5/6Nx mice.To summarize, adenine diet causes a more severe renal insufficiency compared with 5/6Nx.The TF upregulation and the hypercoagulable state were observed in both CKD models.Bleeding tendency was observed only in the adenine model of CKD that recapitulates the whole spectrum of hemostasis abnormalities observed in advanced human CKD.

10.1055/s-010-47205

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