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212 results on '"Sartelet, H."'

1. Neuroblastoma

Author

Plantaz, D., Freycon, C., Schiff, I., Durand, C., Combaret, V., Pagnier, A., Piolat, C., and Sartelet, H.

Published
2023
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4. Characterization of novel interactions with plasma membrane NEU1 reveals new biological functions for the elastin receptor complex in vascular diseases

Author

Tembely, D., primary, Bocquet, O., additional, Kawecki, C., additional, Terryn, C., additional, Schmelzer, C., additional, Heinz, A., additional, Romier-Crouzet, B., additional, Bennasroune, A., additional, Blaise, S., additional, Sartelet, H., additional, Martiny, L., additional, Duca, L., additional, and Maurice, P., additional

Published
2021
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5. TWIST1 expression is associated with high-risk Neuroblastoma and promotes Primary and Metastatic Tumor Growth

Author

Katia Balmas Bourloud, Nardou-Auderset K, Nicolas Jauquier, Nicolo Riggi, Annick Mühlethaler-Mottet, Jean-Marc Joseph, Sepporta M, Sartelet H, Praz, Petit A, Raffaele Renella, and Jean-Yves Scoazec

Subjects
Extracellular matrix, Crosstalk (biology), animal structures, Neuroblastoma, Cancer research, medicine, CRISPR, Cancer, Biology, medicine.disease, Embryonic stem cell, Transcription factor, Metastasis
Abstract

The embryonic transcription factors TWIST1/2 are frequently overexpressed in cancer, acting as multifunctional oncogenes. Here we investigate their role in neuroblastoma (NB), a heterogeneous childhood malignancy ranging from spontaneous regression to dismal outcomes despite multimodal therapy. We first reveal the association of TWIST1 expression with poor survival and metastasis in primary NB, while TWIST2 correlates with good prognosis. Secondly, suppression of TWIST1 by CRISPR/Cas9 results in a reduction of tumor growth and metastasis colonization in immunocompromised mice. Moreover, TWIST1 knockout tumors display a less aggressive cellular morphology and a reduced disruption of the extracellular matrix (ECM) reticulin network. Additionally, we identify a TWIST1-mediated transcriptional program associated with dismal outcome in NB and involved in the control of pathways mainly linked to the signaling, migration, adhesion, the organization of the ECM, and the tumor cells versus tumor stroma crosstalk. Taken together, our findings suggest TWIST1 as novel therapeutic target in NB.

Published
2021

16. Involvement of lysine 1047 in type I collagen-mediated activation of polymorphonuclear neutrophils

Author

Jaisson, S., Sartelet, H., Perreau, C., Blanchevoye, C., Garnotel, R., Gillery, P., Matrice extracellulaire et dynamique cellulaire - UMR 7369 (MEDyC), Université de Reims Champagne-Ardenne (URCA)-SFR CAP Santé (Champagne-Ardenne Picardie Santé), and Université de Reims Champagne-Ardenne (URCA)-Université de Picardie Jules Verne (UPJV)-Université de Reims Champagne-Ardenne (URCA)-Université de Picardie Jules Verne (UPJV)-Centre National de la Recherche Scientifique (CNRS)

Subjects
ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
2008

17. Anticorps polyclonal dirigé contre la protéine EBP

Author

Blanchevoye, C., Delacoux, F., Duca, L., Devy, J., Sartelet, H., Debelle, L., Matrice extracellulaire et dynamique cellulaire - UMR 7369 (MEDyC), Université de Reims Champagne-Ardenne (URCA)-SFR CAP Santé (Champagne-Ardenne Picardie Santé), and Université de Reims Champagne-Ardenne (URCA)-Université de Picardie Jules Verne (UPJV)-Université de Reims Champagne-Ardenne (URCA)-Université de Picardie Jules Verne (UPJV)-Centre National de la Recherche Scientifique (CNRS)

Published
2007

20. Thrombospondin-1 C-terminal-derived peptide protects thyroid cells from ceramide-induced apoptosis through the adenylyl cyclase pathway.

Author

UCL - Autre, Rath, Géraldine, Schneider, C, Dedieu, S, Sartelet, H, Morjani, H, Martiny, L, El Btaouri, H, UCL - Autre, Rath, Géraldine, Schneider, C, Dedieu, S, Sartelet, H, Morjani, H, Martiny, L, and El Btaouri, H

Abstract

Thrombospondin-1, a multi-modular matrix protein is able to interact with a variety of matrix proteins and cell-surface receptors. Thus it is multifunctional. In this work, we examined the role of thrombospondin-1 in ceramide-induced thyroid apoptosis. We focused on the VVM containing sequence localized in the C-terminal domain of the molecule. Primary cultured thyroid cells synthesize thrombospondin-1 depending on their morphological organization. As it leads thyrocytes to organize into monolayers before inducing apoptosis ceramide can modulate this organization. Here, we established that C(2)-ceramide treatment decreased thrombospondin-1 expression by interfering with the adenylyl cyclase pathway, thus leading to apoptosis. Furthermore, we demonstrated that the thrombospondin-1-derived peptide 4N1 (RFYVVMWK) abolished ceramide-induced thyroid cell death by preventing intracellular cAMP levels from dropping. Finally, we reported that 4N1-mediated inhibition of ceramide-induced apoptosis was consistently associated with a down-regulation of the caspase-3 processing. Integrin-associated protein receptor (IAP or CD47) was identified as a molecular relay mediating the observed 4N1 effects. Taken together, our results shed light for the first time on anti-apoptotic activities of the thrombospondin-1-derived peptide 4N1 and provide new information on how thrombospondin-1 may control apoptosis of non-tumoral cells.

Published
2006

21. Thrombospondin 1 : a multifunctional protein implicated in the regulation of tumor growth.

Author

Université de Reims Champagne Ardennes - FRE CNRS 2134, Sid, Brice, Sartelet, H, Bellon, G, El Btaouri, H, Rath, Géraldine, Delorme, N, Haye, B, Martiny, L, Université de Reims Champagne Ardennes - FRE CNRS 2134, Sid, Brice, Sartelet, H, Bellon, G, El Btaouri, H, Rath, Géraldine, Delorme, N, Haye, B, and Martiny, L

Abstract

Thrombospondins belong to a family of extracellular matrix (ECM) proteins widely found from embryonic to adult tissues. The modular structure of thrombospondins contains a series of peptide sequences implicated in a multiplicity of biological functions. Extracellular matrix undergoes important alterations under proteolysis that occurs in pathological processes like tumorigenesis. An elevated secretion of thrombospondin 1 (TSP1) is often observed in tumors and is sometimes considered as a predictive factor. However, the role of TSP1 in cancer progression remains controversial and must be carefully apprehended. The regulation of cell adhesion, proliferation, apoptosis by TSP1 is examined in the present review and it is clear from the literature and from our investigations that TSP1 presents both stimulatory and inhibitory effects. The exposition of cryptic sites upon conformational changes can partially explain this contradiction. More interestingly, the analysis of TSP1-directed intracellular signaling pathways activated through specific receptors or supramolecular receptors docking systems may be useful to discriminate the precise function of TSP1 in tumor progression. The central role played by TSP1 in the control of matrix-degrading enzyme activation and catabolism reveals attractive tracks of research and highlights the involvement of the lipoprotein receptor-related protein (LRP) receptor in these events. Therefore, TSP1-derived peptides constitute a source of potentially active matrikins which could provide essential tools in cancer therapy.

Published
2004

45. Up-regulation of a serine protease inhibitor in astrocytes mediates the neuroprotective activity of transforming growth factor beta1

Author

Buisson A, Nicole O, Docagne F, Sartelet H, Eric T MacKenzie, and Vivien D

Subjects
Neurons, N-Methylaspartate, Serine Proteinase Inhibitors, Cell Death, Up-Regulation, Mice, Neuroprotective Agents, Transforming Growth Factor beta, Astrocytes, Tissue Plasminogen Activator, Plasminogen Activator Inhibitor 1, Animals, Neuroglia, Receptors, Transforming Growth Factor beta
Abstract

Serine proteases play a key role in the fundamental biology of the central nervous system (CNS), and recent data suggest their involvement in the pathophysiology of neurodegenerative diseases. Little is known about the physiological regulation of these proteases in the CNS. Among the multiple growth factors present in the brain, transforming growth factor beta1 (TGF-beta1) has been described as an injury-related growth factor. However, its beneficial or deleterious role remains unclear. In the present study, we investigated the influence of TGF-beta1 in apoptosis and necrosis, two mechanisms involved in ischemic neuronal death. We show that TGF-beta1 exerts a neuroprotective role restricted to necrosis induced by N-methyl-D-aspartate. This effect is observable only in the obligatory presence of TGF-beta1-responsive astrocytes. We demonstrate that this neuroprotective activity is mediated through an up-regulation of a serine protease inhibitor (PAI-1) in astrocytes. These results underline the involvement of serine proteases and extracellular matrix components such as the PAI-1/t-PA axis in the excitotoxic cascade. Moreover, regardless of the underlying mechanisms of t-PA involvement in excitotoxic injury, our observations might warn against the use of tissular plasminogen activator as an alternative therapy for the treatment of hypoxic-ischemic injury in the brain.

49. Analyses of combined Merkel cell carcinomas with neuroblastic components suggests that loss of T antigen expression in Merkel cell carcinoma may result in cell cycle arrest and neuroblastic transdifferentiation.

Author

Kervarrec T, Appenzeller S, Gramlich S, Coyaud E, Bachiri K, Appay R, Macagno N, Tallet A, Bonenfant C, Lecorre Y, Kapfer J, Kettani S, Srinivas N, Lei KC, Lange A, Becker JC, Sarosi EM, Sartelet H, von Deimling A, Touzé A, Guyétant S, Samimi M, Schrama D, and Houben R

Subjects
Humans, Male, Cell Cycle Checkpoints genetics, Biomarkers, Tumor genetics, Biomarkers, Tumor metabolism, Aged, 80 and over, Aged, Neoplasms, Complex and Mixed pathology, Neoplasms, Complex and Mixed genetics, Neoplasms, Complex and Mixed metabolism, Neuroblastoma pathology, Neuroblastoma genetics, Neuroblastoma metabolism, Carcinoma, Merkel Cell pathology, Carcinoma, Merkel Cell virology, Carcinoma, Merkel Cell genetics, Carcinoma, Merkel Cell metabolism, Skin Neoplasms pathology, Skin Neoplasms genetics, Skin Neoplasms virology, Skin Neoplasms metabolism, Antigens, Viral, Tumor genetics, Antigens, Viral, Tumor metabolism, Cell Transdifferentiation, Merkel cell polyomavirus genetics
Abstract

Merkel cell carcinoma (MCC) is an aggressive skin cancer frequently caused by genomic integration of the Merkel cell polyomavirus (MCPyV). MCPyV-negative cases often present as combined MCCs, which represent a distinctive subset of tumors characterized by association of an MCC with a second tumor component, mostly squamous cell carcinoma. Up to now, only exceptional cases of combined MCC with neuroblastic differentiation have been reported. Herein we describe two additional combined MCCs with neuroblastic differentiation and provide comprehensive morphologic, immunohistochemical, transcriptomic, genetic and epigenetic characterization of these tumors, which both arose in elderly men and appeared as an isolated inguinal adenopathy. Microscopic examination revealed biphasic tumors combining a poorly differentiated high-grade carcinoma with a poorly differentiated neuroblastic component lacking signs of proliferation. Immunohistochemical investigation revealed keratin 20 and MCPyV T antigen (TA) in the MCC parts, while neuroblastic differentiation was confirmed in the other component in both cases. A clonal relation of the two components can be deduced from 20 and 14 shared acquired point mutations detected by whole exome analysis in both combined tumors, respectively. Spatial transcriptomics demonstrated a lower expression of stem cell marker genes such as SOX2 and MCM2 in the neuroblastic component. Interestingly, although the neuroblastic part lacked TA expression, the same genomic MCPyV integration and the same large T-truncating mutations were observed in both tumor parts. Given that neuronal transdifferentiation upon TA repression has been reported for MCC cell lines, the most likely scenario for the two combined MCC/neuroblastic tumors is that neuroblastic transdifferentiation resulted from loss of TA expression in a subset of MCC cells. Indeed, DNA methylation profiling suggests an MCC-typical cellular origin for the combined MCC/neuroblastomas. © 2024 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland., (© 2024 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.)

Published
2024
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50. Metabolic syndrome-associated murine aortic wall stiffening is associated with premature elastic fibers aging.

Author

Vanalderwiert L, Henry A, Wahart A, Carvajal Berrio DA, Brauchle EM, El Kaakour L, Schenke-Layland K, Brinckmann J, Steenbock H, Debelle L, Six I, Faury G, Jaisson S, Gillery P, Durlach V, Sartelet H, Maurice P, Bennasroune A, Martiny L, Duca L, Romier B, and Blaise S

Subjects
Animals, Mice, Male, Elastin metabolism, Collagen metabolism, Diabetes Mellitus, Experimental metabolism, Diabetes Mellitus, Experimental pathology, Diabetes Mellitus, Experimental physiopathology, Aging pathology, Aging metabolism, Diabetes Mellitus, Type 2 metabolism, Diabetes Mellitus, Type 2 pathology, Diabetes Mellitus, Type 2 physiopathology, Aging, Premature metabolism, Aging, Premature pathology, Aging, Premature physiopathology, Elastic Tissue metabolism, Elastic Tissue pathology, Vascular Stiffness physiology, Aorta metabolism, Aorta pathology, Aorta physiopathology, Mice, Inbred C57BL, Extracellular Matrix metabolism, Extracellular Matrix pathology, Metabolic Syndrome metabolism, Metabolic Syndrome pathology, Metabolic Syndrome physiopathology
Abstract

Type 2 diabetes (T2D) constitutes a major public health problem, and despite prevention efforts, this pandemic disease is one of the deadliest diseases in the world. In 2022, 6.7 million patients with T2D died prematurely from vascular complications. Indeed, diabetes increases the risk of myocardial infarction or stroke eightfold. The identification of the molecular factors involved in the occurrence of cardiovascular complications and their prevention are therefore major axes. Our hypothesis is that factors brought into play during physiological aging appear prematurely with diabetes progression. Our study focused on the aging of the extracellular matrix (ECM), a major element in the maintenance of vascular homeostasis. We characterized the morphological and functional aspects of aorta, with a focus on the collagen and elastic fibers of diabetic mice aged from 6 mo to nondiabetic mice aged 6 mo and 20 mo. The comparison with the two nondiabetic models (young and old) highlighted an exacerbated activity of proteases, which could explain a disturbance in the collagen accumulation and an excessive degradation of elastic fibers. Moreover, the generation of circulating elastin-derived peptides reflects premature aging of the ECM. These extracellular elements contribute to the appearance of vascular rigidity, often the origin of pathologies such as hypertension and atherosclerosis. In conclusion, we show that diabetic mice aged 6 mo present the same characteristics of ECM wear as those observed in mice aged 20 mo. This accelerated aortic wall remodeling could then explain the early onset of cardiovascular diseases and, therefore, the premature death of patients with T2D. NEW & NOTEWORTHY Aortic elastic fibers of young (6-mo old) individuals with diabetes degrade prematurely and exhibit an appearance like that found in aged (20-mo old) nondiabetic mice. Exacerbated elastolysis and elastin-derived peptide production are characteristic elements, contributing to early aortic wall rigidity and hypertension development. Therefore, limiting this early aging could be a judicious therapeutic approach to reduce cardiovascular complications and premature death in patients with diabetes.

Published
2024
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