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6. Temporal specificity and heterogeneity of the fly immune cells' transcriptional landscape Authors and affiliations

Author

Cattenoz, Pierre, Sakr, Rosy, Pavlidaki, Alexia, Delaporte, Claude, Riba, Andrea, Molina, Nacho, Hariharan, Nivedita, Mukherjee, Tina, Giangrande, Angela, Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), and Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
single cells RNA seq, immune cells, Drosophila melanogaster, wasp infestation, [SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]
Abstract

Immune cells provide defense against the non-self, however recent data suggest roles well beyond innate immunity, in processes as diverse as development, metabolism and tumor progression. Nevertheless, the heterogeneity of these cells remains an open question. Using bulk RNA sequencing we find that the Drosophila immune cells (hemocytes) display distinct features in the embryo, a closed and rapidly developing system, compared to the larva, which is exposed to environmental and metabolic challenges. Through single cell RNA sequencing we identify fourteen hemocyte clusters present in unchallenged larvae and associated with distinct cellular processes e.g. proliferation, phagocytosis, metabolic homeostasis and humoral response. Finally, we characterize the changes occurring in the hemocyte clusters upon wasp infestation that triggers the differentiation of a novel cell type, the lamellocyte. This first molecular atlas provides precious insights and paves the way to study the biology of the Drosophila immune cells in physiological and pathological conditions.

Published
2020

8. Additional file 1: Table S1. of Whole transcriptome analysis of human erythropoietic cells during ontogenesis suggests a role of VEGFA gene as modulator of fetal hemoglobin and pharmacogenomic biomarker of treatment response to hydroxyurea in β-type hemoglobinopathy patients

Author

Chondrou, Vasiliki, Kolovos, Petros, Sgourou, Argyro, Kourakli, Alexandra, Pavlidaki, Alexia, Vlasia Kastrinou, John, Anne, Argiris Symeonidis, Ali, Bassam, Papachatzopoulou, Adamantia, Katsila, Theodora, and Patrinos, George

Abstract

Upregulated genes when (i) peripheral blood is compared to umbilical cord blood and fetal liver (PB vs CB+FL) and (ii) peripheral blood is compared to fetal liver (PB vs FL). Table S2. Downregulated genes when (i) peripheral blood is compared to umbilical cord blood and fetal liver (PB vs CB+FL) and (ii) peripheral blood is compared to fetal liver (PB vs FL). Table S3. Statistical and Hardy-Weinberg analyses on the genotyping data of β-type hemoglobinopathy patients of Hellenic origin and healthy (non-thalassemic) individuals. Table S4. Pairwise linkage disequilibrium (LD) calculations for the tagSNPs of interest across the VEGFA gene (CEU). Figure S1. Differential gene expression when adult peripheral blood is compared to cord blood. A total of 135 genes were over- (FC > 2) or downregulated (FC 2) or downregulated (FC

Published
2017
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9. Whole transcriptome analysis of human erythropoietic cells during ontogenesis suggests a role of VEGFA gene as modulator of fetal hemoglobin and pharmacogenomic biomarker of treatment response to hydroxyurea in β-type hemoglobinopathy patients

Author

Chondrou, Vasiliki, Kolovos, Petros, Sgourou, Argyro, Kourakli, Alexandra, Pavlidaki, Alexia, Kastrinou, Vlasia, John, Anne, Symeonidis, Argiris, Ali, Bassam R., Papachatzopoulou, Adamantia, Katsila, Theodora, Patrinos, George P., Chondrou, Vasiliki, Kolovos, Petros, Sgourou, Argyro, Kourakli, Alexandra, Pavlidaki, Alexia, Kastrinou, Vlasia, John, Anne, Symeonidis, Argiris, Ali, Bassam R., Papachatzopoulou, Adamantia, Katsila, Theodora, and Patrinos, George P.

Abstract

Background: Human erythropoiesis is characterized by distinct gene expression profiles at various developmental stages. Previous studies suggest that fetal-to-adult hemoglobin switch is regulated by a complex mechanism, in which many key players still remain unknown. Here, we report our findings from whole transcriptome analysis of erythroid cells, isolated from erythroid tissues at various developmental stages in an effort to identify distinct molecular signatures of each erythroid tissue. Results: From our in-depth data analysis, pathway analysis, and text mining, we opted to focus on the VEGFA gene, given its gene expression characteristics. Selected VEGFA genomic variants, identified through linkage disequilibrium analysis, were explored further for their association with elevated fetal hemoglobin levels in β-type hemoglobinopathy patients. Our downstream analysis of non-transfusion-dependent β-thalassemia patients, β-thalassemia major patients, compound heterozygous sickle cell disease/β-thalassemia patients receiving hydroxyurea as fetal hemoglobin augmentation treatment, and non-thalassemic individuals indicated that VEGFA genomic variants were associated with disease severity in β-thalassemia patients and hydroxyurea treatment efficacy in SCD/β-thalassemia compound heterozygous patients. Conclusions: Our findings suggest that VEGFA may act as a modifier gene of human globin gene expression and, at the same time, serve as a genomic biomarker in β-type hemoglobinopathy disease severity and hydroxyurea treatment efficacy.

Published
2017

10. Whole transcriptome analysis of human erythropoietic cells during ontogenesis suggests a role of VEGFA gene as modulator of fetal hemoglobin and pharmacogenomic biomarker of treatment response to hydroxyurea in β-type hemoglobinopathy patients

Author

Chondrou, Vasiliki, primary, Kolovos, Petros, additional, Sgourou, Argyro, additional, Kourakli, Alexandra, additional, Pavlidaki, Alexia, additional, Kastrinou, Vlasia, additional, John, Anne, additional, Symeonidis, Argiris, additional, Ali, Bassam R., additional, Papachatzopoulou, Adamantia, additional, Katsila, Theodora, additional, and Patrinos, George P., additional

Published
2017
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11. Whole transcriptome analysis of human erythropoietic cells during ontogenesis suggests a role of VEGFAgene as modulator of fetal hemoglobin and pharmacogenomic biomarker of treatment response to hydroxyurea in β-type hemoglobinopathy patients

Author

Chondrou, Vasiliki, Kolovos, Petros, Sgourou, Argyro, Kourakli, Alexandra, Pavlidaki, Alexia, Kastrinou, Vlasia, John, Anne, Symeonidis, Argiris, Ali, Bassam, Papachatzopoulou, Adamantia, Katsila, Theodora, and Patrinos, George

Abstract

Human erythropoiesis is characterized by distinct gene expression profiles at various developmental stages. Previous studies suggest that fetal-to-adult hemoglobin switch is regulated by a complex mechanism, in which many key players still remain unknown. Here, we report our findings from whole transcriptome analysis of erythroid cells, isolated from erythroid tissues at various developmental stages in an effort to identify distinct molecular signatures of each erythroid tissue. From our in-depth data analysis, pathway analysis, and text mining, we opted to focus on the VEGFAgene, given its gene expression characteristics. Selected VEGFAgenomic variants, identified through linkage disequilibrium analysis, were explored further for their association with elevated fetal hemoglobin levels in β-type hemoglobinopathy patients. Our downstream analysis of non-transfusion-dependent β-thalassemia patients, β-thalassemia major patients, compound heterozygous sickle cell disease/β-thalassemia patients receiving hydroxyurea as fetal hemoglobin augmentation treatment, and non-thalassemic individuals indicated that VEGFAgenomic variants were associated with disease severity in β-thalassemia patients and hydroxyurea treatment efficacy in SCD/β-thalassemia compound heterozygous patients. Our findings suggest that VEGFAmay act as a modifier gene of human globin gene expression and, at the same time, serve as a genomic biomarker in β-type hemoglobinopathy disease severity and hydroxyurea treatment efficacy.

Published
2017
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12. Targeting the MAtrix REgulating MOtif abolishes several hallmarks of cancer, triggering antitumor immunity.

Author

Li C, Kaur A, Pavlidaki A, Spenlé C, Rajnpreht I, Donnadieu E, Salomé N, Molitor A, Carapito R, Wack F, Erne W, Lefebvre O, Averous G, Mitrentsi I, Loustau T, and Orend G

Subjects
Humans, Animals, Mice, Female, Cell Line, Tumor, Breast Neoplasms immunology, Breast Neoplasms drug therapy, Breast Neoplasms metabolism, Breast Neoplasms pathology, Extracellular Matrix metabolism, Signal Transduction drug effects, Peptides pharmacology, Chemokine CXCL12 metabolism, Fibronectins metabolism, Tenascin metabolism, Tumor Microenvironment immunology, Tumor Microenvironment drug effects
Abstract

Tumor-targeted therapies have often been inefficient due to the lack of concomitant control over the tumor microenvironment. Using an immunocompetent autologous breast cancer model, we investigated a MAtrix REgulating MOtif (MAREMO)-mimicking peptide, which inhibits the protumorigenic extracellular matrix (ECM) molecule tenascin-C that activates several cancer hallmarks. In cultured cells, targeting the MAREMO blocks tenascin-C signaling involved in cell adhesion and immune-suppression by inhibiting tenascin-C interactions with fibronectin, TGFβ, CXCL12, and others, thereby blocking downstream events. Using RNASequencing and various genetic, molecular, in situ, and in vivo assays, we demonstrate that the MAREMO peptide similarly blocks multiple tenascin-C functions in vivo. This includes releasing tumor-infiltrating leukocytes, including CD8+ T cells, from the stroma. The MAREMO peptide also triggers interferon signaling, restoring antitumor immunity, contributing to tumor growth inhibition and reduced dissemination. The MAREMO peptide targets tumor cells directly by promoting growth suppression and inhibiting phenotypic plasticity, subsequently enhancing responsiveness to the endogenous death inducer tumor necrosis factor-related apoptosis-inducing ligand, as shown by a loss-of-function approach. Moreover, the MAREMO peptide largely subdues the tumor bed by depleting fibroblasts, repressing tenascin-C and other ECM molecules, and restoring the function of the few remaining blood vessels. In conclusion, targeting tenascin-C with a MAREMO peptide represents a powerful anticancer strategy with a broad inhibition of several cancer hallmarks., Competing Interests: Competing interests statement:The authors declare no competing interest.

Published
2024
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