Giuseppe D’Agostino

ORCID: 0000-0001-8315-7406
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About
Contact & Profiles
Research Areas
  • Genetics and Neurodevelopmental Disorders
  • Liver Disease Diagnosis and Treatment
  • Congenital heart defects research
  • RNA Research and Splicing
  • Circadian rhythm and melatonin
  • Nuclear Receptors and Signaling
  • Cystic Fibrosis Research Advances
  • Neurobiology and Insect Physiology Research
  • RNA modifications and cancer
  • Diet and metabolism studies
  • Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
  • Occupational and environmental lung diseases
  • Viral Infections and Immunology Research
  • Endoplasmic Reticulum Stress and Disease
  • Economic and Financial Impacts of Cancer
  • Autism Spectrum Disorder Research
  • Liver physiology and pathology
  • Alzheimer's disease research and treatments
  • RNA and protein synthesis mechanisms
  • Immune cells in cancer
  • Acute Myeloid Leukemia Research
  • Epigenetics and DNA Methylation
  • Williams Syndrome Research
  • Genomic variations and chromosomal abnormalities
  • Nutritional Studies and Diet

Nanyang Technological University
2020-2025

Plasticell (United Kingdom)
2022-2024

European Institute of Oncology
2014-2024

Istituti di Ricovero e Cura a Carattere Scientifico
2014-2024

The Francis Crick Institute
2023-2024

Stevenage Bioscience Catalyst
2022-2023

National University of Singapore
2018-2020

Duke-NUS Medical School
2019

University of Milan
2018

University of Tübingen
2016

We studied the role of interleukin 11 (IL11) signaling in pathogenesis nonalcoholic steatohepatitis (NASH) using hepatic stellate cells (HSCs), hepatocytes, and mouse models NASH.We stimulated human fibroblasts, HSCs, or hepatocytes with IL11 other cytokines analyzed them by imaging, immunoblot, functional assays enzyme-linked immunosorbent assays. Mice were given injections IL11. disruption receptor subunit alpha1 gene (Il11ra1-/-) mice Il11ra1+/+ fed a high-fat methionine-...

10.1053/j.gastro.2019.05.002 article EN cc-by-nc-nd Gastroenterology 2019-05-10

The adult mammalian heart has limited ability to repair itself after injury. Zebrafish, newts, and neonatal mice can regenerate cardiac tissue, largely by myocyte (CM) proliferation. It is unknown whether hearts of young large mammals regenerate.We examined the regenerative capacity pig in animals (ages 2, 3, or 14 days postnatal) myocardial infarction sham procedure. Myocardial scar left ventricular function were determined magnetic resonance imaging echocardiography. Bromodeoxyuridine...

10.1161/circulationaha.117.031542 article EN Circulation 2018-07-20

Hyperexcitable neurons in brain organoids Individuals with Angelman syndrome experience intellectual disability and seizures throughout their lives. In this condition, ubiquitin-mediated degradation of a key potassium channel is disrupted, allowing for the neuronal excitability network synchronization that leads to seizure. Sun et al. used organoid technology study what happens human mutation ubiquitin ligase implicated syndrome. these vitro models mouse model syndrome, antagonists...

10.1126/science.aav5386 article EN Science 2019-12-20

Microglial phagocytosis is an energetically demanding process that plays a critical role in the removal of toxic protein aggregates Alzheimer’s disease (AD). Recent evidence indicates switch energy production from mitochondrial respiration to glycolysis disrupts this important protective microglial function and may provide therapeutic targets for AD. Here, we demonstrate translocator (TSPO) member its complex, hexokinase-2 (HK), play roles respiratory-glycolytic metabolism phagocytosis....

10.1073/pnas.2209177120 article EN cc-by-nc-nd Proceedings of the National Academy of Sciences 2023-02-14

ABSTRACT Convergent evidence associates endocrine disrupting chemicals (EDCs) with major, increasingly-prevalent human disorders. Regulation requires elucidation of EDC-triggered molecular events causally linked to adverse health outcomes, but two factors limit their identification. First, experiments frequently use individual chemicals, whereas real life entails simultaneous exposure multiple EDCs. Second, population-based and experimental studies are seldom integrated. This drawback was...

10.1101/206664 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2017-10-23

Fibrosis is a common pathology in many cardiac disorders and driven by the activation of resident fibroblasts. The global posttranscriptional mechanisms underlying fibroblast-to-myofibroblast conversion heart have not been explored.Genome-wide changes RNA transcription translation during human fibroblast were monitored with sequencing ribosome profiling. We then used RNA-binding protein-based analyses to identify translational regulators fibrogenic genes. integration occupancy levels 30...

10.1161/circulationaha.119.039596 article EN cc-by Circulation 2019-07-09

Thymus is necessary for lifelong immunological tolerance and immunity. It displays a distinctive epithelial complexity undergoes age-dependent atrophy. Nonetheless, it also retains regenerative capacity, which, if harnessed appropriately, might permit rejuvenation of adaptive By characterizing cortical medullary compartments in the human thymus at single-cell resolution, this study we have defined specific populations, including those that share properties with bona fide stem cells (SCs)...

10.1016/j.devcel.2023.08.017 article EN cc-by Developmental Cell 2023-08-30

Transforming growth factor beta-1 (TGFβ1) is a major driver of vascular smooth muscle cell (VSMC) phenotypic switching, an important pathobiology in arterial disease. We performed RNA-sequencing TGFβ1-stimulated human aortic or VSMCs which revealed large and consistent upregulation Interleukin 11 (IL11). IL11 has unknown function VSMCs, highly express the receptor alpha, suggestive autocrine loop. In vitro, activated ERK signaling, but inhibited STAT3 activity, caused VSMC switching to...

10.1038/s41598-020-74944-7 article EN cc-by Scientific Reports 2020-10-20

Copy number variation (CNV) at 7q11.23 causes Williams-Beuren syndrome (WBS) and 7q microduplication (7Dup), neurodevelopmental disorders (NDDs) featuring intellectual disability accompanied by symmetrically opposite neurocognitive features. Although significant progress has been made in understanding the molecular mechanisms underlying 7q11.23-related pathophysiology, propagation of CNV dosage across gene expression layers their interplay remains elusive. Here we uncovered dosage-dependent...

10.1172/jci168982 article EN cc-by Journal of Clinical Investigation 2024-07-14

Autism spectrum disorder (ASD) is a highly prevalent neurodevelopmental condition affecting almost 1% of children, and represents major unmet medical need with no effective drug treatment available. Duplication at 7q11.23 (7Dup), encompassing 26-28 genes, one the best characterized ASD-causing copy number variations offers unique translational opportunities, because hemideletion same interval causes Williams-Beuren syndrome (WBS), defined by hypersociability language strengths, thereby...

10.1186/s13229-020-00387-6 article EN cc-by Molecular Autism 2020-11-19

Abstract The past few years have witnessed a growth of interest in the historical and philosophical dimensions bioinformatics as discipline. Despite importance addressing issues raised by growing amount biological data, data management is often seen all it has to offer biology. However, emphasis on may come at expense understanding how generates genuine knowledge beyond its instrumental value for bench biologists. Some authors taken first steps management, towards characterization unique...

10.1162/posc_a_00638 article EN Perspectives on Science 2025-01-31

In early 2014, Dr Haruko Obokata and her co-authors caused a global media storm by publishing two scientific papers in Nature on stem cells. The proposed surprisingly simple new method called stimulus-triggered acquisition of pluripotency (STAP) to generate pluripotent cells for research purposes fast inexpensive way. To the dismay many, both were retracted within six months their release due data fabrication falsification. rise fall STAP illustrates impacts open science practices quality...

10.1080/09505431.2017.1316975 article EN Science as Culture 2017-05-02

Abstract Copy number variations (CNVs) at 7q11.23 cause Williams-Beuren (WBS) and 7q microduplication syndromes (7Dup), two neurodevelopmental disorders with shared opposite cognitive-behavioral phenotypes. Using patient-derived isogenic neurons, we integrated transcriptomics, translatomics proteomics to elucidate the molecular underpinnings of this dosage effect. We found that CNVs alterations in neuronal differentiation excitability. Genes related transmission chiefly followed appeared...

10.1101/2022.10.10.511483 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2022-10-10

Abstract Idiopathic pulmonary fibrosis (IPF) remains a progressive disease despite best medical management. We previously identified IL-11 as critical factor for cardiovascular and examine here its role in fibrosis. is consistently upregulated IPF genomic datasets, which we confirmed by histology. Pulmonary fibroblasts stimulated with transform into invasive myofibroblasts whereas from Il11ra deleted mice did not respond to pro-fibrotic stimuli. In the mouse, injection of recombinant Il-11...

10.1101/336537 preprint EN cc-by-nd bioRxiv (Cold Spring Harbor Laboratory) 2018-06-02

The response of an animal to a sensory stimulus depends on the nature and expectations, which are mediated by spontaneous activity. Here, we ask how circadian variation in expectation danger, thus potential threat, is controlled. We focus habenula, mediator threat that functions regulating neuromodulator release, use zebrafish as experimental system. Single cell transcriptomics indicates multiple clock genes expressed throughout while quantitative situ hybridization confirms oscillates....

10.1016/j.ynstr.2021.100403 article EN cc-by-nc-nd Neurobiology of Stress 2021-09-23

Abstract Microglial phagocytosis is an energetically demanding process that plays a critical role in the removal of toxic aggregates beta amyloid (Aβ) Alzheimer’s disease (AD). Recent evidence indicates metabolic programming may breakdown microglia AD, thereby disrupting this important protective function. The mechanisms coordinating mitochondrial metabolism to fuel remain poorly understood, however. Here we demonstrate displacement glucose metabolizing enzyme, hexokinase-II (HK) regulates...

10.1101/2021.12.01.469111 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2021-12-03
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