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DTSTART;TZID=Europe/Madrid:20211203T100000
DTEND;TZID=Europe/Madrid:20211203T120000
DTSTAMP:20260505T181155
CREATED:20210917T110911Z
LAST-MODIFIED:20211123T153308Z
UID:87240-1638525600-1638532800@ibecbarcelona.eu
SUMMARY:Online IBEC Seminar: Arnau Hervera
DESCRIPTION:Therapeutic effects of HDAC3 inhibition on spinal injuries and autoimmune demyelinating diseases\nArnau Hervera\, Molecular and Cellular Neurobiotechnology \nThe molecular mechanisms discriminating between regenerative failure and success remain elusive. While a regeneration-competent peripheral nerve injury mounts a regenerative gene expression response in bipolar dorsal root ganglia (DRG) sensory neurons\, a regeneration-incompetent central spinal cord injury does not. This dichotomic response offered us a unique opportunity to investigate the fundamental biological mechanisms underpinning this regenerative ability. Following a pharmacological screen with small molecule inhibitors targeting key epigenetic enzymes in DRG neurons we identified HDAC3 signaling as a novel candidate\, that hindered axonal regenerative growth. In vivo\, we found that only a peripheral but not a central axonal injury induced an increase in calcium\, activating protein phosphatase 4 (PP4) who in turn dephosphorylates HDAC3 thus impairing its activity and enhancing histone acetylation. Bioinformatics analysis of ex vivo H3K9ac ChIPseq and RNAseq from DRG followed by promoter acetylation and protein expression studies implicated HDAC3 in the regulation of multiple regenerative pathways. Additionally\, we and others have found that\, HDAC3 inhibition is able to modulate the neuroinflammatory environment in the CNS after injury. In that sense\, after CNS injury\, inflammatory phase transitions are poorly orchestrated leading to unresolved exaggerated inflammation that triggers secondary damage and functional deficits. We found that HDAC3 inhibition also altered the cytokinome after SCI\, and we are currently characterizing the effects of this inhibition on the functions of different immune cells after SCI. Additionally\, HDAC3 inhibition has been also previously described to play important roles in neuronal survival\, lymphocyte differentiation and myelination\, together with neuroinflammation\, all these processes are essential regulators on the development and outcome of autoimmune demyelinating diseases\, such as MS. In this direction\, we are also currently studying the potential therapeutic effects of HDAC3 inhibition in the multiple sclerosis mouse model Experimental Autoimmune Encephalitis (EAE)\, as well as their underlying mechanisms\, in neuroinflammation autoantigen presentation\, lymphocyte differentiation\, demyelination\, remyelination and oligodendrocyte survival and differentiation. \nThis seminar will be held using the GoToMeeting app
URL:https://ibecbarcelona.eu/es/event/online-ibec-seminar-arnau-hervera/
CATEGORIES:IBEC Seminar
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DTSTART;TZID=Europe/Madrid:20211210T100000
DTEND;TZID=Europe/Madrid:20211210T120000
DTSTAMP:20260505T181155
CREATED:20210901T150722Z
LAST-MODIFIED:20211129T105930Z
UID:86925-1639130400-1639137600@ibecbarcelona.eu
SUMMARY:Online IBEC Seminar: Irene Marco
DESCRIPTION:Updates on a new lab at IBEC: hyperpolarised magnetic resonance for real-time\, in situ monitoring of cell metabolism\nIrene Marco\, Molecular Imaging for Precision Medicine group at IBEC \nThere is a clinical need for non-invasive and reliable markers to diagnose\, stage and evaluate treatment response in many diseases such as cancer or non-alcoholic fatty liver disease. \nMagnetic resonance (MR) methods now have the potential to revolutionise in the identification of such biomarkers in real time.  Spectroscopic identification and quantitation of metabolites via carbon-13 chemical shifts can be combined with imaging (MRI) to simultaneously probe spatial (biodistribution) and temporal (kinetics) aspects of metabolism in vivo. These capabilities are enabled by so-called hyperpolarised (HP) MR techniques\, including Dynamic Nuclear Polarisation (DNP)\, which can transiently boost the carbon-13 MR signals by several orders of magnitude\, compared to traditional methods. DNP enables real-time measurement of enzymatic reactions in cell suspensions and in vivo. Multiple HP 13C-labelled substrates have provided insights in several metabolic pathways\, including glycolysis\, the pentose-phosphate pathway and the cellular redox state. I will present the potential of DNP to study metabolism in cell suspensions\, tissue ex vivo and animals in vivo. Also\, I will talk about the progress we have made at IBEC in the past couple of months and how we plan to implement HP MR to monitor metabolism in organs-in-chips. \nThis seminar will be held at Tower I\, 11th floor Baobab room\, there will be 30 avialable seats\, the free spots will be assigned on a first come first served basis. If you wish to attend this seminar online\, please write to ibeccommunications@ibecbarcelona.eu. \nMore information about Irene Marco’s research here
URL:https://ibecbarcelona.eu/es/event/online-ibec-seminar-irene-marco/
CATEGORIES:IBEC Seminar
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DTSTART;TZID=Europe/Madrid:20211217T100000
DTEND;TZID=Europe/Madrid:20211217T120000
DTSTAMP:20260505T181155
CREATED:20210909T094506Z
LAST-MODIFIED:20211209T123245Z
UID:87094-1639735200-1639742400@ibecbarcelona.eu
SUMMARY:PhD Discussions: Enrico Almici and Albert Manzano
DESCRIPTION:Investigating Pathological Extracellular Matrix Architecture\nThe composition and architecture of the extracellular matrix (ECM)\, and their dynamic alterations\, play an important regulatory role on numerous cellular processes. Furthermore\, structural and biochemical properties of the ECM are central in regulating cell behavior via mechanical\, chemical and topological cues detected by receptors in the cell membrane which induce cytoskeleton rearrangement and/or cell nucleus gene expression. Indeed\, distinct ECM architectures are encountered in the native stroma\, which depend on tissue type\, function and composition. For instance\, ECM anisotropy and stiffness are associated with altered ECM degradation and remodeling in cancer. In turn\, this architecture favors tumor progression and invasion. Moreover\, numerous diseases are associated with mutations in genes encoding ECM components\, leading to deficient mechanical properties and altered ECM structure. Thus\, there is an increasing interest to exploit and consolidate this knowledge to improve patients’ treatment and care. In my work I focused on Collagen-VI related muscular dystrophies and Non-small cell lung cancer\, to investigate in vitro and in patient tissues ECM-related biomarkers to be implemented in clinical setting. I employed automatic image segmentation to quantify fibrillar characteristics and investigate the association with the clinicopathological information from patients. Ultimately this analysis along with the tools presented is promising for addressing the need of novel descriptors\, to stratify patients and evaluate their response to experimental treatments. \nEnrico Almici\, Nanobioengineering \nPersonalizing pediatric leukemia treatment using cell-based functional assays and microfluidics\nCancer personalized medicine improves treatment by testing different drugs in samples from every individual patient to select the best option in every case\, maximizing efficacy and reducing side effects. Pediatric B-cell Precursor Acute Lymphoblastic Leukemia (BCP-ALL) has an acceptable cure rate\, however\, almost 10% of the cases are refractory to standard-of-care treatments\, showing an urgent need for new therapeutic options. Here\, we use Dynamic BH3 Profiling (DBP)\, a new assay that uses synthetic peptides mimicking the pro-apoptotic effect of the BH3 family of proteins\, to predict treatment efficacy and anti-apoptotic adaptations conferring treatment resistance. Applying DBP in two BCP-ALL cell lines we identified new treatment options including both targeted agents and chemotherapies. We were also able to describe the mechanistic response of these cells after treatment\, which acquired resistance using anti-apoptotic proteins that were later overcome using specific inhibitors called BH3 mimetics. Importantly\, this resistance mechanism was also seen in patient-derived xenografts opening the use of these new combinations with BH3 mimetics in BCP-ALL patients. In the second part of the presentation\, we developed a new version of the DBP protocol. Actual cytometry-based DBP requires a large number of viable cells which are easily obtained in liquid tumors but not in solid tumor biopsies\, limiting the number of treatments that can be explored. To solve this problem\, we developed a microfluidic-based DBP that drastically reduces cell requirement to perform the assay and helps to automatize the process to be implemented as a routinely clinical technique. We validated this microfluidic-based DBP using two gastrointestinal stromal tumor (GIST) cell lines obtaining similar results between the new protocol and the cytometry-based DBP. Finally\, we used a primary GIST sample to identify a treatment combination that induced apoptosis to these patient cells\, which proves that the microfluidic-based DBP can help to personalize solid cancers treatment. \nAlbert Manzano\, Nanobioengineering \nThis PhD Discussion session will be held at Tower I\, 11th floor Baobab room\, there will be 30 avialable seats\, the free spots will be assigned on a first come first served basis.
URL:https://ibecbarcelona.eu/es/event/phd-discussions-enrico-almici-and-giulia-fornabaio/
CATEGORIES:PhD Discussions Session
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