About
I am scientist who is passionate about bringing pre-clinical drug products into the…
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While automation holds immense potential for the CGT industry, it's not a magic solution. To truly unlock its benefits, you need the right expertise.…
While automation holds immense potential for the CGT industry, it's not a magic solution. To truly unlock its benefits, you need the right expertise.…
Liked by David Roig-Carles
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An often-asked question is "can your Dextramer® reagents activate T cells?". To answer your questions, we developed a novel type of reagent (PAX)…
An often-asked question is "can your Dextramer® reagents activate T cells?". To answer your questions, we developed a novel type of reagent (PAX)…
Liked by David Roig-Carles
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Exciting news! We have successfully deployed the first cGMP Cell Shuttle in Cellares' IDMO Smart Factory in Bridgewater, NJ. This marks an important…
Exciting news! We have successfully deployed the first cGMP Cell Shuttle in Cellares' IDMO Smart Factory in Bridgewater, NJ. This marks an important…
Liked by David Roig-Carles
Experience
Education
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The Open University
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Investigating the role of endothelial extracellular vesicles and microRNA-155 in cerebrovascular function and inflammation.
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Licenses & Certifications
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Personal Licence for Animal Research Category A and B
Home Office
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Cambridge Certificate in Advanced English (CAE)
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Publications
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Endothelial-Derived Extracellular Vesicles Induce Cerebrovascular Dysfunction in Inflammation
Pharmaceutics
Blood–brain barrier (BBB) dysfunction is a key hallmark in the pathology of many neuroinflammatory disorders. Extracellular vesicles (EVs) are lipid membrane-enclosed carriers of molecular cargo that are involved in cell-to-cell communication. Circulating endothelial EVs are increased in the plasma of patients with neurological disorders, and immune cell-derived EVs are known to modulate cerebrovascular functions. However, little is known about whether brain endothelial cell (BEC)-derived EVs…
Blood–brain barrier (BBB) dysfunction is a key hallmark in the pathology of many neuroinflammatory disorders. Extracellular vesicles (EVs) are lipid membrane-enclosed carriers of molecular cargo that are involved in cell-to-cell communication. Circulating endothelial EVs are increased in the plasma of patients with neurological disorders, and immune cell-derived EVs are known to modulate cerebrovascular functions. However, little is known about whether brain endothelial cell (BEC)-derived EVs themselves contribute to BBB dysfunction. Human cerebral microvascular cells (hCMEC/D3) were treated with TNFα and IFNy, and the EVs were isolated and characterised. The effect of EVs on BBB transendothelial resistance (TEER) and leukocyte adhesion in hCMEC/D3 cells was measured by electric substrate cell-substrate impedance sensing and the flow-based T-cell adhesion assay. EV-induced molecular changes in recipient hCMEC/D3 cells were analysed by RT-qPCR and Western blotting. A stimulation of naïve hCMEC/D3 cells with small EVs (sEVs) reduced the TEER and increased the shear-resistant T-cell adhesion. The levels of microRNA-155, VCAM1 and ICAM1 were increased in sEV-treated hCMEC/D3 cells. Blocking the expression of VCAM1, but not of ICAM1, prevented sEV-mediated T-cell adhesion to brain endothelia. These results suggest that sEVs derived from inflamed BECs promote cerebrovascular dysfunction. These findings may provide new insights into the mechanisms involving neuroinflammatory disorders.
Other authorsSee publication -
The Long Non-Coding RNA H19 Drives the Proliferation of Diffuse Intrinsic Pontine Glioma with H3K27 Mutation
IJMS
Diffuse intrinsic pontine glioma (DIPG) is an incurable paediatric malignancy. Identifying the molecular drivers of DIPG progression is of the utmost importance. Long non-coding RNAs (lncRNAs) represent a large family of disease- and tissue-specific transcripts, whose functions have not yet been elucidated in DIPG. Herein, we studied the oncogenic role of the development-associated H19 lncRNA in DIPG. Bioinformatic analyses of clinical datasets were used to measure the expression of H19 lncRNA…
Diffuse intrinsic pontine glioma (DIPG) is an incurable paediatric malignancy. Identifying the molecular drivers of DIPG progression is of the utmost importance. Long non-coding RNAs (lncRNAs) represent a large family of disease- and tissue-specific transcripts, whose functions have not yet been elucidated in DIPG. Herein, we studied the oncogenic role of the development-associated H19 lncRNA in DIPG. Bioinformatic analyses of clinical datasets were used to measure the expression of H19 lncRNA in paediatric high-grade gliomas (pedHGGs). The expression and sub-cellular location of H19 lncRNA were validated in DIPG cell lines. Locked nucleic acid antisense oligonucleotides were designed to test the function of H19 in DIPG cells. We found that H19 expression was higher in DIPG vs. normal brain tissue and other pedHGGs. H19 knockdown resulted in decreased cell proliferation and survival in DIPG cells. Mechanistically, H19 buffers let-7 microRNAs, resulting in the up-regulation of oncogenic let-7 target (e.g., SULF2 and OSMR). H19 is the first functionally characterized lncRNA in DIPG and a promising therapeutic candidate for treating this incurable cancer.
Other authorsSee publication -
The evolutionarily conserved long non-coding RNA LINC00261 drives neuroendocrine prostate cancer proliferation and metastasis via distinct nuclear and cytoplasmic mechanisms
Molecular Oncology
Metastatic neuroendocrine prostate cancer (NEPC) is a highly aggressive disease, whose incidence is rising. Long noncoding RNAs (lncRNAs) represent a large family of disease‐ and tissue‐specific transcripts, most of which are still functionally uncharacterized. Thus, we set out to identify the highly conserved lncRNAs that play a central role in NEPC pathogenesis. To this end, we performed transcriptomic analyses of donor‐matched patient‐derived xenograft models (PDXs) with immunohistologic…
Metastatic neuroendocrine prostate cancer (NEPC) is a highly aggressive disease, whose incidence is rising. Long noncoding RNAs (lncRNAs) represent a large family of disease‐ and tissue‐specific transcripts, most of which are still functionally uncharacterized. Thus, we set out to identify the highly conserved lncRNAs that play a central role in NEPC pathogenesis. To this end, we performed transcriptomic analyses of donor‐matched patient‐derived xenograft models (PDXs) with immunohistologic features of prostate adenocarcinoma (AR+/PSA+) or NEPC (AR−/SYN+/CHGA+) and through differential expression analyses identified lncRNAs that were upregulated upon neuroendocrine transdifferentiation. These genes were prioritized for functional assessment based on the level of conservation in vertebrates. Here, LINC00261 emerged as the top gene with over 3229‐fold upregulation in NEPC. Consistently, LINC00261 expression was significantly upregulated in NEPC specimens in multiple patient cohorts. Knockdown of LINC00261 in PC‐3 cells dramatically attenuated its proliferative and metastatic abilities, which are explained by parallel downregulation of CBX2 and FOXA2 through distinct molecular mechanisms. In the cell cytoplasm, LINC00261 binds to and sequesters miR‐8485 from targeting the CBX2 mRNA, while inside the nucleus, LINC00261 functions as a transcriptional scaffold to induce SMAD‐driven expression of the FOXA2 gene. For the first time, these results demonstrate hyperactivation of the LINC00261‐CBX2‐FOXA2 axes in NEPC to drive proliferation and metastasis, and that LINC00261 may be utilized as a therapeutic target and a biomarker for this incurable disease.
Other authorsSee publication -
PPARγ agonist-loaded PLGA-PEG nanocarriers as a potential treatment for Alzheimer’s disease: in vitro and in vivo studies
International Journal of Nanomedicine
OBJECTIVE:
The first aim of this study was to develop a nanocarrier that could transport the peroxisome proliferator-activated receptor agonist, pioglitazone (PGZ) across brain endothelium and examine the mechanism of nanoparticle transcytosis. The second aim was to determine whether these nanocarriers could successfully treat a mouse model of Alzheimer's disease (AD).
METHODS:
PGZ-loaded nanoparticles (PGZ-NPs) were synthesized by the solvent displacement technique, following a…OBJECTIVE:
The first aim of this study was to develop a nanocarrier that could transport the peroxisome proliferator-activated receptor agonist, pioglitazone (PGZ) across brain endothelium and examine the mechanism of nanoparticle transcytosis. The second aim was to determine whether these nanocarriers could successfully treat a mouse model of Alzheimer's disease (AD).
METHODS:
PGZ-loaded nanoparticles (PGZ-NPs) were synthesized by the solvent displacement technique, following a factorial design using poly (lactic-co-glycolic acid) polyethylene glycol (PLGA-PEG). The transport of the carriers was assessed in vitro, using a human brain endothelial cell line, cytotoxicity assays, fluorescence-tagged nanocarriers, fluorescence-activated cell sorting, confocal and transmission electron microscopy. The effectiveness of the treatment was assessed in APP/PS1 mice in a behavioral assay and by measuring the cortical deposition of β-amyloid.
RESULTS:
Incorporation of PGZ into the carriers promoted a 50x greater uptake into brain endothelium compared with the free drug and the carriers showed a delayed release profile of PGZ in vitro. In the doses used, the nanocarriers were not toxic for the endothelial cells, nor did they alter the permeability of the blood-brain barrier model. Electron microscopy indicated that the nanocarriers were transported from the apical to the basal surface of the endothelium by vesicular transcytosis. An efficacy test carried out in APP/PS1 transgenic mice showed a reduction of memory deficit in mice chronically treated with PGZ-NPs. Deposition of β-amyloid in the cerebral cortex, measured by immunohistochemistry and image analysis, was correspondingly reduced.
CONCLUSION:
PLGA-PEG nanocarriers cross brain endothelium by transcytosis and can be loaded with a pharmaceutical agent to effectively treat a mouse model of AD.Other authorsSee publication -
MicroRNAs in Brain Endothelium and Inflammation
Springer International
Blood-brain barrier (BBB) dysfunction, characterised by increased permeability across brain endothelium and/or leukocyte extravasation into CNS tissue, is associated with changes in the gene expression profile of brain endothelium and is therefore potentially controlled by epigenetic factors. MicroRNAs (miRNAs) are single-stranded, short, non-coding RNA molecules that mediate post-transcriptional gene silencing. Recent studies have demonstrated alterations of miRNA expression at the BBB in…
Blood-brain barrier (BBB) dysfunction, characterised by increased permeability across brain endothelium and/or leukocyte extravasation into CNS tissue, is associated with changes in the gene expression profile of brain endothelium and is therefore potentially controlled by epigenetic factors. MicroRNAs (miRNAs) are single-stranded, short, non-coding RNA molecules that mediate post-transcriptional gene silencing. Recent studies have demonstrated alterations of miRNA expression at the BBB in experimental autoimmune encephalomyelitis, in multiple sclerosis, and in cytokine-stimulated human brain endothelial cells. These results suggest that brain endothelial miRNAs play a role in the pathophysiology of the BBB in inflammation. In this chapter, we will first give an overview of miRNA biology and then review the current knowledge of the role of miRNAs in regulating BBB function, particularly in the context of multiple sclerosis
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Don't let the noise distract you. This industry is doing some incredible work. The future is bright! What would you name the other…
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We are pleased to share the publication of a new paper in Human Reproduction Open, where our investigators, Dr. Felipe Vilella and Dr. Carlos Simon…
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🌟 Excited to share that our research has been published in Nature Immunology! I’m thrilled to have contributed to this study, where we discovered…
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A pinch of salt to the rescue🧂#celltherapies
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