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Development of iPSC-derived Disease Models - https://lnkd.in/eTcBhWm Human induced pluripotent stem cell (iPSC)-based models are a valuable resource for studying disease mechanisms in vitro at the cellular level[1], screening potential new therapeutics[2], and investigating the propensity and mechanism for the development of toxic side effects caused by a drug treatment[3]. Such iPSC-based models enable research to be performed under defined experimental conditions and in a reproducible manner. Through our extensive Global Tissue Network and alliances, REPROCELL can source a variety of diseased and healthy tissue samples (for example skin, blood or urine cells) for use with REPROCELL reprogramming technologies to generate iPSC lines on behalf of our clients. Tissues and cells that we source are fully anonymized and consented for use in all types of iPSC-based projects, and they come with valuable donor demographic information. We can also perform whole genome sequencing or molecular characterization of tissue or primary cells to provide further genetic information or confirm disease-relevant mutations. Read more at: https://lnkd.in/eTcBhWm #ipsc #genomesequencing #stemcells

Nanostraws uniquely enable edits of sensitive genes!  In a recent paper, we show that nanostraws greatly reduce stress levels in human primary blood stem cells when editing genes connected to the rare bone marrow disorder Diamond-Blackfan anemia (DBA). CRISPR based editing of genes such as RPS19 sensitize the cells to stress and is catastrophic to the cells if combined with electroporation based transfection.  Nanostraws allow for many more cells to be recovered and used for downstream processing and/or disease modelling. This will have a profound impact on the way we can study DBA. This study was performed in collaboration with Prof. Stefan Karlsson and Prof. Jonas Larsson, Lund University. Read more in Haematologica https://lnkd.in/dhsrNN2N #NAVANbio #nanotechnology #lunduniversity #nanolund #stemcell

📃Scientific paper: Disruption of MAM integrity in mutant FUS oligodendroglial progenitors from hiPSCs Abstract: Amyotrophic lateral sclerosis (ALS) is a rapidly progressive and fatal neurodegenerative disorder, characterized by selective loss of motor neurons (MNs). A number of causative genetic mutations underlie the disease, including mutations in the fused in sarcoma ( FUS ) gene, which can lead to both juvenile and late-onset ALS. Although ALS results from MN death, there is evidence that dysfunctional glial cells, including oligodendroglia, contribute to neurodegeneration. Here, we used human induced pluripotent stem cells (hiPSCs) with a R521H or a P525L mutation in FUS and their isogenic controls to generate oligodendrocyte progenitor cells (OPCs) by inducing SOX10 expression from a TET-On SOX10 cassette. Mutant and control iPSCs differentiated efficiently into OPCs. RNA sequencing identified a myelin sheath-related phenotype in mutant OPCs. Lipidomic studies demonstrated defects in myelin-related lipids, with a reduction of glycerophospholipids in mutant OPCs. Interestingly, FUS ^ R521H OPCs displayed a decrease in the phosphatidylcholine/phosphatidylethanolamine ratio, known to be associated with maintaining membrane integrity. A proximity ligation assay further indicated that mitochondria-associated endoplasmic reticulum membranes (MAM) were diminished in both mutant FUS OPCs. Moreover, both mutant FUS OPCs displayed increased susceptibility to ER stress when exposed to thapsigargin, and exhibited impaired mitochondrial respiration and reduced Ca^2+ signaling from ... Continued on ES/IODE ➡️ https://etcse.fr/VUvlC ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you. #amyotrophiclateralsclerosis #als #charcot

Use of stem cells in disease modeling‼️ Cells derived from the tissue affected by a particular disease can be used to understand the mechanisms responsible for disease or can serve as a model for drug discovery or testing. Relevant cells (orange or green) can be obtained either directly from the tissue or by differentiation from specific adult stem cells (blue). Alternatively, if the disease has an inherited genetic origin, then any somatic cells (lime green) can be used to produce iPS cells, which can in turn be differentiated to the required tissue cell type.

ChIP-seq Data Analysis (part-2) SNAIL-1 in the TRANSFAC database In Part-1 of this series analysis of ChIP-seq data publicly available in GSE127183 is presented. This ChIP-seq dataset provides in vivo binding regions of the SNAIL-1 transcription factor in colorectal cancer cells. This video demonstrates the SNAIL-1 Locus Report in the integrated TRANSFAC + HumanPSD + TRANSPATH database. Here we demonstrate details about the SNAIL-1 transcription factor both as a gene and as a protein. First, we demonstrate associations of SNAIL-1 with several neoplasms as a biomarker. It is known to be associated with about 40 different diseases, the top associated are stomach, breast, colorectal and prostatic neoplasms. The next part of the Locus Report demonstrates tissue and organ-specific expression of SNAIL-1. SNAIL-1 transcription factor is known to bind to its sites in several promoters, and also to play a role in several pathways including the epithelial to mesenchymal transition. It is important to note that SNAIL-1 binds and regulates its own promoter thus forming a short feedback loop. There are several matrices for SNAIL-1 collected in TRANSFAC. There are several factors that regulate SNAIL-1 promoters including EGR-1, AR, GLI-1, c-Jun, SRF, Smad-2, HIF-1. Next, the interaction of SNAIL-1 with several FDA-approved drugs and other small molecules are reviewed. From the Locus Report, we briefly jump into several other types of Reports including the Drug Report and Pathway Report as well as into the TRANSFAC Transcription Factor Classification. The details on SNAIL-1 interactions with different proteins and TFs are shown, among them beta-catenin forms a complex with SNAIL-1 and this pathway is already known to be important in colon carcinoma. We review post-translational modifications of SNAIL-1 including type of modification, modified amino acid and also the enzyme responsible for the particular modification. Locus Report in the integrated TRANSFAC + HumanPSD + TRANSPATH database helps to understand the role of SNAIL-1 and can significantly facilitate the biological interpretation of the results obtained by the bioinformatics analysis. #genexplain #bioinformatics #TRANSFAC #science #dataanalysis #dataanalytics #pathways #analysis #research #cancerresearch #transcription #molecules #biomarkers

📃Scientific paper: Phloretin suppresses neuroinflammation by autophagy-mediated Nrf2 activation in macrophages Abstract: Background Macrophages play a dual role in neuroinflammatory disorders such as multiple sclerosis (MS). They are involved in lesion onset and progression but can also promote the resolution of inflammation and repair of damaged tissue. In this study, we investigate if and how phloretin, a flavonoid abundantly present in apples and strawberries, lowers the inflammatory phenotype of macrophages and suppresses neuroinflammation. Methods Transcriptional changes in mouse bone marrow-derived macrophages upon phloretin exposure were assessed by bulk RNA sequencing. Underlying pathways related to inflammation, oxidative stress response and autophagy were validated by quantitative PCR, fluorescent and absorbance assays, nuclear factor erythroid 2–related factor 2 (Nrf2) knockout mice, western blot, and immunofluorescence. The experimental autoimmune encephalomyelitis (EAE) model was used to study the impact of phloretin on neuroinflammation in vivo and confirm underlying mechanisms. Results We show that phloretin reduces the inflammatory phenotype of macrophages and markedly suppresses neuroinflammation in EAE. Phloretin mediates its effect by activating the Nrf2 signaling pathway. Nrf2 activation was attributed to 5′ AMP-activated protein kinase (AMPK)-dependent activation of autophagy and subsequent kelch-like ECH-associated protein 1 (Keap1) degradation. Conclusions This study opens future perspectives for phloretin as a therapeutic strategy for neuroinflammatory disorde... Continued on ES/IODE ➡️ https://etcse.fr/1v2Wf ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you.

I'm pleased to see a recent study in Frontiers in Cardiovascular Medicine using Cellartis DEF-CS 500 stem cell medium for single-cell survival after CRISPR gene editing! The study demonstrated that using DEF-CS 500 significantly improved the survival and functionality of edited cells, enabling researchers to generate disease models using hiPSCs to study cardiac dysfunction more effectively. This highlights the medium's effectiveness and reliability in challenging stem cell applications. https://lnkd.in/g_-AQZWD

I'm proud to announce our latest publication in BMC: Cell Communication and Signaling. We shed light on the calcium electroporation (CaEP) and its impact on two established endothelial cell lines, EA.hy926 and HMEC-1, and studied their viability, cytoskeleton, adherens junctions, and intracellular Ca2+ regulation. EA.hy926 cells displayed higher CaEP susceptibility and distinct Ca2+ kinetics compared to HMEC-1, as evidenced by spectrofluorometric measurements. RNA sequencing revealed significant differences in gene expression related to cytoskeleton and Ca2+ signaling between the two cell lines. Our findings suggest that differences in CaEP response and Ca2+ regulation between EA.hy926 and HMEC-1 are attributed to their distinct transcriptomic profiles. This study provides valuable insights for selecting endothelial cell models based on research objectives.   Check out the full article for more details https://lnkd.in/dCsfq8AP   #Research #CaEP #CancerTherapy #TissueEngineering #Bioinformatics #Electroporation #Calcium

Role of long-noncoding RNA in diabetic atherosclerosis Diabetes accelerates the development of atherosclerosis, increasing the incidence of cardiovascular events. In atherosclerosis, immune cells called macrophages release molecules such as chemokines and cytokines, causing inflammation and leading to arterial plaque formation. However, significant gaps persist in understanding the exact molecular mechanisms controlling this increased inflammatory response in individuals with diabetes. In a new, preclinical study, researchers identified a long non-coding RNA (lncRNA) sequence that could help them unravel the complex processes underlying diabetic atherosclerosis, potentially paving the way for future therapeutic interventions in humans. Through genetic analysis of a mouse model of diabetic atherosclerosis, the research team identified a specific sequence of long-noncoding RNA, they named MERRICAL, which is involved in recruiting macrophages to the arterial wall. As atherosclerosis progressed in these mice, the researchers found a notable increase in the expression of MERRICAL at arterial lesions—areas where atherosclerosis plaque built up and damaged the arteries. #ScienceMission #ScienceNewsHighlights https://lnkd.in/gyPzACqq

Have you heard the term “translational research?" At Retina Foundation, it’s one of the core activities that we do. In simple terms, translational research is the process of turning scientific discoveries made in the lab into real-world treatments and therapies that can benefit patients. It's about bridging the gap between basic science and clinical practice. In practical terms it is demonstrated by our laboratories being literally across the hall for our clinics. This proximity is rarely found in other institutions and is one of the many factors that makes the research at the Retina Foundation so unique. In retinal research, this means taking groundbreaking findings from our laboratories at Retina Foundation and moving them through rigorous testing and clinical trials. The findings can be anything from a novel gene therapy to an advanced imaging technique to discovering possible individualized therapies for patients using their own stem cells. With each clinical trial, we are working to move from theoretical to improved vision and enhanced quality of life for patients with retinal disease. Translational research is where science meets patient care. It’s a collaborative process that involves researchers, clinicians and patients working together to turn potential treatments into actual solutions. Every step we take in this field brings us closer to new therapies that can make a real difference in people's lives.