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227 results for “multipotency”
Storage conditions affect the composition of the lyophilized secretome of multipotent mesenchymal stromal cells - graphs
<p>Figures for artcile Rogulska, O., Vackova, I., Prazak, S. <em>et al.</em> Storage conditions affect the composition of the lyophilized secretome of multipotent mesenchymal stromal cells. <em>Sci Rep</em> 14, 10243 (2024). https://doi.org/10.1038/s41598-024-60787-z</p> <p><span>Fig. 1. Preservation of the growth factors and cytokines in the lyophilized MSC-derived conditioned medium after 3 months of storage at different temperatures (N=3). Data is presented as Median (Q1; Q3). * - the values are significantly (p<0.05) lower compared to the -80°C group; # - the values are significantly (p<0.05) lower compared to the -20°C group. The values are related to non-lyophilized MSC-sec stored for the same time (3 months) in a frozen state at −80°C.</span></p> <p><span> </span><span>Fig. 2. The preservation of growth factors and cytokines in the lyophilized MSC-derived conditioned medium after 30 months of storage at different temperatures (N=3). Data is presented as Median (Q1; Q3). * - the values are significantly (p<0.05) lower compared to the -80°C group; # - the values are significantly (p<0.05) lower compared to the -20°C group; ° - the values are significantly (p<0.05) lower compared to the 4°C group. The values are related to non-lyophilized MSC-sec stored for the same time (30 months) in a frozen state at −80°C.</span></p> <p><span> </span><span>Fig. 3. The preservation levels of the whole lyophilized MSC-sec cocktail, determined as the median of the preservation values for each of the MSC-sec components. The v</span><span>alues are related to non-lyophilized MSC-sec stored for the same time in a frozen state at −80°C.</span></p>
Tabular and image data of article "Morphing cholinesterase inhibitor amiridine into multipotent drugs for the treatment of Alzheimer's disease"
<p>The search for novel drugs to address the medical needs of Alzheimer’s disease (AD) is an ongoing process relying on the discovery of disease-modifying agents. Given the complexity of the disease, such an aim can be pursued by developing so-called multi-target directed ligands (MTDLs) that will impact the disease pathophysiology more<br>comprehensively. Herewith, we contemplated the therapeutic efficacy of an amiridine drug acting as a cholinesterase inhibitor by converting it into a novel class of novel MTDLs. Applying the linking approach, we have paired amiridine as a core building block with memantine/adamantylamine, trolox, and substituted benzothiazole moieties to generate novel MTDLs endowed with additional properties like N-methyl-D-aspartate (NMDA) receptor affinity, antioxidant capacity, and anti-amyloid properties, respectively. The top-ranked amiridine-based compound 5d was also inspected by in silico to reveal the butyrylcholinesterase binding differences with its close structural analogue 5b. Our study provides insight into the discovery of novel amiridinebased drugs by broadening their target-engaged profile from cholinesterase inhibitors towards MTDLs with potential implications in AD therapy.</p> <p><strong>Table 1. </strong>hBChE inhibitory activities of 5c-d, 7c and 7 g and reference compounds (amiridine hydrochloride and THA); their cytotoxicity profile on SH-SY5Y cell line, and predictions of BBB penetration.</p> <p>T<strong>able 2</strong>. Relative inhibitions (RIs) of 5c-d and 7 m and reference compound memantine at recombinant human GluN1/GluN2B NMDA receptor expressed in HEK293 cells.</p> <p><strong>Fig_1</strong>. Chemical structures of rivastigmine, galantamine, and tacrine as representatives of cholinesterase inhibitors. Approaches to novel drugs for AD treatment on the selected candidates are displayed.</p> <p><strong>Fig_2</strong>. Examples of previously published amiridine-based derivatives and design strategy applied in the current study below, using various pharmacophores.</p> <p><strong>Fig_3</strong>. Top scored docking pose of 5b (A) and 5d (B) highlighting the key findings responsible for compound activity/inactivity. For the sake of clarity, superimposed ligands are aligned in the Fig. C with respect to key amino acid residue W82 to demonstrate the binding difference. Compounds 5b and 5d are colored in salmon and yellow, respectively. Essential amino acid residues responsible for ligand anchoring are rendered in green. Important interactions of different origin are displayed with dashed black lines. The figure was created with The PyMOL Molecular Graphics System, v. 2.5.2.</p> <p><strong>Scheme 1</strong>. Preparation of the amiridine-based compounds 5a-d. Reagents and conditions: <strong>a)</strong> 2-chloroacetyl chloride (4 eq.), CHCl3, 90 ◦C, overnight, 8, 54%, 11, 90%, 12, 52%; <strong>b)</strong> CH3CN, K2CO3, KI, reflux, 3 h, 5a, 54%, 5b, 54%; <strong>c)</strong> amiridine (1.1 eq), CH3CN, K2CO3, KI, reflux, overnight, 5c, 48%, 5d, 41%.</p> <p><strong>Scheme 2</strong>. Preparation of intermediate 13 and final compound 6. Reagents and conditions: <strong>a)</strong> potassium phthalimide, CH3CN, reflux, 3 h, then an excess of NH2NH2⋅H2O, reflux, overnight, 57%; <strong>b)</strong> DMF, TEA, BOP, room temperature, 2 days, 86%.</p> <p><strong>Scheme 3</strong>. Preparation of amiridine-benzothiazole derivatives 7a-m. Reagents and conditions: <strong>a)</strong> for 7a: 2-chlorobenzothiazole, 110 ◦C, overnight, 32%; for 7b-m: corresponding 2-chlorobenzothiazole, DIPEA, 100 ◦C, overnight, 21–77%.</p>
Erythropoietin directly remodels the clonal composition of murine hematopoietic multipotent progenitor cells
<p>## In version 1 of the repository the scRNAseq data was corrupted -- in version 2 this has been corrected and the bam files of both scRNAseq runs have been uploaded ##</p> <p>This dataset consists of the raw sequencing files of 9 independent barcoding experiments and of one 10X Genomics scRNAseq experiment. These are the source files for the main figures of the associated publication.</p> <p>HSPCs (C-Kit+ Sca1+ CD150+ Flt3-) or MPP2 (C-Kit+ Sca1+ Flt3- CD150+ CD48+) were isolated form mouse bone marrow through flushing, MACS-enrichment and sorting. The cells were barcoded by spin infection for 6h, and cultured in StemSpanMedium SFEM with 50 ng/ml mSCF (STEMCELL Technologies) for 16h with or without human recombinant EPO (Eprex, erythropoietin alpha, Janssen) at 1000 ng/ml or 160 ng/ml. At this stage scRNAseq was perfromed on the 10X Chromium platfom (10X Genomics), or cells were transplanted by tail vein injection into 6Gy irradiated recipient mice. When appropirate an additional injection of EPO 133ug/kg was given at the moment of transplantation. Different mature hematopoietic cells were isolated form the transplanted mice after 4 weeks or 16 weeks.</p> <p>For barcoding experiments, a three-step PCR was performed to amplify barcode sequences, to add Read1 and Read2 Illumina sequencing adapters, P5 and P3 flow cell attachment sites as well as plate and sample indices. Libraries were sequenced on an Illumina HiSeq SR65 with 10% of PhiX spike-in. For scRNAseq experiment, libraries were made using the Chromium SIngle Cell 3' v2 kit and sequencing was performed on a HiSeq PE26-98.</p> <p>The repository encompasses the following datasets:</p> <ul> <li>A1006.tar.gz -- AE05Low -- HSPCs EPO 160 ng/ml + injection 4 weeks -- main figure 2</li> <li>A1007.tar.gz -- AE05High -- HSPCs EPO 1000 ng/ml + injection 4 weeks -- main figure 2</li> <li>A984.tar.gz -- AE03Low -- HSPCs EPO 160 ng/ml 4 weeks -- main figure 2 and HSPC part of main figure 4</li> <li>A1008.tar.gz -- AE03High -- HSPCs EPO 1000 ng/ml 4 weeks -- main figure 1, 2 and DC part of main figure 3</li> <li>A1012.tar.gz -- AE04Low -- HSPCs EPO 160 ng/ml 4 months -- main figure 8</li> <li>A1013.tar.gz -- AE04High -- HSPCs EPO 1000 ng/ml 4 months -- main figure 8</li> <li>A1105.tar.gz -- AE07part1 -- HSPCs EPO 1000 ng/ml 4 weeks part 1 -- MkP part of main figure 3</li> <li>A1107.tar.gz -- AE07part2 -- HSPCs EPO 1000 ng/ml 4 weeks part 2 -- MkP part of main figure 3</li> <li>A1166.tar.gz -- AE13part1 -- HSPCs EPO 1000 ng/ml 4 weeks part 1 -- HSPC part of main figure 4</li> <li>A1166.tar.gz -- AE13part2 -- HSPCs EPO 1000 ng/ml 4 weeks part 2 -- HSPC part of main figure 4</li> <li>D757_3697.tar.gz -- LP26MPP2 -- MPP2 EPO 1000 ng/ml 4 weeks -- main figure 7</li> </ul> <p>In version two of the repository the scRNAseq data is changed into:</p> <ul> <li>possorted_genome_bam_T1.bam -- 10X of EPO exposed (T1) HSPCs -- main figure 5 and 6</li> <li>possorted_genome_bam_T2.bam -- 10X of control (T2) HSPCs -- main figure 5 and 6</li> </ul> <p>The folder for each barcode experiment encompasses fastq files for each sample index used in the experiment. These have to be further de-multiplexed by plate index and barcode reads have to be called. These, and all subsequent processing steps till the making of the main figures are described in the github folder accompanying the associated publication.</p> <p> </p> <p> </p> <p> </p> <p> </p>
PKHhigh/CD133+/CD24− Renal Stem-Like Cells Isolated from Human Nephrospheres Exhibit In Vitro Multipotency.
<p>The mechanism upon which human kidneys undergo regeneration is debated, though different lineage-tracing mouse models have tried to explain the cellular types and the mechanisms involved. Different sources of human renal progenitors have been proposed, but it is difficult to argue whether these populations have the same capacities that have been described in mice. Using the nephrosphere (NS) model, we isolated the quiescent population of adult human renal stem-like PKH<sup>high</sup>/CD133+/CD24− cells (RSC). The aim of this study was to deepen the RSC in vitro multipotency capacity. RSC, not expressing endothelial markers, generated secondary nephrospheres containing CD31+/vWf+ cells and cytokeratin positive cells, indicating the coexistence of endothelial and epithelial commitment. RSC cultured on decellularized human renal scaffolds generated endothelial structures together with the proximal and distal tubular structures. CD31+ endothelial committed progenitors sorted from nephrospheres generated spheroids with endothelial-like sprouts in Matrigel. We also demonstrated the double commitment toward endothelial and epithelial lineages of single RSC. The ability of the plastic RSC population to recapitulate the development of tubular epithelial and endothelial renal lineages makes these cells a good tool for the creation of organoids with translational relevance for studying the parenchymal and endothelial cell interactions and developing new therapeutic strategies.</p>
Safety Study of Multipotent Progenitor Cells for Immunomodulation Therapy After Liver Transplantation
ClinicalTrials.gov study NCT01841632. IPD Sharing: Not stated. Countries: 1. Publications: 2.
EBF1 primes B-lymphoid enhancers and limits the myeloid bias in murine multipotent progenitors
<p>Haematopoietic stem cells (HSC) and multipotent progenitors (MPP) generate all cells of the blood system. Despite their multipotency, MPPs display poorly understood lineage bias. Here, we examine whether lineage-specifying transcription factors, such as the B-lineage determinant EBF1, regulate lineage preference in early progenitors. We detect low level EBF1 expression in myeloid-biased MPP3 and lymphoid-biased MPP4 cells, coinciding with expression of the myeloid determinant C/EBPα. Hematopoietic deletion of <em>Ebf1</em> results in enhanced myelopoiesis and reduced HSC repopulation capacity. <em>Ebf1</em>-deficient MPP3 and MPP4 cells exhibit augmented myeloid differentiation potential and a myeloid-enriched transcriptome that is inversely correlated with <em>Cebpa</em>-deficient progenitors. Correspondingly, EBF1 binds the <em>Cebpa</em> enhancer and <em>Ebf1</em>-deficient MPP3 and MPP4 cells upregulate <em>Cebpa </em>expression. In addition, EBF1 primes the chromatin of B-lymphoid enhancers specifically in MPP3 cells. Thus, our study implicates EBF1 in regulating myeloid/lymphoid fate bias in MPPs by constraining C/EBPα -driven myelopoiesis and priming the B-lymphoid fate.</p>
Analysis of the Osteogenic Potential of Multipotent Cells From Different Anatomical Regions
ClinicalTrials.gov study NCT03369457. IPD Sharing: NO. Countries: 1. Publications: 1.
Allogeneic Multipotent Stromal Cell Treatment for Acute Kidney Injury Following Cardiac Surgery
ClinicalTrials.gov study NCT00733876. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Efficacy of Bone-marrow-derived and Placenta-derived Multipotent Mesenchymal Stem / Stromal Cells for Osteoarthritis
ClinicalTrials.gov study NCT04453111. IPD Sharing: NO. Countries: 1. Publications: 1.
Data from: Notch and Nodal control expression of a forkhead factor in the specification network of a multipotent progenitor population in sea urchin
Indirect development, where embryogenesis gives rise to a larval form, requires that some cells retain developmental potency until they contribute to the different tissues in the adult, including the germ line, in a later, post-embryonic phase. In sea urchins, the coelomic pouches are the major contributor to the adult but how coelomic pouch cells (CPCs) are specified during embryogenesis is unknown. We here identify the key signaling inputs into the CPC specification network and show the forkhead factor foxY is the first transcription factor specifically expressed in CPC progenitors. Through dissection of its cis-regulatory apparatus we determine that the foxY expression pattern is the result of two signaling inputs: First, Delta/Notch signaling activates foxY in CPC progenitors and, second, Nodal signaling restricts its expression to the left side, where the adult rudiment will form, through direct repression by the Nodal target pitx2. A third signal, Hedgehog, is required for coelomic pouch morphogenesis and institution of laterality but does not directly affect foxY transcription. Knockdown of foxY results in failure to form coelomic pouches and disrupts expression of virtually all transcription factors known to be expressed in this cell type. Our experiments place foxY at the top of the regulatory hierarchy underlying specification of a cell type maintaining developmental potency.
Autologous Multipotent Mesenchymal Stromal Cells in the Treatment of Amyotrophic Lateral Sclerosis
ClinicalTrials.gov study NCT03828123. IPD Sharing: Not stated. Countries: 0. Publications: 1.
Data from: Influence of factors of cryopreservation and hypothermic storage on survival and functional parameters of multipotent stromal cells of placental origin
Open the record for dataset details and reuse information.
Data from: Notch and Nodal control expression of a forkhead factor in the specification network of a multipotent progenitor population in sea urchin
Open the record for dataset details and reuse information.
OCT4-SOX2 dimers reshape the epigenome to promote neural crest multipotency
GEO Series GSE163961. Gallus gallus; Homo sapiens. 98 samples. Type: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing.
Dynamic analysis of gene expression and genome wide transcription factor binding during lineage-specification of multipotent progenitors [ER]
GEO Series GSE49990. Mus musculus. 16 samples. Type: Expression profiling by array.
Fate changes leading to multipotency of isolated mesenchymal cells [Expression: Population_vs_Clone]
GEO Series GSE48545. Mus musculus. 6 samples. Type: Expression profiling by array.
Influence of temperature fluctuations during cryopreservation on vital parameters, plasticity, and transgene expression of placental multipotent stromal cells
GEO Series GSE85097. Homo sapiens. 10 samples. Type: Expression profiling by array.
Diabetes Enhances the Proliferation of Adult Pancreatic Multipotent Progenitor Cells and Biases Their Differentiation to More Beta-Cell Production
GEO Series GSE66817. Mus musculus. 4 samples. Type: Expression profiling by high throughput sequencing.
PBRM-1/PBAF-regulated genes in a multipotent progenitor in C. elegans
GEO Series GSE249603. Caenorhabditis elegans. 10 samples. Type: Expression profiling by high throughput sequencing.
Lymphatic vessels arise from a niche of multipotent angioblasts within the floor of the cardinal vein
GEO Series GSE65751. Danio rerio. 4 samples. Type: Expression profiling by high throughput sequencing.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.