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Exosome Diagnostics rose stem cell derived exosome
Rose Stem Cell Derived Exosome, supplied by Exosome Diagnostics, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/stem+cells/derived+exosome+like+plant/pm42278464-52-6-9
Average 86 stars, based on 1 article reviews

rose stem cell derived exosome - by Bioz Stars, 2026-11

86/100 stars

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Infection:

Article Title: A pH-responsive hydrogel based on polysaccharides incorporated with honeysuckle-derived exosome-like nanovesicles for the management of infected wound.
Article Snippet: The management of infected wounds is a major clinical challenge because the healing process is often obstructed by several related pathological factors, such as drug-resistant microbial infections, persistent inflammatory responses, oxidative stress, and impaired angiogenesis.. In this study, we developed an injectable hydrogel (CTO-Ho) designed using honeysuckle-derived exosome-like nanovesicles (HoNVs) incorporated into a dynamic network created from carboxymethyl chitosan (CMCS), tannic acid (TA), and oxidised sodium alginate (OSA).. HoNVs were isolated from fresh honeysuckle and characterised.

other:

Article Title: Biomimetic fusion nanosystem from ginger exosomes and tumor cell membranes: boosting PLK1-targeted therapy in BRCA-heterogeneous HGSOC.
Article Snippet: Exploring the bioactivity of MicroRNAs Originated from Plant-derived Exosome-like Nanoparticles (PELNs): current perspectives.

Article Title: Plant-Derived Exosome-Like Nanoparticles in Neurodegenerative Diseases: From Dual Bioactive-Delivery Roles to Translational Challenges
Article Snippet: Lycium barbarum L.-derived exosome-like nanoparticles loaded with isoliquiritigenin and incorporated into 3D-printed biomimetic scaffolds promoted spinal cord injury repair, suggesting that PELNs can be integrated with tissue-engineering platforms to provide both biological and structural support.96 In this hybrid system, plant-derived vesicles may regulate the post-injury inflammatory microenvironment, reduce excessive apoptosis or autophagy, and support axonal regeneration., This example is especially valuable because it moves PELNs beyond simple drug delivery and positions them as components of bioactive regenerative systems.

Article Title: Tower-shaped super-adhesive microneedles loaded with vitamin A-containing Bletilla striata vesicles: temporally regulated Inflammation resolution and ECM remodeling for scarless wound healing.
Article Snippet: Emerging Plant-Derived Exosome-Like Particles Reveal Key Therapeutic Benefits.

Derivative Assay:

Article Title: Nanomaterials targeting ferroptosis for osteoarthritis treatment: a systematic review of preclinical evidence.
Article Snippet: .. By enabling multifunctional, diseasecontextualized targeting, such platforms hold the potential to overcome key translational barriers—but their success will depend on careful design, standardized production, and comprehensive preclinical evaluation. (3) Green and Bio-Inspired NMs: Plant-Derived Exosome Nanovesicles and Herbal Self-Assembled Platforms in OA–Ferroptosis Research Green nanotechnology represents a sustainable and bio-inspired strategy for the design and application of NMs, aiming to minimize environmental impact while harnessing renewable, non-toxic, and naturally derived resources [128]. ..

Image Search Results

HCC cells promote MC migration and sustain MC proliferation. (A, B) Timer3.0 database analysis of SCF expression in tumors and correlation analysis between SCF and MCs; (C) ELISA detection of SCF levels in tumor tissues and adjacent tissues; (D) Correlation analysis between TAMC density and SCF concentration in HCC tumor tissues; (E): Flow cytometry identification of expanded hMCs at week 4; (F, G) Transwell assay for hMC migration capacity; (H, I) Flow cytometry for hMC proliferation; (J, K) Flow cytometry for hMC cell cycle. Data are presented as mean ± SD. Figure (B) used independent samples t ‐tests ( n = 59). (D) Spearman 's rank correlation analysis ( n = 59); (G/I/K), one‐way ANOVA with Tukey's post‐hoc multiple comparison test ( N = 3). * indicates p < 0.05; *** indicates p < 0.001.

Journal: Journal of Biochemical and Molecular Toxicology

Article Title: Tumor‐Associated Mast Cells Drive Immunosuppression and Resistance to Anti‐PD‐1 Therapy in Hepatocellular Carcinoma Through CCL17/CCR4‐mediated Regulatory T‐Cell Recruitment

doi: 10.1002/jbt.71127

Figure Lengend Snippet: HCC cells promote MC migration and sustain MC proliferation. (A, B) Timer3.0 database analysis of SCF expression in tumors and correlation analysis between SCF and MCs; (C) ELISA detection of SCF levels in tumor tissues and adjacent tissues; (D) Correlation analysis between TAMC density and SCF concentration in HCC tumor tissues; (E): Flow cytometry identification of expanded hMCs at week 4; (F, G) Transwell assay for hMC migration capacity; (H, I) Flow cytometry for hMC proliferation; (J, K) Flow cytometry for hMC cell cycle. Data are presented as mean ± SD. Figure (B) used independent samples t ‐tests ( n = 59). (D) Spearman 's rank correlation analysis ( n = 59); (G/I/K), one‐way ANOVA with Tukey's post‐hoc multiple comparison test ( N = 3). * indicates p < 0.05; *** indicates p < 0.001.

Article Snippet: The following kits were utilized: human SCF ELISA Kit (E‐EL‐H1299, Elabscience), human CCL1 ELISA kit (ab314600, Abcam), human CCL5 ELISA kit (ab174446, Abcam), human CCL17 ELISA kit (ab183366, Abcam), Human CCL22 ELISA Kit (ab242931, Abcam), Human CCL28 ELISA Kit (ab99988, Abcam), Human Granzyme B ELISA Kit (E‐EL‐H1617, Elabscience), Human Interferon‐γ (IFN‐γ) ELISA Kit (E‐EL‐H0108, Elabscience), Human TNF‐α ELISA Kit (E‐EL‐H0109, Elabscience), Human Perforin 1 ELISA Kit (E‐EL‐H1123, Elabscience), Mouse Granzyme B ELISA Kit (E‐EL‐M0594, Elabscience), Mouse IFN‐γ ELISA Kit (E‐EL‐M0048, Elabscience), Mouse TNF‐α ELISA Kit (E‐EL‐M3063, Elabscience), and Mouse Perforin ELISA Kit (E‐EL‐M0890, Elabscience).

Techniques: Migration, Analysis, Expressing, Enzyme-linked Immunosorbent Assay, Concentration Assay, Flow Cytometry, Transwell Assay, Comparison, X-Ray Photoelectron Spectroscopy

TAMCs recruit Tregs into the tumor microenvironment by secreting chemokines. (A) ELISA detection of CCL1, CCL5, CCL17, CCL22, and CCL28 secretion by TAMCs (after subtracting CCL1, CCL5, CCL17, CCL22, and CCL28 levels in TCCS); (B) ELISA detection of CCL17 levels in tumor tissues and adjacent tissues; (C) Correlation analysis between TAMCs and CCL17 concentration; D: Correlation analysis between Tregs and CCL17 concentration; (E, F) Transwell migration assay to assess Treg migration capacity. Data are presented as mean ± SD. (A, B), independent samples t ‐tests ( N = 3); (C, D) Spearman 's rank correlation analysis ( n = 59); (F), one‐way ANOVA and Tukey's multiple comparison test ( N = 3). * indicates p < 0.05, ** indicates p < 0.01, *** indicates p < 0.001.

Journal: Journal of Biochemical and Molecular Toxicology

doi: 10.1002/jbt.71127

Figure Lengend Snippet: TAMCs recruit Tregs into the tumor microenvironment by secreting chemokines. (A) ELISA detection of CCL1, CCL5, CCL17, CCL22, and CCL28 secretion by TAMCs (after subtracting CCL1, CCL5, CCL17, CCL22, and CCL28 levels in TCCS); (B) ELISA detection of CCL17 levels in tumor tissues and adjacent tissues; (C) Correlation analysis between TAMCs and CCL17 concentration; D: Correlation analysis between Tregs and CCL17 concentration; (E, F) Transwell migration assay to assess Treg migration capacity. Data are presented as mean ± SD. (A, B), independent samples t ‐tests ( N = 3); (C, D) Spearman 's rank correlation analysis ( n = 59); (F), one‐way ANOVA and Tukey's multiple comparison test ( N = 3). * indicates p < 0.05, ** indicates p < 0.01, *** indicates p < 0.001.

Techniques: Enzyme-linked Immunosorbent Assay, Analysis, Concentration Assay, Transwell Migration Assay, Migration, Comparison

The TAMCs‐Tregs axis inhibits CD8 + T cell function. (A, B) Flow cytometry analysis of Treg‐mediated suppression of CD8 + T cell proliferation; (C–F) ELISA for Granzyme B, IFN‐γ, TNF‐α, and Perforin in supernatants from CD8 + T cell proliferation assays. Data are presented as mean ± SD. One‐way ANOVA was performed, followed by Tukey's multiple comparison test for post‐hoc analysis ( N = 3). * indicates p < 0.05, ** indicates p < 0.01, *** indicates p < 0.001.

Journal: Journal of Biochemical and Molecular Toxicology

doi: 10.1002/jbt.71127

Figure Lengend Snippet: The TAMCs‐Tregs axis inhibits CD8 + T cell function. (A, B) Flow cytometry analysis of Treg‐mediated suppression of CD8 + T cell proliferation; (C–F) ELISA for Granzyme B, IFN‐γ, TNF‐α, and Perforin in supernatants from CD8 + T cell proliferation assays. Data are presented as mean ± SD. One‐way ANOVA was performed, followed by Tukey's multiple comparison test for post‐hoc analysis ( N = 3). * indicates p < 0.05, ** indicates p < 0.01, *** indicates p < 0.001.

Techniques: Cell Function Assay, Flow Cytometry, Analysis, Enzyme-linked Immunosorbent Assay, Comparison

Combination therapy of anti‐PD‐1 antibody and CCR4 antagonists reshapes the tumor immune microenvironment in HCC. (A–F) Flow cytometry analysis of immune cell proportions (MCs, Tregs, CD8 + T cells) in tumor tissue; G–K: ELISA detection of Granzyme B, IFN‐γ, TNF‐α, Perforin, and CCL17 levels. Data are presented as mean ± SD. One‐way ANOVA was performed, followed by Tukey's multiple comparison test for post‐hoc analysis ( n = 6). * indicates p < 0.05, ** indicates p < 0.01, *** indicates p < 0.001.

Journal: Journal of Biochemical and Molecular Toxicology

doi: 10.1002/jbt.71127

Figure Lengend Snippet: Combination therapy of anti‐PD‐1 antibody and CCR4 antagonists reshapes the tumor immune microenvironment in HCC. (A–F) Flow cytometry analysis of immune cell proportions (MCs, Tregs, CD8 + T cells) in tumor tissue; G–K: ELISA detection of Granzyme B, IFN‐γ, TNF‐α, Perforin, and CCL17 levels. Data are presented as mean ± SD. One‐way ANOVA was performed, followed by Tukey's multiple comparison test for post‐hoc analysis ( n = 6). * indicates p < 0.05, ** indicates p < 0.01, *** indicates p < 0.001.

Techniques: Flow Cytometry, Analysis, Immune Cell, Tissue, Enzyme-linked Immunosorbent Assay, Comparison

Validation of the synergistic antitumor efficacy of the triple‐drug therapy in an in situ Hepa1‐6 HCC model. (A) Representative images of in situ tumors; (B): Tumor volume in each group; (C) Tumor weight in each group; (D) Average ratio of liver weight to body weight; (E, F): Ki67 immunohistochemical staining and quantitative analysis; (G–L) Flow cytometry detection of the proportions of various immune cells (mast cells, Tregs, CD8 + T cells); (M) ELISA detection of Granzyme B, IFN‐γ, TNF‐α, and perforin levels. Data are presented as mean ± SD. One‐way ANOVA was performed, followed by Tukey's multiple comparison test for post‐hoc analysis ( n = 6).

Journal: Journal of Biochemical and Molecular Toxicology

doi: 10.1002/jbt.71127

Figure Lengend Snippet: Validation of the synergistic antitumor efficacy of the triple‐drug therapy in an in situ Hepa1‐6 HCC model. (A) Representative images of in situ tumors; (B): Tumor volume in each group; (C) Tumor weight in each group; (D) Average ratio of liver weight to body weight; (E, F): Ki67 immunohistochemical staining and quantitative analysis; (G–L) Flow cytometry detection of the proportions of various immune cells (mast cells, Tregs, CD8 + T cells); (M) ELISA detection of Granzyme B, IFN‐γ, TNF‐α, and perforin levels. Data are presented as mean ± SD. One‐way ANOVA was performed, followed by Tukey's multiple comparison test for post‐hoc analysis ( n = 6).

Techniques: Biomarker Discovery, In Situ, Immunohistochemical staining, Staining, Analysis, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Comparison

(A) Predicted cell cycle phase in ChP organoid scRNA-seq shown on FA plot and proportion per phase across time. (B) Live cell images of H9-FUCCI cell-cycle reporter line D14-D70. Reporter labels G1/G0 in orange (mKO2-CDT1) and S/G2 in green (mAG-GEM). Images from D35 onwards focus on organoid cysts. Scale bar: 100µm. (C) Percentage of cells in G1/G0 and in S/G2 quantified by flow cytometry across ChP organoid differentiation. Multiple organoids were pooled for each sample (n=3). (D) Human fetal ChP at 8pcw showing heterogeneous cell division. In localised region (arrows) epithelial cells (TTR, grey) are highly proliferative (KI67, green), whilst proliferation elsewhere is largely limited to stromal regions (star, TAGLN, magenta). Scale bar: 500µm. (E) Progressive decline of proliferation (KI67, magenta) in ChP epithelium (TTR, green) across development, in human fetal ChP sections from 8 to 14 pcw. Dashed lines separate epithelial from stromal layers. Example of proliferative cells in epithelium (arrow) and stroma (star). Scale bar: 100µm. (F) Confocal images of organoids labelled for epithelial cells (NKCC1, green) and EdU (magenta) with EdU added at mid (D45-49) and later (D79-80) stages of differentiation. Percentage of EdU+ cells was quantified in NKCC1+ cyst epithelium (n=5). Scale bar: 100µm. Significant difference in average EdU frequency between early and later time points, t-test * p < 0.05. (G) Distribution of proliferation across organoid cyst after 1 week of 1uM EdU exposure. Relative distance of EdU+ cells measured from the nearest end. Points represent average distances per organoid (n= 6). Representative image, labelled for TTR (green), EdU (magenta) and nuclei (dapi, blue). Scale bar: 1mm. (H) Expression of cyclin-dependent kinase inhibitor CDKN1A (p21) in ChP organoid scRNA-seq. (I) Module score for senescence associated transcriptomic signature (SaTS) upregulated genes across differentiation time in epithelial lineage cells. (J) Top differentially expressed genes between p21+ and p21-cells within the ChP epithelial lineage. Dot size indicates the percentage of cells in each time period expressing the gene, colour scale shows average gene expression. (K) ChP organoids collected across time, immunostained for p21 (green) and KI67 (magenta). Scale bar: 100 µm. (L) Quantification of p21-positive epithelial cells over time in ChP differentiation. Points represent average values for organoids (n = 3-4). ANOVA followed by Tukey HSD, * p<0.05. Nuclei are stained with DAPI (blue) throughout. “N” indicates independent organoid batches. Cell lines are indicated by point shape in plots: solid triangle H1, open circle H9.

Journal: bioRxiv

Article Title: Human Choroid Plexus Organoids Progress to Postnatal-like Maturation and Reveal a Closing Window of Developmental Plasticity

doi: 10.64898/2026.10.12.758506

Figure Lengend Snippet: (A) Predicted cell cycle phase in ChP organoid scRNA-seq shown on FA plot and proportion per phase across time. (B) Live cell images of H9-FUCCI cell-cycle reporter line D14-D70. Reporter labels G1/G0 in orange (mKO2-CDT1) and S/G2 in green (mAG-GEM). Images from D35 onwards focus on organoid cysts. Scale bar: 100µm. (C) Percentage of cells in G1/G0 and in S/G2 quantified by flow cytometry across ChP organoid differentiation. Multiple organoids were pooled for each sample (n=3). (D) Human fetal ChP at 8pcw showing heterogeneous cell division. In localised region (arrows) epithelial cells (TTR, grey) are highly proliferative (KI67, green), whilst proliferation elsewhere is largely limited to stromal regions (star, TAGLN, magenta). Scale bar: 500µm. (E) Progressive decline of proliferation (KI67, magenta) in ChP epithelium (TTR, green) across development, in human fetal ChP sections from 8 to 14 pcw. Dashed lines separate epithelial from stromal layers. Example of proliferative cells in epithelium (arrow) and stroma (star). Scale bar: 100µm. (F) Confocal images of organoids labelled for epithelial cells (NKCC1, green) and EdU (magenta) with EdU added at mid (D45-49) and later (D79-80) stages of differentiation. Percentage of EdU+ cells was quantified in NKCC1+ cyst epithelium (n=5). Scale bar: 100µm. Significant difference in average EdU frequency between early and later time points, t-test * p < 0.05. (G) Distribution of proliferation across organoid cyst after 1 week of 1uM EdU exposure. Relative distance of EdU+ cells measured from the nearest end. Points represent average distances per organoid (n= 6). Representative image, labelled for TTR (green), EdU (magenta) and nuclei (dapi, blue). Scale bar: 1mm. (H) Expression of cyclin-dependent kinase inhibitor CDKN1A (p21) in ChP organoid scRNA-seq. (I) Module score for senescence associated transcriptomic signature (SaTS) upregulated genes across differentiation time in epithelial lineage cells. (J) Top differentially expressed genes between p21+ and p21-cells within the ChP epithelial lineage. Dot size indicates the percentage of cells in each time period expressing the gene, colour scale shows average gene expression. (K) ChP organoids collected across time, immunostained for p21 (green) and KI67 (magenta). Scale bar: 100 µm. (L) Quantification of p21-positive epithelial cells over time in ChP differentiation. Points represent average values for organoids (n = 3-4). ANOVA followed by Tukey HSD, * p<0.05. Nuclei are stained with DAPI (blue) throughout. “N” indicates independent organoid batches. Cell lines are indicated by point shape in plots: solid triangle H1, open circle H9.

Article Snippet: Human embryonic stem (hES) cells H9 and H1 (WiCell WA09, WA01) and the human induced pluripotent stem cell (hiPSC) line KOLF2.1J (Jackson Laboratory, JIPSC1000) were approved for use by the Medicines and Healthcare products Regulatory Agency (Reference #SCSC23-57).

Techniques: Flow Cytometry, Organoids, Confocal, Expressing, Gene Expression, Staining

(A) Multi-ciliation gene score from Lewis and Stracker projected on FA plot. (B) Dotplot of cilia gene expression in epithelial lineage cells over time. Dot size indicates the percentage of cells expressing the gene, colour scale shows average gene expression scaled per gene. (C) TP73 expression peaks in developing ChP epithelium. Organoids across differentiation immunostained for TP73 (green) and ARL13B (magenta). Scale bar: 100µm. Quantification of TP73 intensity over time, points represent organoids from separate differentiations (n=4), Cell lines are indicated by point shape: solid triangle H1, open circle H9. ANOVA followed by Tukey HSD, * p <0.05. (D) ChP epithelial cilia (ARL13B, fire) morphology across differentiation in immunostained organoid sections. Scale bar: 10µm. (E) ChP organoid cilia classified according to morphology: long cilia (grey), short, clustered cilia (light green) and scattered multi-cilia (dark green). Representative ARL13B-labelled images for each class, nuclei labelled with dapi (grey). Proportion of cilia per class over time, plotted as mean with standard error bars. Two-way ANOVA and Tukey multiple-comparison test, (n=4-5). Long cilia significantly decreases over time (adj. p < 0.0001 for D40-50 vs all other ages and D80-90 vs D100+; adj. p =< 0.01), with corresponding increases in clustered cilia (adj. p < 0.001 D40-50 vs all other ages) and scattered cilia (adj. p < 0.05 D40-50 vs D60-70 and D80-90; adj. p < 0.0001 D40-50 vs D100+; adj. p < 0.001 D60-70 vs D100+; adj. p < 0.01 D80-90 vs D100+). (F) Schematic of CAPture-MS proteomics workflow. Organoid samples collected at D20, D40 and D80. (G) Venn diagrams of proteins passing filtering criteria: full protein list (left) and within the centrosome-cilia database (CCDB, right) (Table S6). (H) Diagram of ciliary architecture and representative proteins identified at all three timepoints. (I) Heatmap of D20-only enriched proteins (log2foldchange compared to bead-only > 2.3, normalised to CEP135). Colour scale from low (yellow) to high (purple). (J) Heatmap of proteins enriched at both D40 and D80 (same filtering and colour scale as in I). (K) CAPture-MS intensity of MYH14 and Spastin across organoid timepoints. Values shown as log₂-fold change over bead-only, normalised to CEP135. (L) Heatmap of D80-only enriched CCDB annotated proteins D80 (same filtering and colour scale as in I). (M) CAPture-MS intensity of KATNA1 across organoid timepoints (same filtering and colour scale as in I). (N) Cilia complexes across D20 to D80 organoid development. Immunostaining for ARL13B (magenta) with PCNT (grey, top) or MYH14 (green, bottom). Dashed lines mark PCNT+ basal body regions. Scale bar: 1µm. (O) CAPture-MS intensity of CCDC170 across organoid timepoints (same filtering and colour scale as in I). (P) Representative images of CCDC170+ cilia complexes (green) at day D40 and D60 with cilia labelled by ARL13B (green) and nuclei by dapi (blue). Scale bar: 1µm.

Journal: bioRxiv

Article Title: Human Choroid Plexus Organoids Progress to Postnatal-like Maturation and Reveal a Closing Window of Developmental Plasticity

doi: 10.64898/2026.10.12.758506

Figure Lengend Snippet: (A) Multi-ciliation gene score from Lewis and Stracker projected on FA plot. (B) Dotplot of cilia gene expression in epithelial lineage cells over time. Dot size indicates the percentage of cells expressing the gene, colour scale shows average gene expression scaled per gene. (C) TP73 expression peaks in developing ChP epithelium. Organoids across differentiation immunostained for TP73 (green) and ARL13B (magenta). Scale bar: 100µm. Quantification of TP73 intensity over time, points represent organoids from separate differentiations (n=4), Cell lines are indicated by point shape: solid triangle H1, open circle H9. ANOVA followed by Tukey HSD, * p <0.05. (D) ChP epithelial cilia (ARL13B, fire) morphology across differentiation in immunostained organoid sections. Scale bar: 10µm. (E) ChP organoid cilia classified according to morphology: long cilia (grey), short, clustered cilia (light green) and scattered multi-cilia (dark green). Representative ARL13B-labelled images for each class, nuclei labelled with dapi (grey). Proportion of cilia per class over time, plotted as mean with standard error bars. Two-way ANOVA and Tukey multiple-comparison test, (n=4-5). Long cilia significantly decreases over time (adj. p < 0.0001 for D40-50 vs all other ages and D80-90 vs D100+; adj. p =< 0.01), with corresponding increases in clustered cilia (adj. p < 0.001 D40-50 vs all other ages) and scattered cilia (adj. p < 0.05 D40-50 vs D60-70 and D80-90; adj. p < 0.0001 D40-50 vs D100+; adj. p < 0.001 D60-70 vs D100+; adj. p < 0.01 D80-90 vs D100+). (F) Schematic of CAPture-MS proteomics workflow. Organoid samples collected at D20, D40 and D80. (G) Venn diagrams of proteins passing filtering criteria: full protein list (left) and within the centrosome-cilia database (CCDB, right) (Table S6). (H) Diagram of ciliary architecture and representative proteins identified at all three timepoints. (I) Heatmap of D20-only enriched proteins (log2foldchange compared to bead-only > 2.3, normalised to CEP135). Colour scale from low (yellow) to high (purple). (J) Heatmap of proteins enriched at both D40 and D80 (same filtering and colour scale as in I). (K) CAPture-MS intensity of MYH14 and Spastin across organoid timepoints. Values shown as log₂-fold change over bead-only, normalised to CEP135. (L) Heatmap of D80-only enriched CCDB annotated proteins D80 (same filtering and colour scale as in I). (M) CAPture-MS intensity of KATNA1 across organoid timepoints (same filtering and colour scale as in I). (N) Cilia complexes across D20 to D80 organoid development. Immunostaining for ARL13B (magenta) with PCNT (grey, top) or MYH14 (green, bottom). Dashed lines mark PCNT+ basal body regions. Scale bar: 1µm. (O) CAPture-MS intensity of CCDC170 across organoid timepoints (same filtering and colour scale as in I). (P) Representative images of CCDC170+ cilia complexes (green) at day D40 and D60 with cilia labelled by ARL13B (green) and nuclei by dapi (blue). Scale bar: 1µm.

Techniques: Gene Expression, Expressing, Organoids, Morphology, Comparison, Immunostaining

(A) Cilia length over time in ChP organoid epithelium. Points represent individual cilia. Cilia measured across organoids from separate differentiations, n = 4-5. (B) Principle component plot of CAPture-MS proteomics data showing progressive separation of organoid timepoints along PC1 consistent with differentiation trajectory, as well as PC2, revealing differences between bead only (BO) versus CAPture samples. Point colour indicates sample (timepoint or bead-only), labelled by cell line used. A total of 9,045 protein features passed quality control filtering. (C) Volcano plot showing differences between H1 and H9 cell lines at day 40. Axes display log2 fold change and - log10(adjusted P-value). No differences were observed between the H1 and H9 datasets, suggesting that the results are robust across the two independent human embryonic cell line-derived organoids. Differential expression performed using the LIMMA linear model. (D) Gene Ontology (GO) term enrichment analysis of proteins identified in isolated centrosome samples. Bar chart shows fold enrichment of the top 7 GO cellular component terms associated with cilia and centrosomes for proteins in isolated centrosome samples at D20, 40 and 80. The GO term of nuclear protein-containing complex (GO:0140513) was used as a negative control. (E) Heatmap showing proteins recorded above filtering threshold (log2 fold change compared to bead-only > 2.3) at only D40 and present in CCDB database. Protein level as log2foldchange from bead-only normalised by CEP135, from low (yellow) to high (purple), absent from >= 1 replicate excluded (white). (F) Cilia number per cluster across time in ChP organoid. Points represent average cilia number per organoid from different batches, n=3-4. ANOVA and Tukey multiple-comparison test. * p < 0.05. (G) Average PCNT-positive basal body area increased across organoid differentiation day. Points represent different differentiation batches, n=3-4. ANOVA and Tukey multiple-comparison test. * p < 0.05, ** p < 0.01. (H) Fluorescent intensity of MYH14 in cilia basal bodies (defined by PCNT signal) in ChP epithelium over time. Points represent batches, n=3-4. Difference in mean fluorescent intensity tested by ANOVA, ns. (I) Localisation of MYH14 across organoid differentiation day. MYH14 intensity measured in PCNT+ basal body divided by MYH14 intensity in background area. Points calculated from average of ROIs per organoid and represent separate differentiation batches (n = 3-4). ANOVA and Tukey multiple-comparison test. * p < 0.05. (J) Additional representative confocal images showing typical range of cilia and basal body complexes across ChP organoid differentiation. Immunostaining with antibodies against PCNT (grey), ARL13B (magenta) and MYH14 (green). PCNT+ basal body regions indicated with dashed lines. Scale bar: 1µm. (K) Additional representative image of day 40 organoid immunostained with antibodies against CCDC170 (green) and ARL13B (magenta). Scale bar: 1µm. (L) Proportion of cilia complexes that contain CCDC170 signal across differentiation day. Points represent different differentiation batches, n = 3-4. ANOVA test ns. Cell lines are indicated by point shape in plots F-I & L: solid triangle H1 and open circle H9.

Journal: bioRxiv

Article Title: Human Choroid Plexus Organoids Progress to Postnatal-like Maturation and Reveal a Closing Window of Developmental Plasticity

doi: 10.64898/2026.10.12.758506

Figure Lengend Snippet: (A) Cilia length over time in ChP organoid epithelium. Points represent individual cilia. Cilia measured across organoids from separate differentiations, n = 4-5. (B) Principle component plot of CAPture-MS proteomics data showing progressive separation of organoid timepoints along PC1 consistent with differentiation trajectory, as well as PC2, revealing differences between bead only (BO) versus CAPture samples. Point colour indicates sample (timepoint or bead-only), labelled by cell line used. A total of 9,045 protein features passed quality control filtering. (C) Volcano plot showing differences between H1 and H9 cell lines at day 40. Axes display log2 fold change and - log10(adjusted P-value). No differences were observed between the H1 and H9 datasets, suggesting that the results are robust across the two independent human embryonic cell line-derived organoids. Differential expression performed using the LIMMA linear model. (D) Gene Ontology (GO) term enrichment analysis of proteins identified in isolated centrosome samples. Bar chart shows fold enrichment of the top 7 GO cellular component terms associated with cilia and centrosomes for proteins in isolated centrosome samples at D20, 40 and 80. The GO term of nuclear protein-containing complex (GO:0140513) was used as a negative control. (E) Heatmap showing proteins recorded above filtering threshold (log2 fold change compared to bead-only > 2.3) at only D40 and present in CCDB database. Protein level as log2foldchange from bead-only normalised by CEP135, from low (yellow) to high (purple), absent from >= 1 replicate excluded (white). (F) Cilia number per cluster across time in ChP organoid. Points represent average cilia number per organoid from different batches, n=3-4. ANOVA and Tukey multiple-comparison test. * p < 0.05. (G) Average PCNT-positive basal body area increased across organoid differentiation day. Points represent different differentiation batches, n=3-4. ANOVA and Tukey multiple-comparison test. * p < 0.05, ** p < 0.01. (H) Fluorescent intensity of MYH14 in cilia basal bodies (defined by PCNT signal) in ChP epithelium over time. Points represent batches, n=3-4. Difference in mean fluorescent intensity tested by ANOVA, ns. (I) Localisation of MYH14 across organoid differentiation day. MYH14 intensity measured in PCNT+ basal body divided by MYH14 intensity in background area. Points calculated from average of ROIs per organoid and represent separate differentiation batches (n = 3-4). ANOVA and Tukey multiple-comparison test. * p < 0.05. (J) Additional representative confocal images showing typical range of cilia and basal body complexes across ChP organoid differentiation. Immunostaining with antibodies against PCNT (grey), ARL13B (magenta) and MYH14 (green). PCNT+ basal body regions indicated with dashed lines. Scale bar: 1µm. (K) Additional representative image of day 40 organoid immunostained with antibodies against CCDC170 (green) and ARL13B (magenta). Scale bar: 1µm. (L) Proportion of cilia complexes that contain CCDC170 signal across differentiation day. Points represent different differentiation batches, n = 3-4. ANOVA test ns. Cell lines are indicated by point shape in plots F-I & L: solid triangle H1 and open circle H9.

Techniques: Organoids, QC/EQA/Proficiency, Derivative Assay, Quantitative Proteomics, Analysis, Isolation, Negative Control, Comparison, Confocal, Immunostaining, Significance Assay

Journal: bioRxiv

Article Title: Human Choroid Plexus Organoids Progress to Postnatal-like Maturation and Reveal a Closing Window of Developmental Plasticity

doi: 10.64898/2026.10.12.758506

Figure Lengend Snippet: (A) FA plot coloured by geneset score for transmembrane transport genes (module 5). (B) Pseudobulk expression heatmap of epithelial module 5 transmembrane transport genes across time in ChP organoid epithelial lineage cells grouped by age. (C) Pseudobulk expression heatmap of module 5 transmembrane transport genes in mouse ChP epithelial cells across ages . Selected genes significantly increased in adult vs embryonic epithelial cells. (D) Violin plot of Slc5a5 increasing with age in mouse ChP epithelial cells . Schematic indicates localisation of selected adult-enriched ion transporters on the ChP epithelium. (E) Quantification of SLC5A5 intensity measured by line profile perpendicular to the epithelial layer. Points represent average per organoid (n=3-4), cell lines are indicated by point shape: solid triangle H1, open circle H9. One-way ANOVA with Tukey HSD, * p <0.05 ** p< 0.01. (F) ChP organoid sections across differentiation immunostained for SLC5A5 (green). Scale bar: 100 µm. (G) Pseudobulk expression heatmap of mouse ChP epithelium adult-upregulated genes in ChP organoids epithelial lineage over time, grouped by age. (H) Heatmap showing similarity between organoid mature epithelial cells and adult human ChP epithelial cells. Adult ChP single-nuclei RNA (snRNA) sequencing data Mount Sinai cohort. Colour scale represents Euclidean distance between cluster centroids in scVI latent space. (I) Dotplot showing gene expression of selected mature epithelial markers across organoid epithelial subtypes (light grey) and adult epithelial cells (dark grey). Adult ChP snRNA sequencing data Mount Sinai cohort. Top 10 shared upregulated genes in ‘Mature epithelial 2’-organoid cluster and ‘Epithelial’-adult cluster highlighted. Point size represents percentage of cells expressing gene and colour scale shows average expression. (J) Violin plots showing expression of selected markers of adult ChP epithelium across time in ChP organoid epithelial lineage cells. (K) Secreted CSF proteins with gene expression enriched in mature epithelial cells in ChP organoids. Left: Dotplot of gene expression in all cells over time in ChP organoids. Dot size indicates percentage of cells expressing the gene and colour scale shows average gene expression. Right: Heatmap coloured by protein levels detected in iCSF by mass spec . Proteins in bold were also detected in adult human CSF. (L) Day 60 ChP organoid immunostained for ENPP2 (green). Scale bar: 100µm, inset 20µm. (M) Schematic of changes to epithelial cells in ChP organoids over differentiation time. Nuclei labelled with dapi (blue).

Techniques: Expressing, Organoids, Sequencing, Gene Expression, Mass Spectrometry

Journal: bioRxiv

Article Title: Human Choroid Plexus Organoids Progress to Postnatal-like Maturation and Reveal a Closing Window of Developmental Plasticity

doi: 10.64898/2026.10.12.758506

Figure Lengend Snippet: (A) Schematic of VPA treatment. ChP organoids were treated with 1mM VPA from D40 (Early Treatment) or D60 (Late Treatment). Treatment lasted 20 days before collection or a 20-day recovery (Rec). Alternatively, treatment lasted 40 days. (B) ChP cyst collapsed after VPA treatment at both time windows and recovered after VPA removal only after early treatment, representative brightfield images. (C) Cyst tissue contrast over time for early VPA treatment, starting at D40. Points represent mean value with standard error bars. Transition from VPA to recovery for VPA:Rec samples indicated by dashed line. (D) D80 ChP epithelial cilia (ARL13B, fire) across conditions of early VPA treatment. Nuclei stained with dapi, grey. Scale bar: 10µm. (E) D100 ChP epithelial cilia (ARL13B, fire) across conditions of late VPA treatment. Nuclei stained with dapi, grey. Scale bar: 10µm. (F) D80 ChP organoid cilia classified according to morphology described in . Proportion of cilia across treatment conditions, plotted as mean with standard error bars. Two-way ANOVA and Tukey multiple-comparison test, n=4 with 30-50 cells/condition/experiment. Long cilia significantly increased after 40 days of VPA exposure (adj. p < 0.0001 for VPA vs CT, p <0.01 for VPA vs VPA:Rec), while all cilia populations returned to control levels after recovery (adj. p = n.s for VPA:Rec vs CT). (G) Nuclear aspect ratio (longest axis / shortest axis) across conditions for early VPA treatment (n=2). (H) D100 ChP organoid cilia classified according to morphology described in : long cilia (grey) short, clustered cilia (light green) and scattered multi-cilia (dark green). Proportion of cilia across treatment conditions, plotted as mean with standard error bars. n=2 with 30-50 cells/condition/experiment. (I) Nuclear aspect ratio (longest axis / shortest axis) across conditions for late VPA treatment. Points show average for batch, n=2. (J) Early VPA exposure decreased expression of secretion markers (green) in D80 ChP epithelium and expression was restored in recovery condition. Immunostained against TTR (top) and SLC5A5 (bottom). Nuclei labelled with dapi (blue). Scale bar: 20µm. (K) Late VPA exposure decreased expression of secretion markers (green) in D100 ChP epithelium and remained low in recovery condition. Immunostained against TTR (top) and SLC5A5 (bottom). Nuclei labelled with dapi (blue). Scale bar: 20µm. (L) Apical localisation of SLC5A5 is disrupted by early VPA treatment, measured at D80. Example intensity profile of SLC5A5 along a line perpendicular to ChP epithelium. (M) Peak SLC5A5 intensity across early VPA treatment conditions at D80. Normalised to control (n=5). (N) Apical localisation of SLC5A5 is disrupted by late VPA treatment, measured at D100. Example intensity profile of SLC5A5 along a line perpendicular to ChP epithelium. (O) Peak SLC5A5 intensity across late VPA treatment conditions at D100. Normalised to control (n=5). (P) Expression of selected genes following early VPA treatment, measured at D80. Expression calculated as 2 -ddCT , normalised by housekeepers and relative to control (n=5). (Q) Schematic of changes to ChP following VPA treatment and treatment washout at early and late timepoints. Data point on graphs represent independent organoid batches (“n”). Cell lines are indicated by point shape in G, I, M & O: solid triangle H1, open circle H9 and solid square KOLF2.1J. Statistical test used across three conditions: One-way ANOVA and Tukey multiple comparison test. *p <0.05, **p<0.01, ***p<0.001.

Techniques: Organoids, Brightfield, Tissue, Staining, Morphology, Comparison, Control, Expressing

(A) Tight junctions remain intact following VPA-treatment at both timepoints. Immunostaining of D80 (early treatment) and D100 (late treatment) organoids against ZO-1 (red). Nuclei labelled with dapi (blue). Scale bar: 20µm. (B) Epithelial nuclei morphology changes over time. Nuclei stained with dapi (cyan). Scale bar: 10µm. (C) Nuclear aspect ratio decreases as ChP epithelium over time, consistent with a rounder cell nucleus. Nuclear aspect ratio calculated as major axis (a)/minor axis (b) from maximally projected images. Points represent average from batches, n=4 (with 30-50 nuclei/condition/experiment). One-way ANOVA and Tukey multiple-comparison test * p <0.05, ** p <0.01, *** p <0.001. (D) Epithelial nuclei morphology across conditions in early VPA treatments, analysed at D80. Nuclei stained with dapi (cyan). Scale bar: 10µm. (E) Epithelial nuclei morphology across conditions in late VPA treatments, analysed at D100. Nuclei stained with dapi (cyan). Scale bar: 10µm. (F) VPA treatment for 20 days decreased secretion markers at both treatment timepoints. Organoids immunostained against TTR (top) and SLC5A5 (bottom). Intensity measurements at D60 (early treatment) and D80 (late treatment). Points represent batches, n=3-5. T-test, ns in all cases. (G) Intensity of TTR across early (left) and late (right) VPA treatment. Normalised to control. Points indicate batches, n=3. One-way ANOVA, ns. Cell lines are indicated by point shape in plots: solid triangle H1, open circle H9 and solid square KOLF2.1J.

Journal: bioRxiv

Article Title: Human Choroid Plexus Organoids Progress to Postnatal-like Maturation and Reveal a Closing Window of Developmental Plasticity

doi: 10.64898/2026.10.12.758506

Figure Lengend Snippet: (A) Tight junctions remain intact following VPA-treatment at both timepoints. Immunostaining of D80 (early treatment) and D100 (late treatment) organoids against ZO-1 (red). Nuclei labelled with dapi (blue). Scale bar: 20µm. (B) Epithelial nuclei morphology changes over time. Nuclei stained with dapi (cyan). Scale bar: 10µm. (C) Nuclear aspect ratio decreases as ChP epithelium over time, consistent with a rounder cell nucleus. Nuclear aspect ratio calculated as major axis (a)/minor axis (b) from maximally projected images. Points represent average from batches, n=4 (with 30-50 nuclei/condition/experiment). One-way ANOVA and Tukey multiple-comparison test * p <0.05, ** p <0.01, *** p <0.001. (D) Epithelial nuclei morphology across conditions in early VPA treatments, analysed at D80. Nuclei stained with dapi (cyan). Scale bar: 10µm. (E) Epithelial nuclei morphology across conditions in late VPA treatments, analysed at D100. Nuclei stained with dapi (cyan). Scale bar: 10µm. (F) VPA treatment for 20 days decreased secretion markers at both treatment timepoints. Organoids immunostained against TTR (top) and SLC5A5 (bottom). Intensity measurements at D60 (early treatment) and D80 (late treatment). Points represent batches, n=3-5. T-test, ns in all cases. (G) Intensity of TTR across early (left) and late (right) VPA treatment. Normalised to control. Points indicate batches, n=3. One-way ANOVA, ns. Cell lines are indicated by point shape in plots: solid triangle H1, open circle H9 and solid square KOLF2.1J.

Techniques: Immunostaining, Organoids, Morphology, Staining, Comparison, Control

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