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mesenchymal stem cell adipocyte differentiation medium  (PromoCell)


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    Structured Review

    PromoCell mesenchymal stem cell adipocyte differentiation medium
    Single-cell RNA sequencing profiling of joint cell populations following extracellular vesicle (EVs) treatment. (a) The UMAP plot displaying the classification of joint cell populations into ten distinct clusters under three conditions: WT, PBS-treated (PBS), and EVs-treated (EVs). ( b ) Cell typing of clusters based on gene expression. Cluster 1 (NK cells), Cluster 2 (T cells), Cluster 3 (pre-B cells), Cluster 4 (Neutrophils), Cluster 5 (B cells), Cluster 6 (Chondrocyte progenitor cells), Cluster 7 (Hematopoietic progenitors), Cluster 8 <t>(Mesenchymal</t> cells), Cluster 9 (Plasma cells), and Cluster 10 (Erythroblasts). ( c ) Heatmap displaying the expression of representative marker genes for each cluster, including Col12a1 for the
    Mesenchymal Stem Cell Adipocyte Differentiation Medium, supplied by PromoCell, used in various techniques. Bioz Stars score: 97/100, based on 312 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mesenchymal stem cell adipocyte differentiation medium/product/PromoCell
    Average 97 stars, based on 312 article reviews
    mesenchymal stem cell adipocyte differentiation medium - by Bioz Stars, 2026-03
    97/100 stars

    Images

    1) Product Images from "Extracellular vesicles derived from adipose-derived mesenchymal stem/stromal cells prevent synovial inflammation and attenuate cartilage degeneration in rodent osteoarthritis"

    Article Title: Extracellular vesicles derived from adipose-derived mesenchymal stem/stromal cells prevent synovial inflammation and attenuate cartilage degeneration in rodent osteoarthritis

    Journal: Regenerative Therapy

    doi: 10.1016/j.reth.2025.101056

    Single-cell RNA sequencing profiling of joint cell populations following extracellular vesicle (EVs) treatment. (a) The UMAP plot displaying the classification of joint cell populations into ten distinct clusters under three conditions: WT, PBS-treated (PBS), and EVs-treated (EVs). ( b ) Cell typing of clusters based on gene expression. Cluster 1 (NK cells), Cluster 2 (T cells), Cluster 3 (pre-B cells), Cluster 4 (Neutrophils), Cluster 5 (B cells), Cluster 6 (Chondrocyte progenitor cells), Cluster 7 (Hematopoietic progenitors), Cluster 8 (Mesenchymal cells), Cluster 9 (Plasma cells), and Cluster 10 (Erythroblasts). ( c ) Heatmap displaying the expression of representative marker genes for each cluster, including Col12a1 for the
    Figure Legend Snippet: Single-cell RNA sequencing profiling of joint cell populations following extracellular vesicle (EVs) treatment. (a) The UMAP plot displaying the classification of joint cell populations into ten distinct clusters under three conditions: WT, PBS-treated (PBS), and EVs-treated (EVs). ( b ) Cell typing of clusters based on gene expression. Cluster 1 (NK cells), Cluster 2 (T cells), Cluster 3 (pre-B cells), Cluster 4 (Neutrophils), Cluster 5 (B cells), Cluster 6 (Chondrocyte progenitor cells), Cluster 7 (Hematopoietic progenitors), Cluster 8 (Mesenchymal cells), Cluster 9 (Plasma cells), and Cluster 10 (Erythroblasts). ( c ) Heatmap displaying the expression of representative marker genes for each cluster, including Col12a1 for the "Chondrocyte" cluster, and Col1a1 for the "Mesenchymal cell" cluster, and CD45/CD14 for the "Hematopoietic" cluster.

    Techniques Used: RNA Sequencing, Gene Expression, Clinical Proteomics, Expressing, Marker

    Differential gene expression besed on Single-cell RNA sequencing of joint cell clusters following extracellular vesicle (EVs) treatment . ( a-d ) Comparison of gene expression in EVs, PBS, and WT groups (a) in Cluster 6 (chondrocyte progenitors) (COL2A1, COL1A2, PRG4, MMP3, CCL2, and FGF18). ( b ) in Cluster 1 (NK cells) (CD14, MRC1, CD163, CD86, CD80, and NOS2). ( c ) in Cluster 8 (Mesenchymal cells) (COL2A1, COL1A2, PRG4, CCL2, and FGF18) ( d ) in Cluster 4 (Neutrophils) (APOE, AGPAT4, HAPLN1, CDKN1C, MET, and CEMIP2). (e) Flow cytometry analysis confirmed that the proportion of CD11b + CD163 + M2 macrophages was approximately 2.5-fold higher in the EVs-treated group compared to the PBS-treated group.
    Figure Legend Snippet: Differential gene expression besed on Single-cell RNA sequencing of joint cell clusters following extracellular vesicle (EVs) treatment . ( a-d ) Comparison of gene expression in EVs, PBS, and WT groups (a) in Cluster 6 (chondrocyte progenitors) (COL2A1, COL1A2, PRG4, MMP3, CCL2, and FGF18). ( b ) in Cluster 1 (NK cells) (CD14, MRC1, CD163, CD86, CD80, and NOS2). ( c ) in Cluster 8 (Mesenchymal cells) (COL2A1, COL1A2, PRG4, CCL2, and FGF18) ( d ) in Cluster 4 (Neutrophils) (APOE, AGPAT4, HAPLN1, CDKN1C, MET, and CEMIP2). (e) Flow cytometry analysis confirmed that the proportion of CD11b + CD163 + M2 macrophages was approximately 2.5-fold higher in the EVs-treated group compared to the PBS-treated group.

    Techniques Used: Gene Expression, RNA Sequencing, Comparison, Flow Cytometry



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    Image Search Results


    Single-cell RNA sequencing profiling of joint cell populations following extracellular vesicle (EVs) treatment. (a) The UMAP plot displaying the classification of joint cell populations into ten distinct clusters under three conditions: WT, PBS-treated (PBS), and EVs-treated (EVs). ( b ) Cell typing of clusters based on gene expression. Cluster 1 (NK cells), Cluster 2 (T cells), Cluster 3 (pre-B cells), Cluster 4 (Neutrophils), Cluster 5 (B cells), Cluster 6 (Chondrocyte progenitor cells), Cluster 7 (Hematopoietic progenitors), Cluster 8 (Mesenchymal cells), Cluster 9 (Plasma cells), and Cluster 10 (Erythroblasts). ( c ) Heatmap displaying the expression of representative marker genes for each cluster, including Col12a1 for the

    Journal: Regenerative Therapy

    Article Title: Extracellular vesicles derived from adipose-derived mesenchymal stem/stromal cells prevent synovial inflammation and attenuate cartilage degeneration in rodent osteoarthritis

    doi: 10.1016/j.reth.2025.101056

    Figure Lengend Snippet: Single-cell RNA sequencing profiling of joint cell populations following extracellular vesicle (EVs) treatment. (a) The UMAP plot displaying the classification of joint cell populations into ten distinct clusters under three conditions: WT, PBS-treated (PBS), and EVs-treated (EVs). ( b ) Cell typing of clusters based on gene expression. Cluster 1 (NK cells), Cluster 2 (T cells), Cluster 3 (pre-B cells), Cluster 4 (Neutrophils), Cluster 5 (B cells), Cluster 6 (Chondrocyte progenitor cells), Cluster 7 (Hematopoietic progenitors), Cluster 8 (Mesenchymal cells), Cluster 9 (Plasma cells), and Cluster 10 (Erythroblasts). ( c ) Heatmap displaying the expression of representative marker genes for each cluster, including Col12a1 for the "Chondrocyte" cluster, and Col1a1 for the "Mesenchymal cell" cluster, and CD45/CD14 for the "Hematopoietic" cluster.

    Article Snippet: For adipocyte differentiation, either BioMirai Lab's induction kit or PromoCell's mesenchymal stem cell adipocyte differentiation medium was used, with Oil Red O staining to assess lipid accumulation.

    Techniques: RNA Sequencing, Gene Expression, Clinical Proteomics, Expressing, Marker

    Differential gene expression besed on Single-cell RNA sequencing of joint cell clusters following extracellular vesicle (EVs) treatment . ( a-d ) Comparison of gene expression in EVs, PBS, and WT groups (a) in Cluster 6 (chondrocyte progenitors) (COL2A1, COL1A2, PRG4, MMP3, CCL2, and FGF18). ( b ) in Cluster 1 (NK cells) (CD14, MRC1, CD163, CD86, CD80, and NOS2). ( c ) in Cluster 8 (Mesenchymal cells) (COL2A1, COL1A2, PRG4, CCL2, and FGF18) ( d ) in Cluster 4 (Neutrophils) (APOE, AGPAT4, HAPLN1, CDKN1C, MET, and CEMIP2). (e) Flow cytometry analysis confirmed that the proportion of CD11b + CD163 + M2 macrophages was approximately 2.5-fold higher in the EVs-treated group compared to the PBS-treated group.

    Journal: Regenerative Therapy

    Article Title: Extracellular vesicles derived from adipose-derived mesenchymal stem/stromal cells prevent synovial inflammation and attenuate cartilage degeneration in rodent osteoarthritis

    doi: 10.1016/j.reth.2025.101056

    Figure Lengend Snippet: Differential gene expression besed on Single-cell RNA sequencing of joint cell clusters following extracellular vesicle (EVs) treatment . ( a-d ) Comparison of gene expression in EVs, PBS, and WT groups (a) in Cluster 6 (chondrocyte progenitors) (COL2A1, COL1A2, PRG4, MMP3, CCL2, and FGF18). ( b ) in Cluster 1 (NK cells) (CD14, MRC1, CD163, CD86, CD80, and NOS2). ( c ) in Cluster 8 (Mesenchymal cells) (COL2A1, COL1A2, PRG4, CCL2, and FGF18) ( d ) in Cluster 4 (Neutrophils) (APOE, AGPAT4, HAPLN1, CDKN1C, MET, and CEMIP2). (e) Flow cytometry analysis confirmed that the proportion of CD11b + CD163 + M2 macrophages was approximately 2.5-fold higher in the EVs-treated group compared to the PBS-treated group.

    Article Snippet: For adipocyte differentiation, either BioMirai Lab's induction kit or PromoCell's mesenchymal stem cell adipocyte differentiation medium was used, with Oil Red O staining to assess lipid accumulation.

    Techniques: Gene Expression, RNA Sequencing, Comparison, Flow Cytometry

    The Ireb2 D826V/D826V mutation results in increased body weight and lipid content in mice. (A) Human IREB2 mRNA expression is significantly reduced in obese individuals compared to lean individuals (n = 16 biological replicates for both lean and obese groups, *P < 0.05, relative to the lean group); (B) Mice with the Ireb2 D826V/D826V mutation exhibit greater body weight compared to WT mice; (C) 16 weeks Ireb2 D826V/D826V mutant mice demonstrate increased fat mass in epWAT and SAT relative to WT mice; (D) Triglyceride (TG) content is elevated in the epWAT and SAT of Ireb2 D826V/D826V mutant mice compared to WT mice; (E) Serum TG content is also increased in Ireb2 D826V/D826V mutant mice relative to WT mice; (F) Serum total cholesterol is increased in Ireb2 D826V/D826V mutant mice; (G) Food intake remains comparable between Ireb2 D826V/D826V mutant mice and WT mice; (H) Ireb2 D826V/D826V mutation slightly increased the fasting blood glucose level; (I) IPGTT detection and (J) ITT detection for WT and Ireb2 D826V/D826V mice; (K) Hypertrophic adipocytes are observed in the epWAT of Ireb2 D826V/D826V mutant mice compared to WT mice; (L) Similarly, hypertrophic adipocytes are present in the SAT of Ireb2 D826V/D826V mutant mice compared to WT mice (scale bar = 50 μm, B-J n = 5 biological replicates, *P < 0.05, **P < 0.01, ***P < 0.001, relative to the WT group using Student’s t-test).

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: The D826V point mutation in IREB2 induces lipogenesis in adipose tissues

    doi: 10.3389/fcell.2026.1724485

    Figure Lengend Snippet: The Ireb2 D826V/D826V mutation results in increased body weight and lipid content in mice. (A) Human IREB2 mRNA expression is significantly reduced in obese individuals compared to lean individuals (n = 16 biological replicates for both lean and obese groups, *P < 0.05, relative to the lean group); (B) Mice with the Ireb2 D826V/D826V mutation exhibit greater body weight compared to WT mice; (C) 16 weeks Ireb2 D826V/D826V mutant mice demonstrate increased fat mass in epWAT and SAT relative to WT mice; (D) Triglyceride (TG) content is elevated in the epWAT and SAT of Ireb2 D826V/D826V mutant mice compared to WT mice; (E) Serum TG content is also increased in Ireb2 D826V/D826V mutant mice relative to WT mice; (F) Serum total cholesterol is increased in Ireb2 D826V/D826V mutant mice; (G) Food intake remains comparable between Ireb2 D826V/D826V mutant mice and WT mice; (H) Ireb2 D826V/D826V mutation slightly increased the fasting blood glucose level; (I) IPGTT detection and (J) ITT detection for WT and Ireb2 D826V/D826V mice; (K) Hypertrophic adipocytes are observed in the epWAT of Ireb2 D826V/D826V mutant mice compared to WT mice; (L) Similarly, hypertrophic adipocytes are present in the SAT of Ireb2 D826V/D826V mutant mice compared to WT mice (scale bar = 50 μm, B-J n = 5 biological replicates, *P < 0.05, **P < 0.01, ***P < 0.001, relative to the WT group using Student’s t-test).

    Article Snippet: Differentiation of Ireb2 D826V/D826V and WT pre-adipocytes into adipocytes was induced using media containing insulin (HY- P73243 , 10 mg/mL, Medchemexpress, China), dexamethasone (HY-14648,10 μM, Medchemexpress, China), 3-isobutyl-1-methylxanthine (HY-12318, IBMX, 0.5 M, Medchemexpress, China), indomethacin (HY-14397, 125 nM, Medchemexpress, China), and rosiglitazone (HY-17386, 1 μM, Medchemexpress, China) for 5 days, followed by treatment with insulin (10 mg/mL) for an additional 2 days.

    Techniques: Mutagenesis, Expressing

    In vitro experiments demonstrated that the Ireb2 D826V/D826V mutation enhances lipid biosynthesis in mature adipocytes. (A) Oil Red O staining was performed on WT and Ireb2 D826V/D826V mature adipocytes; (B) The Ireb2 D826V/D826V mutation led to an increase in TG content in mature adipocytes; (C) The mutation also elevated fatty acid content in mature adipocytes; (D) Western blot analysis was conducted to assess the expression of proteins related to fatty acid and triglyceride biosynthesis, as well as IREB2 and FTH1, in mature adipocytes; (E) Relative band intensity analysis was carried out for IREB2 and FTH1 proteins; (F) Relative band intensity analysis was conducted for EGR1 and FGFR4 proteins; (G) Relative band intensity analysis was performed for FASN, ACACA, and ACLY proteins; (H) Lipogenic related mRNA expression in Ireb2 D826V/D826V adipocytes and Ireb2 D826V/D826V + deferoxamine adipocytes; (I) TG content in Ireb2 D826V/D826V adipocytes and Ireb2 D826V/D826V + deferoxamine adipocytes; (J) FA content in Ireb2 D826V/D826V adipocytes and Ireb2 D826V/D826V + deferoxamine adipocytes. (A-C n = 5 biological replicates; D-G n = 3 biological replicates, H-J n = 4 biological replicates, *P < 0.05, **P < 0.01, ***P < 0.001, (A-G) compared with the WT group using Student’s t-test; (H-J) compared with the Ireb2 D826V/D826V group using Student’s t-test.

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: The D826V point mutation in IREB2 induces lipogenesis in adipose tissues

    doi: 10.3389/fcell.2026.1724485

    Figure Lengend Snippet: In vitro experiments demonstrated that the Ireb2 D826V/D826V mutation enhances lipid biosynthesis in mature adipocytes. (A) Oil Red O staining was performed on WT and Ireb2 D826V/D826V mature adipocytes; (B) The Ireb2 D826V/D826V mutation led to an increase in TG content in mature adipocytes; (C) The mutation also elevated fatty acid content in mature adipocytes; (D) Western blot analysis was conducted to assess the expression of proteins related to fatty acid and triglyceride biosynthesis, as well as IREB2 and FTH1, in mature adipocytes; (E) Relative band intensity analysis was carried out for IREB2 and FTH1 proteins; (F) Relative band intensity analysis was conducted for EGR1 and FGFR4 proteins; (G) Relative band intensity analysis was performed for FASN, ACACA, and ACLY proteins; (H) Lipogenic related mRNA expression in Ireb2 D826V/D826V adipocytes and Ireb2 D826V/D826V + deferoxamine adipocytes; (I) TG content in Ireb2 D826V/D826V adipocytes and Ireb2 D826V/D826V + deferoxamine adipocytes; (J) FA content in Ireb2 D826V/D826V adipocytes and Ireb2 D826V/D826V + deferoxamine adipocytes. (A-C n = 5 biological replicates; D-G n = 3 biological replicates, H-J n = 4 biological replicates, *P < 0.05, **P < 0.01, ***P < 0.001, (A-G) compared with the WT group using Student’s t-test; (H-J) compared with the Ireb2 D826V/D826V group using Student’s t-test.

    Article Snippet: Differentiation of Ireb2 D826V/D826V and WT pre-adipocytes into adipocytes was induced using media containing insulin (HY- P73243 , 10 mg/mL, Medchemexpress, China), dexamethasone (HY-14648,10 μM, Medchemexpress, China), 3-isobutyl-1-methylxanthine (HY-12318, IBMX, 0.5 M, Medchemexpress, China), indomethacin (HY-14397, 125 nM, Medchemexpress, China), and rosiglitazone (HY-17386, 1 μM, Medchemexpress, China) for 5 days, followed by treatment with insulin (10 mg/mL) for an additional 2 days.

    Techniques: In Vitro, Mutagenesis, Staining, Western Blot, Expressing