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Dawley Inc bmscs
Bmscs, supplied by Dawley Inc, 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/bmscs/bmscs/pmc13264244-208-0-8
Average 86 stars, based on 1 article reviews

bmscs - by Bioz Stars, 2026-10

86/100 stars

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In Vitro:

Article Title: Hierarchical biomimetic scaffold with directional guidance and photothermal properties for the repair of critical-sized bone defects.
Article Snippet: .. AR TIC LE IN PR ES S ARTICLE IN PRESS In Vitro Osteogenic Activity of the MS-BP/TCP Scaffold As previously reported, BMSCs were isolated from female Sprague-Dawley rats (4 weeks old)[28]. ..

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Article Title: Effects Of Jiawei Qiwei Baizhu Powder-Containing Serum On The Proliferation And Osteogenic Differentiation Of Rat Bone Marrow Mesenchymal Stem Cells By Enhancing Proliferation And Alkaline Phosphatase Activity
Article Snippet: .. BMSCs were isolated from Sprague–Dawley rats using the whole bone marrow adherence method and identified by flow cytometry. ..

Article Title: Dendrobine promotes osteogenesis-angiogenesis in postmenopausal osteoporosis by inhibiting Hippo signaling pathway.
Article Snippet: 3 Wuhan Fourth Hospital, No.473 Hanzheng Street, Wuhan, Hubei, China Abstract Postmenopausal osteoporosis (PMOP) is a skeletal disorder marked by progressive bone mineral density decline and increased susceptibility to fractures.. Accumulating evidence indicates that coupled osteogenesis and angiogenesis are indispensable for bone remodeling and repair.. This study investigated the therapeutic potential of dendrobine in concurrently modulating osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) and angiogenic activity in the context of PMOP.

Article Title: LOC100912399 regulates osteogenic differentiation of bone marrow mesenchymal stem cells through modulating p38MAPK signaling-mediated oxidative stress and apoptosis.
Article Snippet: .. Methods: BMSCs were isolated from the tibiae and fibulae of Sprague-Dawley (SD) rat pups and cultured to the third passage. ..

Article Title: Wnt5a‐Induced Exosomes From Bone Marrow Mesenchymal Stem Cells Promote Spinal Cord Injury Repair by Modulating Immune Cell Phenotypes and Alleviating Neuroinflammation via the NF ‐ κB Pathway
Article Snippet: .. BMSCs were derived from the bone marrow of Sprague–Dawley (SD) rats and have been characterized in previous research [ ], while NSCs and microglia were isolated from the spinal cords of neonatal rats and characterized in this study. .. BMSCs were cultured in Dulbecco's Modified Eagle Medium (DMEM; Thermo Fisher) supplemented with 10% fetal bovine serum (FBS; Thermo Fisher) and 100 U/mL penicillin–streptomycin (Thermo Fisher), maintained at 37°C in a 5% CO 2 incubator.

Article Title: A cell-free lipid sterosomal therapeutic enables bone regeneration via USP18-mediated noncanonical S1P signaling
Article Snippet: .. BMSCs were isolated from the femurs of 4-week-old Sprague-Dawley (SD) rats, as previously described[ ]. .. Cells were maintained in α-minimum essential medium (α-MEM, Gibco) supplemented with 10% fetal bovine serum (FBS, Gibco) and 1% penicillin–streptomycin (P/S, Gibco).

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Screening of the quinonoid compounds for the treatment of GIOP. (A) Flowchart depicting the screening process of the quinonoid compounds library. The schematic diagram was created by using BioRender.com. (B) Volcano diagram showing the effects of the 153 quinonoid compounds on Runx2 expression in BMSCs. Red and blue dots indicate the specific compounds that up- and down-regulate Runx2 expression in BMSCs, respectively. (C) Heat map showing the effect of the compounds on ALP activity in primary BMSCs. Color from blue to red indicates the ALP activity in primary BMSCs from low to high. (D) Measurement of intracellular ROS level in primary BMSCs treated with three potential compounds by using the fluorescent dye DCFDA. (E) Chemical structure of DUB, the final candidate among the screened drugs. (F) MTT assay for the proliferation of BMSCs treated with different doses of DUB for 2 and 10 days, under osteogenic induction conditions with or without 10 μM Dex. (G) Representative images and quantitative analysis of mineralized nodule formation via Alizarin Red S (ARS) staining in primary BMSCs treated with DUB at a series of concentrations, under osteogenic induction conditions with or without 10 μM Dex. (H) Western blot and quantification for the expression of osteogenesis-related proteins in primary BMSCs under different treatments. (I) Oil Red O staining and quantifications for lipid droplets in primary BMSCs of different groups. n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ∗∗∗ p < 0.001 by one-way ANOVA. Scale bars: 200 μm (G), and 50 μm (I).

Journal: Bioactive Materials

Article Title: Screening of a quinonoid compounds library identifies decylubiquinone as an antioxidant and anti-apoptotic agent against glucocorticoid-induced osteoporosis via CD39/CD73/adenosine axis

doi: 10.1016/j.bioactmat.2026.03.062

Figure Lengend Snippet: Screening of the quinonoid compounds for the treatment of GIOP. (A) Flowchart depicting the screening process of the quinonoid compounds library. The schematic diagram was created by using BioRender.com. (B) Volcano diagram showing the effects of the 153 quinonoid compounds on Runx2 expression in BMSCs. Red and blue dots indicate the specific compounds that up- and down-regulate Runx2 expression in BMSCs, respectively. (C) Heat map showing the effect of the compounds on ALP activity in primary BMSCs. Color from blue to red indicates the ALP activity in primary BMSCs from low to high. (D) Measurement of intracellular ROS level in primary BMSCs treated with three potential compounds by using the fluorescent dye DCFDA. (E) Chemical structure of DUB, the final candidate among the screened drugs. (F) MTT assay for the proliferation of BMSCs treated with different doses of DUB for 2 and 10 days, under osteogenic induction conditions with or without 10 μM Dex. (G) Representative images and quantitative analysis of mineralized nodule formation via Alizarin Red S (ARS) staining in primary BMSCs treated with DUB at a series of concentrations, under osteogenic induction conditions with or without 10 μM Dex. (H) Western blot and quantification for the expression of osteogenesis-related proteins in primary BMSCs under different treatments. (I) Oil Red O staining and quantifications for lipid droplets in primary BMSCs of different groups. n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ∗∗∗ p < 0.001 by one-way ANOVA. Scale bars: 200 μm (G), and 50 μm (I).

Article Snippet: For DUB@Lip uptake assay in vitro , primary BMSCs were incubated with DUB@Lip labeled with IR-780 (HY-D1063, MedChemExpress, Shanghai, China) in culture medium.

Techniques: Expressing, Activity Assay, MTT Assay, Staining, Western Blot, In Vitro

The effect of DUB on the CD39/CD73/ADO axis. ( A ) The volcano plot showing the differential metabolites in the serum of mice of different groups, as indicated by LC-MS/MS metabolomics analysis. ( B ) The Venn diagram illustrates the overlapping differential metabolites across different groups. ( C ) Heatmap showing the differential metabolites as indicated by Venn analysis. Pseudo-color from blue to red indicated the relative expression level of the metabolites ranges from low to high. ( D ) Relative extracellular ADO level in the serum and bone marrow (BM) in mice of different groups. ( E ) Relative extracellular ATP level in the bone marrow (BM) in mice of different groups. ( F-G ) Western blot and RT-qPCR for CD39 and CD73 expressions in primary BMSCs of different groups. ( H ) Relative extracellular ATP and ADO levels in the conditioned medium (CM) in primary BMSCs under different treatments. ( I ) Western blot validation for the knockdown deficiency of CD39 and CD73 after transfection with si Entpd1 and si Nt 5e, respectively. ( J ) Extracellular ATP and ADO concentrations in the conditioned medium (CM) in primary BMSCs from different groups following transfection with si Entpd1 and si Nt5e . n = 4 mice (A-C) in each group for the high-throughput metabolomics analysis, 8 mice (D-E) in each group for in vivo assays, and 4 independent repeats (F-J) by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA.

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.03.062

Figure Lengend Snippet: The effect of DUB on the CD39/CD73/ADO axis. ( A ) The volcano plot showing the differential metabolites in the serum of mice of different groups, as indicated by LC-MS/MS metabolomics analysis. ( B ) The Venn diagram illustrates the overlapping differential metabolites across different groups. ( C ) Heatmap showing the differential metabolites as indicated by Venn analysis. Pseudo-color from blue to red indicated the relative expression level of the metabolites ranges from low to high. ( D ) Relative extracellular ADO level in the serum and bone marrow (BM) in mice of different groups. ( E ) Relative extracellular ATP level in the bone marrow (BM) in mice of different groups. ( F-G ) Western blot and RT-qPCR for CD39 and CD73 expressions in primary BMSCs of different groups. ( H ) Relative extracellular ATP and ADO levels in the conditioned medium (CM) in primary BMSCs under different treatments. ( I ) Western blot validation for the knockdown deficiency of CD39 and CD73 after transfection with si Entpd1 and si Nt 5e, respectively. ( J ) Extracellular ATP and ADO concentrations in the conditioned medium (CM) in primary BMSCs from different groups following transfection with si Entpd1 and si Nt5e . n = 4 mice (A-C) in each group for the high-throughput metabolomics analysis, 8 mice (D-E) in each group for in vivo assays, and 4 independent repeats (F-J) by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA.

Article Snippet: For DUB@Lip uptake assay in vitro , primary BMSCs were incubated with DUB@Lip labeled with IR-780 (HY-D1063, MedChemExpress, Shanghai, China) in culture medium.

Techniques: Liquid Chromatography with Mass Spectroscopy, Expressing, Western Blot, Quantitative RT-PCR, Biomarker Discovery, Knockdown, Transfection, High Throughput Screening Assay, In Vivo, In Vitro

Roles of the CD39/CD73 axis on DUB's multidirectional protection effects in Dex-treated primary BMSCs. ( A ) ELISA for ROS clearance-related enzyme T-SOD and ROS damage biomarkers 8-OHdG, AOPP, and MDA in primary BMSCs of different groups. ( B ) Western blot and quantification for the expression of ROS clearance-related proteins in primary BMSCs of different groups. ( C ) Representative images and quantitative analysis of immunofluorescence staining for MitoSox (red) in primary BMSCs of different groups, and nuclei were stained with Hoechst (blue). ( D ) Western blot and quantification for the expression of apoptosis-related proteins in primary BMSCs of different groups. ( E ) Cellular apoptosis detection in primary BMSCs of different groups by Annexin V-FITC and PI dual-staining assessment via flow cytometry. The proportion of cells in each quadrant was indicated in the plot. ( F ) Tunel (red) staining and quantification of apoptotic cells in primary BMSCs of different groups, and nuclei were stained with DAPI (blue). ( G ) Representative images and quantitative analysis of Alizarin Red S staining for mineralization in primary BMSCs of different groups under osteogenic conditions. ( H ) Western blot and quantification for the expression of osteogenesis-related proteins in primary BMSCs of different groups. n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bars: 50 μm (C), 25 μm (F), and 200 μm (G).

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.03.062

Figure Lengend Snippet: Roles of the CD39/CD73 axis on DUB's multidirectional protection effects in Dex-treated primary BMSCs. ( A ) ELISA for ROS clearance-related enzyme T-SOD and ROS damage biomarkers 8-OHdG, AOPP, and MDA in primary BMSCs of different groups. ( B ) Western blot and quantification for the expression of ROS clearance-related proteins in primary BMSCs of different groups. ( C ) Representative images and quantitative analysis of immunofluorescence staining for MitoSox (red) in primary BMSCs of different groups, and nuclei were stained with Hoechst (blue). ( D ) Western blot and quantification for the expression of apoptosis-related proteins in primary BMSCs of different groups. ( E ) Cellular apoptosis detection in primary BMSCs of different groups by Annexin V-FITC and PI dual-staining assessment via flow cytometry. The proportion of cells in each quadrant was indicated in the plot. ( F ) Tunel (red) staining and quantification of apoptotic cells in primary BMSCs of different groups, and nuclei were stained with DAPI (blue). ( G ) Representative images and quantitative analysis of Alizarin Red S staining for mineralization in primary BMSCs of different groups under osteogenic conditions. ( H ) Western blot and quantification for the expression of osteogenesis-related proteins in primary BMSCs of different groups. n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bars: 50 μm (C), 25 μm (F), and 200 μm (G).

Article Snippet: For DUB@Lip uptake assay in vitro , primary BMSCs were incubated with DUB@Lip labeled with IR-780 (HY-D1063, MedChemExpress, Shanghai, China) in culture medium.

Techniques: Enzyme-linked Immunosorbent Assay, Western Blot, Expressing, Immunofluorescence, Staining, Flow Cytometry, TUNEL Assay, In Vitro

The effect of ADO supplements on primary BMSCs. ( A ) MTT assay for the proliferation of BMSCs treated with different doses of ADO for 2 days and 10 days under osteogenic induction conditions with or without 10 μM Dex. ( B-C ) Representative images and quantitative analysis of mineralized nodule areas by Alizarin Red S staining in primary BMSCs treated with gradient doses of ADO under osteogenic induction with or without 10 μM Dex. ( D ) Western blot and quantification for the expression of osteogenesis-related proteins in primary BMSCs of different groups. ( E ) ELISA for ROS clearance-related enzyme T-SOD and ROS damage biomarkers 8-OHdG, AOPP, and MDA in primary BMSCs of different groups. ( F ) Western blot and quantification for the expression of ROS clearance-related proteins in primary BMSCs of different groups. ( G ) Representative images and quantitative analysis of immunofluorescence staining for MitoSox (red) in primary BMSCs of different groups, and nuclei were stained with Hoechst (blue). ( H ) Western blot and quantification for the expression of apoptosis-related proteins in primary BMSCs of different groups. ( I ) Cellular apoptosis detection in primary BMSCs of different groups by Annexin V-FITC and PI dual-staining assessment via flow cytometry. The proportion of cells in each quadrant was indicated in the plot. ( J ) Tunel (red) staining and quantification of apoptotic cells in primary BMSCs of different groups, and nuclei were stained with DAPI (blue). n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bars: 200 μm (B), 50 μm (G), and 25 μm (J).

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.03.062

Figure Lengend Snippet: The effect of ADO supplements on primary BMSCs. ( A ) MTT assay for the proliferation of BMSCs treated with different doses of ADO for 2 days and 10 days under osteogenic induction conditions with or without 10 μM Dex. ( B-C ) Representative images and quantitative analysis of mineralized nodule areas by Alizarin Red S staining in primary BMSCs treated with gradient doses of ADO under osteogenic induction with or without 10 μM Dex. ( D ) Western blot and quantification for the expression of osteogenesis-related proteins in primary BMSCs of different groups. ( E ) ELISA for ROS clearance-related enzyme T-SOD and ROS damage biomarkers 8-OHdG, AOPP, and MDA in primary BMSCs of different groups. ( F ) Western blot and quantification for the expression of ROS clearance-related proteins in primary BMSCs of different groups. ( G ) Representative images and quantitative analysis of immunofluorescence staining for MitoSox (red) in primary BMSCs of different groups, and nuclei were stained with Hoechst (blue). ( H ) Western blot and quantification for the expression of apoptosis-related proteins in primary BMSCs of different groups. ( I ) Cellular apoptosis detection in primary BMSCs of different groups by Annexin V-FITC and PI dual-staining assessment via flow cytometry. The proportion of cells in each quadrant was indicated in the plot. ( J ) Tunel (red) staining and quantification of apoptotic cells in primary BMSCs of different groups, and nuclei were stained with DAPI (blue). n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bars: 200 μm (B), 50 μm (G), and 25 μm (J).

Article Snippet: For DUB@Lip uptake assay in vitro , primary BMSCs were incubated with DUB@Lip labeled with IR-780 (HY-D1063, MedChemExpress, Shanghai, China) in culture medium.

Techniques: MTT Assay, Staining, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Flow Cytometry, TUNEL Assay, In Vitro

Roles of A 2b R in ADO-mediated activation of the cAMP/PKA/CREB pathway in primary BMSCs. ( A ) Principal component analysis (PCA) of RNA-seq data from primary BMSCs treated with Dex or Dex + ADO. ( B ) The volcano plot presented the differentially expressed genes (DEGs) as determined by RNA-Seq in primary BMSCs treated with Dex or Dex + ADO. ( C ) Gene Ontology (GO) enrichment analysis in the biological process category for DEGs as determined by RNA-Seq in primary BMSCs treated with Dex, or Dex + ADO. ( D ) The molecular docking of ADO with mus musculus A 1 R, A 2a R, A 2b R, and A 3 R proteins. ADO is displayed in Cyan. The surrounding residues in the binding pocket are shown in green (forming a non-hydrogen bond with ADO) or magenta (forming a hydrogen bond with ADO). The hydrogen bond is labeled as yellow dashed lines. The backbone of the receptor is depicted as gray. ( E ) RT-qPCR analysis of the mRNA levels of Adora1 , Adora2a , Adora2b , and Adora3 in primary BMSCs treated with vehicle, Dex, or Dex + ADO. ( F ) RT-qPCR analysis for the expression of Runx2 in primary BMSCs of different groups. (G) Gene Set Enrichment Analysis (GSEA) plot showing the differentially expressed pathway (cAMP) between the Dex group and the Dex + ADO group as indicated by Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. ( H ) Western blot validation for the knockdown deficiency of A 2b R after transfection with si Adora2b . ( I ) ELISA analysis for the relative intracellular cAMP levels in BMSCs of different groups. ( J ) Western blot and quantification for the expression of PKA, p-PKA, CREB, and p-CREB in primary BMSCs. ( K ) Representative images and quantitative analysis of Alizarin Red S staining for mineralization deposit in primary BMSCs of different groups under osteogenic conditions. n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ns p > 0.05, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bar: 200 μm (K).

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.03.062

Figure Lengend Snippet: Roles of A 2b R in ADO-mediated activation of the cAMP/PKA/CREB pathway in primary BMSCs. ( A ) Principal component analysis (PCA) of RNA-seq data from primary BMSCs treated with Dex or Dex + ADO. ( B ) The volcano plot presented the differentially expressed genes (DEGs) as determined by RNA-Seq in primary BMSCs treated with Dex or Dex + ADO. ( C ) Gene Ontology (GO) enrichment analysis in the biological process category for DEGs as determined by RNA-Seq in primary BMSCs treated with Dex, or Dex + ADO. ( D ) The molecular docking of ADO with mus musculus A 1 R, A 2a R, A 2b R, and A 3 R proteins. ADO is displayed in Cyan. The surrounding residues in the binding pocket are shown in green (forming a non-hydrogen bond with ADO) or magenta (forming a hydrogen bond with ADO). The hydrogen bond is labeled as yellow dashed lines. The backbone of the receptor is depicted as gray. ( E ) RT-qPCR analysis of the mRNA levels of Adora1 , Adora2a , Adora2b , and Adora3 in primary BMSCs treated with vehicle, Dex, or Dex + ADO. ( F ) RT-qPCR analysis for the expression of Runx2 in primary BMSCs of different groups. (G) Gene Set Enrichment Analysis (GSEA) plot showing the differentially expressed pathway (cAMP) between the Dex group and the Dex + ADO group as indicated by Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. ( H ) Western blot validation for the knockdown deficiency of A 2b R after transfection with si Adora2b . ( I ) ELISA analysis for the relative intracellular cAMP levels in BMSCs of different groups. ( J ) Western blot and quantification for the expression of PKA, p-PKA, CREB, and p-CREB in primary BMSCs. ( K ) Representative images and quantitative analysis of Alizarin Red S staining for mineralization deposit in primary BMSCs of different groups under osteogenic conditions. n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ns p > 0.05, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bar: 200 μm (K).

Article Snippet: For DUB@Lip uptake assay in vitro , primary BMSCs were incubated with DUB@Lip labeled with IR-780 (HY-D1063, MedChemExpress, Shanghai, China) in culture medium.

Techniques: Activation Assay, RNA Sequencing, Binding Assay, Labeling, Quantitative RT-PCR, Expressing, Western Blot, Biomarker Discovery, Knockdown, Transfection, Enzyme-linked Immunosorbent Assay, Staining, In Vitro

$Establishment of DUB-loaded bone-targeted liposomal delivery system. ( A ) Representative images and quantitative analysis of mineralized nodule formation via Alizarin Red S (ARS) staining in primary BMSCs for the effect of DUB@Lip on osteogenesis differentiation under conditions of 10 μM Dex. ( B ) RT-qPCR for the expression of osteogenesis-related genes in primary BMSCs of different groups. ( C-D ) In vitro cellular uptake assay of IR-780-labeled DUB@Lip liposomes in primary BMSCs by confocal microscopy and flow cytometry. ( E-F ) Evaluation of bone-targeting capacity and pharmacokinetic analysis of DUB@Lip and DUB@TLip via ex vivo fluorescence imaging. ( G-H ) Representative reconstructed images and quantification for Tb.BV/TV, Tb.N, Tb.Th, Tb.Sp, and Ct.Th in femora in mice of different groups by Micro-CT. ( I ) H&E staining and quantification for trabecular bone area in distal femora in mice of different groups. ( J ) Masson staining and quantification for collagen deposition fraction (collagen area/trabecular bone area) in distal femora in mice of different groups. n = 4 independent repeats by using different biological samples in each group for in vitro experiments, or 8 mice per group for in vivo assays. Data were means ± s.e.m. ns p > 0.05, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bars: 200 μm (A-B), 2 mm (G left & right bottom), 1 mm (G right top), and 100 μm (I-J).$

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.03.062

Figure Lengend Snippet: Establishment of DUB-loaded bone-targeted liposomal delivery system. ( A ) Representative images and quantitative analysis of mineralized nodule formation via Alizarin Red S (ARS) staining in primary BMSCs for the effect of DUB@Lip on osteogenesis differentiation under conditions of 10 μM Dex. ( B ) RT-qPCR for the expression of osteogenesis-related genes in primary BMSCs of different groups. ( C-D ) In vitro cellular uptake assay of IR-780-labeled DUB@Lip liposomes in primary BMSCs by confocal microscopy and flow cytometry. ( E-F ) Evaluation of bone-targeting capacity and pharmacokinetic analysis of DUB@Lip and DUB@TLip via ex vivo fluorescence imaging. ( G-H ) Representative reconstructed images and quantification for Tb.BV/TV, Tb.N, Tb.Th, Tb.Sp, and Ct.Th in femora in mice of different groups by Micro-CT. ( I ) H&E staining and quantification for trabecular bone area in distal femora in mice of different groups. ( J ) Masson staining and quantification for collagen deposition fraction (collagen area/trabecular bone area) in distal femora in mice of different groups. n = 4 independent repeats by using different biological samples in each group for in vitro experiments, or 8 mice per group for in vivo assays. Data were means ± s.e.m. ns p > 0.05, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bars: 200 μm (A-B), 2 mm (G left & right bottom), 1 mm (G right top), and 100 μm (I-J).

Article Snippet: For DUB@Lip uptake assay in vitro , primary BMSCs were incubated with DUB@Lip labeled with IR-780 (HY-D1063, MedChemExpress, Shanghai, China) in culture medium.

Techniques: Staining, Quantitative RT-PCR, Expressing, In Vitro, Labeling, Liposomes, Confocal Microscopy, Flow Cytometry, Ex Vivo, Fluorescence, Imaging, Micro-CT, In Vivo

CCL promotes METTL3 protein stability. A Cytotoxicity of CCL on BMSCs assessed by CCK-8 assay (n = 3). B - C ALP ( B ) and ARS ( C ) staining evaluating osteogenic differentiation of BMSCs treated with CCL (n = 3); scale bar = 200 µm. D Colorimetric quantification of global m. 6 A levels in cellular RNA (n = 3). E – F METTL3 expression detected by RT-qPCR ( E ) and WB ( F ) (n = 3). G METTL3 protein expression in CCL-treated cells at specified time points after CHX administration (n = 3). H METTL3 expression in bone tissue detected by IHC (n = 8); scale bar = 200 µm. Comparisons among three or more groups were performed by one-way or two-way ANOVA followed by Tukey’s post-hoc test. * P < 0.05

Journal: Journal of Molecular Histology

Article Title: Cuscuta chinensis Lam. extract alleviates ovariectomy-induced osteoporosis by inhibiting VCP-mediated METTL3 protein degradation

doi: 10.1007/s10735-026-10846-8

Figure Lengend Snippet: CCL promotes METTL3 protein stability. A Cytotoxicity of CCL on BMSCs assessed by CCK-8 assay (n = 3). B - C ALP ( B ) and ARS ( C ) staining evaluating osteogenic differentiation of BMSCs treated with CCL (n = 3); scale bar = 200 µm. D Colorimetric quantification of global m. 6 A levels in cellular RNA (n = 3). E – F METTL3 expression detected by RT-qPCR ( E ) and WB ( F ) (n = 3). G METTL3 protein expression in CCL-treated cells at specified time points after CHX administration (n = 3). H METTL3 expression in bone tissue detected by IHC (n = 8); scale bar = 200 µm. Comparisons among three or more groups were performed by one-way or two-way ANOVA followed by Tukey’s post-hoc test. * P < 0.05

Article Snippet: The potential cytotoxic effects of CCL on BMSCs were assessed using a CCK-8 (HY-K0301, MCE).

Techniques: CCK-8 Assay, Staining, Expressing, Quantitative RT-PCR

METTL3 knockdown inhibits the pro-osteogenic differentiation effects of CCL. BMSCs were transfected with METTL3-targeting shRNAs. A – B Knockdown efficiency was verified by (A) RT-qPCR and (B) WB (n = 3). C – D Osteogenic differentiation was assessed in CCL-treated, METTL3-knockdown BMSCs by ( C ) ALP and ( D ) ARS staining (n = 3); scale bar = 200 µm. E – F Expression of COL1A1, RUNX2, and BGLAP (OCN) was detected by ( E ) RT-qPCR and ( F ) WB (n = 3). Two-group comparisons were conducted applying the t-test, while comparisons among multiple groups were carried out via one-way ANOVA, followed by Tukey’s post-hoc test. * P < 0.05

Journal: Journal of Molecular Histology

Article Title: Cuscuta chinensis Lam. extract alleviates ovariectomy-induced osteoporosis by inhibiting VCP-mediated METTL3 protein degradation

doi: 10.1007/s10735-026-10846-8

Figure Lengend Snippet: METTL3 knockdown inhibits the pro-osteogenic differentiation effects of CCL. BMSCs were transfected with METTL3-targeting shRNAs. A – B Knockdown efficiency was verified by (A) RT-qPCR and (B) WB (n = 3). C – D Osteogenic differentiation was assessed in CCL-treated, METTL3-knockdown BMSCs by ( C ) ALP and ( D ) ARS staining (n = 3); scale bar = 200 µm. E – F Expression of COL1A1, RUNX2, and BGLAP (OCN) was detected by ( E ) RT-qPCR and ( F ) WB (n = 3). Two-group comparisons were conducted applying the t-test, while comparisons among multiple groups were carried out via one-way ANOVA, followed by Tukey’s post-hoc test. * P < 0.05

Article Snippet: The potential cytotoxic effects of CCL on BMSCs were assessed using a CCK-8 (HY-K0301, MCE).

Techniques: Knockdown, Transfection, Quantitative RT-PCR, Staining, Expressing

CCL promotes osteogenic differentiation by targeting VCP to inhibit METTL3 protein degradation. BMSC cell lines stably overexpressing VCP, or both VCP and METTL3, were established. A WB analysis of VCP and METTL3 protein expression (n = 3). B – C Osteogenic differentiation was assessed in CCL-treated BMSCs by (B) ALP and (C) ARS staining (n = 3); scale bar = 200 µm. D – E Expression of the osteogenic markers COL1A1, RUNX2, and BGLAP (OCN) detected by D RT-qPCR and E WB (n = 3). Comparisons among three or more groups were performed by one-way ANOVA followed by Tukey’s post-hoc test. * P < 0.05

Journal: Journal of Molecular Histology

Article Title: Cuscuta chinensis Lam. extract alleviates ovariectomy-induced osteoporosis by inhibiting VCP-mediated METTL3 protein degradation

doi: 10.1007/s10735-026-10846-8

Figure Lengend Snippet: CCL promotes osteogenic differentiation by targeting VCP to inhibit METTL3 protein degradation. BMSC cell lines stably overexpressing VCP, or both VCP and METTL3, were established. A WB analysis of VCP and METTL3 protein expression (n = 3). B – C Osteogenic differentiation was assessed in CCL-treated BMSCs by (B) ALP and (C) ARS staining (n = 3); scale bar = 200 µm. D – E Expression of the osteogenic markers COL1A1, RUNX2, and BGLAP (OCN) detected by D RT-qPCR and E WB (n = 3). Comparisons among three or more groups were performed by one-way ANOVA followed by Tukey’s post-hoc test. * P < 0.05

Article Snippet: The potential cytotoxic effects of CCL on BMSCs were assessed using a CCK-8 (HY-K0301, MCE).

Techniques: Stable Transfection, Expressing, Staining, Quantitative RT-PCR

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