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Journal: Stem cell research & therapy
Article Title: PRMT1 inhibition enhances the cardioprotective effect of adipose-derived mesenchymal stem cells against myocardial infarction through RUNX1.
doi: 10.1186/s13287-025-04409-z
Figure Lengend Snippet: Fig. 3 PRMT1 inhibition increases the expression of MMP-10, PlGF and TGF-β2 in ADSCs. (A) Volcano plot comparing changes in genes with up-regulated or down-regulated expression in ADSCs treated with vehicle or Furamidine (10 µM) for 24 h (n = 3). (B) GO (Gene ontology) was used to analyze the bubble map of differential gene-enriched molecules in ADSCs. (C) Heat map of mRNA expression profile of ADSCs treated with vehicle or Furamidine. (D) ADSCs treated with Furamidine (10 µM, 24 h) showed changes in mRNA expression levels of target genes (n = 6). (E) The mRNA expression levels of target genes in ADSCs infected with Ad-control or Ad-shPRMT1 (MOI 200, 24 h) (n = 6). (F, G) Western blotting and protein quantitative analysis showed the protein changes of target genes after ADSCs were infected with adenovirus for 48 h (n = 6). Full-length blots are presented in Supplementary Fig. 4D. Data are presented as mean ± SEM and were analyzed using student’s t test, *P < 0.05
Article Snippet: The primary antibodies used in this study included: anti-PRMT1 rabbit monoclonal antibody (2449 S, 1:1000; Cell Signaling Technology, MA, USA), anti-cleaved caspase-3 rabbit polyclonal antibody (9664 S, 1:1000; Cell Signaling Technology, MA, USA), anti-MMP-10 rabbit polyclonal antibody (A3033, 1:1000; Abclonal Technology, Wuhan, China), anti-TGF-β2 rabbit polyclonal antibody (19999-1-AP, 1:1000; Proteintech, Wuhan, China),
Techniques: Inhibition, Expressing, Infection, Control, Western Blot
Journal: Stem cell research & therapy
Article Title: PRMT1 inhibition enhances the cardioprotective effect of adipose-derived mesenchymal stem cells against myocardial infarction through RUNX1.
doi: 10.1186/s13287-025-04409-z
Figure Lengend Snippet: Fig. 4 PRMT1 inhibition promotes proliferation and migration of ADSCs through RUNX1-mediated MMP-10/PlGF/TGF-β2 expression in ADSCs. (A) Pre dicted transcription factors binding to the target Mmp10, Plgf and Tgfb2 genes promoter region. The promoter region is defined as 2000 bp upstream of the target gene transcription starting point. (B) Predict possible binding sites in the gene promoter region and transcription factor RUNX1. (C, D) The relationship between PRMT1 and RUNX1 was detected by Co-IP experiment. (E, F) ADSCs were treated with Furamidine (10 µM) and Ro5-3335 (50 µM) for 48 h. Full-length blots are presented in Supplementary Fig. 4E, F. Western blotting and quantitative analysis of MMP-10, PlGF, and TGF-β2 protein levels (n = 6). Full-length blots are presented in Supplementary Fig. 5A. (G) Changes in cell proliferation were detected by CCK-8 after ADSCs were treated with Furamidine and Ro5-3335 for 24 h (n = 6). (H, I) Representative images of crystal violet staining. The migration ability of ADSCs was observed by transwell assay after treatment with Furamidine and Ro5-3335 (n = 4). Scale bar: 50 μm. All data are presented as mean ± SEM and were analyzed by one-way ANOVA, *P < 0.05
Article Snippet: The primary antibodies used in this study included: anti-PRMT1 rabbit monoclonal antibody (2449 S, 1:1000; Cell Signaling Technology, MA, USA), anti-cleaved caspase-3 rabbit polyclonal antibody (9664 S, 1:1000; Cell Signaling Technology, MA, USA), anti-MMP-10 rabbit polyclonal antibody (A3033, 1:1000; Abclonal Technology, Wuhan, China), anti-TGF-β2 rabbit polyclonal antibody (19999-1-AP, 1:1000; Proteintech, Wuhan, China),
Techniques: Inhibition, Migration, Expressing, Binding Assay, Co-Immunoprecipitation Assay, Western Blot, CCK-8 Assay, Staining, Transwell Assay
Journal: Stem cell research & therapy
Article Title: PRMT1 inhibition enhances the cardioprotective effect of adipose-derived mesenchymal stem cells against myocardial infarction through RUNX1.
doi: 10.1186/s13287-025-04409-z
Figure Lengend Snippet: Fig. 8 Schematic illustration of inhibition of PRMT1 improve the therapeutic efficacy of ADSCs for MI. After MI, the level of PRMT1 in ADSCs transplanted into the infarct border zone increased under stress, and by interacting with RUNX1, the transcription-promoting effect of RUNX1 on Mmp10, Plgf and Tgfb2 was inhibited, resulting in impaired retention and survival of ADSCs, and inadequate cardioprotective effects (left). After knockdown of PRMT1, the released RUNX1 promoted the expression of Mmp10, Plgf and Tgfb2 in ADSCs, improved the retention rate of implanted ADSCs, and enhanced cardiopro tective effects of ADSCs (right). The Figure was created with BioRender software (https://biorender.com/)
Article Snippet: The primary antibodies used in this study included: anti-PRMT1 rabbit monoclonal antibody (2449 S, 1:1000; Cell Signaling Technology, MA, USA), anti-cleaved caspase-3 rabbit polyclonal antibody (9664 S, 1:1000; Cell Signaling Technology, MA, USA), anti-MMP-10 rabbit polyclonal antibody (A3033, 1:1000; Abclonal Technology, Wuhan, China), anti-TGF-β2 rabbit polyclonal antibody (19999-1-AP, 1:1000; Proteintech, Wuhan, China),
Techniques: Inhibition, Drug discovery, Knockdown, Expressing, Software
Journal: Life (Basel, Switzerland)
Article Title: Placental Pathology and Placental Growth Factor (PlGF)/Vascular Endothelial Growth Factor Receptor-1 (VEGFR-1) Pathway Expression Evaluation in Fetal Congenital Heart Defects.
doi: 10.3390/life15060837
Figure Lengend Snippet: Figure 2. Representative micrographs displaying the placental immunohistochemical localization of the placental growth factor (PlGF) in (a) the syncytiotrophoblast (strong staining; magnification 20×), (c) decidual cells (strong staining; magnification 20×), and (e) villous endothelial cells (moderate staining; magnification 20×) and the vascular endothelial growth factor receptor-1 (VEGFR-1) in (b) the syncytiotrophoblast (strong staining; magnification 10×), (d) decidual cells (strong staining; magnification 20×), and (f) villous endothelial cells (strong staining; magnification 40×).
Article Snippet: Tissues were then incubated for 1 h at RT with primary
Techniques: Immunohistochemical staining, Staining
Journal: Life (Basel, Switzerland)
Article Title: Placental Pathology and Placental Growth Factor (PlGF)/Vascular Endothelial Growth Factor Receptor-1 (VEGFR-1) Pathway Expression Evaluation in Fetal Congenital Heart Defects.
doi: 10.3390/life15060837
Figure Lengend Snippet: Figure 3. Comparative evaluation of placental immunostaining intensities at the level of syncytiotro- phoblast, decidual cells, and villous endothelial cells for (a) the placental growth factor (PlGF) and (b) the vascular endothelial growth factor receptor-1 (VEGFR-1) (** p < 0.001; **** p < 0.00001; ns, no significance).
Article Snippet: Tissues were then incubated for 1 h at RT with primary
Techniques: Immunostaining