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Characterization of hAECs and hUC-MSCs. A Schematic illustration of the experimental design for comparing the effects of hAECs and hUC-MSCs on ovarian function. B , C Morphological feature and flow cytometric analysis of hAECs and hUC-MSCs. D , E Representative images of double immunofluorescence staining for OCT4 and <t>CK18</t> or N-cadherin in hAECs and hUC-MSCs. F Multilineage differentiation potential of hUC-MSCs into osteoblasts, adipocytes, and chondrocytes, as assessed by Alizarin Red, Oil Red O, and Alcian Blue staining, respectively. Scale bars represent 25, 50, 100 and 200 μm
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Characterization of hAECs and hUC-MSCs. A Schematic illustration of the experimental design for comparing the effects of hAECs and hUC-MSCs on ovarian function. B , C Morphological feature and flow cytometric analysis of hAECs and hUC-MSCs. D , E Representative images of double immunofluorescence staining for OCT4 and <t>CK18</t> or N-cadherin in hAECs and hUC-MSCs. F Multilineage differentiation potential of hUC-MSCs into osteoblasts, adipocytes, and chondrocytes, as assessed by Alizarin Red, Oil Red O, and Alcian Blue staining, respectively. Scale bars represent 25, 50, 100 and 200 μm
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Characterization of hAECs and hUC-MSCs. A Schematic illustration of the experimental design for comparing the effects of hAECs and hUC-MSCs on ovarian function. B , C Morphological feature and flow cytometric analysis of hAECs and hUC-MSCs. D , E Representative images of double immunofluorescence staining for OCT4 and <t>CK18</t> or N-cadherin in hAECs and hUC-MSCs. F Multilineage differentiation potential of hUC-MSCs into osteoblasts, adipocytes, and chondrocytes, as assessed by Alizarin Red, Oil Red O, and Alcian Blue staining, respectively. Scale bars represent 25, 50, 100 and 200 μm
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Pharmacological inhibition of RTK signaling with sunitinib suppresses proliferation and induces apoptosis in BPH epithelial cells. a Growth curves of BPH-1 cells treated with sunitinib or DMSO for up to 60 h, measured by MTT assay. b Representative images and quantification of colony formation in BPH-1 cells under the sunitinib or DMSO treatments. c BrdU incorporation assays showing reduced proliferative activity in BPH-1 cells after sunitinib treatment; BrdU-positive cells were visualized by immunofluorescence (BrdU, green; DAPI, blue). d Flow cytometric analysis of apoptosis in BPH-1 cells following 96 h treatment with sunitinib, assessed by Annexin V/PI staining. e Growth curves of primary luminal epithelial cells isolated from BPH tissues (n = 3 patient-derived cultures) treated with sunitinib or DMSO. f Representative images and spheroid diameter quantification of BPH-derived prostate organoids cultured for 1 week with sunitinib or DMSO; luminal epithelial identity confirmed by <t>KRT18</t> immunofluorescence (green) with DAPI nuclear staining (blue). Scale bars: 1.0 cm. g Flow cytometric quantification of apoptosis in BPH-derived primary luminal epithelial cells after 96 h treatment with sunitinib. h Comparison of prostate weight in normal or testosterone-induced BPH mice treated with placebo, finasteride, or sunitinib for 8 weeks. i Representative IHC staining of Ki-67 and quantification of Ki-67 positive epithelial cells in mouse prostates from the indicated groups. Scale bars: 100 μm. Data are presented as mean ± SD from at least three independent experiments or biological replicates. Statistical significance was determined by Student’s t -test; * P < 0.05, ** P < 0.01, *** P < 0.001; n.s, not significant
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Pharmacological inhibition of RTK signaling with sunitinib suppresses proliferation and induces apoptosis in BPH epithelial cells. a Growth curves of BPH-1 cells treated with sunitinib or DMSO for up to 60 h, measured by MTT assay. b Representative images and quantification of colony formation in BPH-1 cells under the sunitinib or DMSO treatments. c BrdU incorporation assays showing reduced proliferative activity in BPH-1 cells after sunitinib treatment; BrdU-positive cells were visualized by immunofluorescence (BrdU, green; DAPI, blue). d Flow cytometric analysis of apoptosis in BPH-1 cells following 96 h treatment with sunitinib, assessed by Annexin V/PI staining. e Growth curves of primary luminal epithelial cells isolated from BPH tissues (n = 3 patient-derived cultures) treated with sunitinib or DMSO. f Representative images and spheroid diameter quantification of BPH-derived prostate organoids cultured for 1 week with sunitinib or DMSO; luminal epithelial identity confirmed by <t>KRT18</t> immunofluorescence (green) with DAPI nuclear staining (blue). Scale bars: 1.0 cm. g Flow cytometric quantification of apoptosis in BPH-derived primary luminal epithelial cells after 96 h treatment with sunitinib. h Comparison of prostate weight in normal or testosterone-induced BPH mice treated with placebo, finasteride, or sunitinib for 8 weeks. i Representative IHC staining of Ki-67 and quantification of Ki-67 positive epithelial cells in mouse prostates from the indicated groups. Scale bars: 100 μm. Data are presented as mean ± SD from at least three independent experiments or biological replicates. Statistical significance was determined by Student’s t -test; * P < 0.05, ** P < 0.01, *** P < 0.001; n.s, not significant
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Pharmacological inhibition of RTK signaling with sunitinib suppresses proliferation and induces apoptosis in BPH epithelial cells. a Growth curves of BPH-1 cells treated with sunitinib or DMSO for up to 60 h, measured by MTT assay. b Representative images and quantification of colony formation in BPH-1 cells under the sunitinib or DMSO treatments. c BrdU incorporation assays showing reduced proliferative activity in BPH-1 cells after sunitinib treatment; BrdU-positive cells were visualized by immunofluorescence (BrdU, green; DAPI, blue). d Flow cytometric analysis of apoptosis in BPH-1 cells following 96 h treatment with sunitinib, assessed by Annexin V/PI staining. e Growth curves of primary luminal epithelial cells isolated from BPH tissues (n = 3 patient-derived cultures) treated with sunitinib or DMSO. f Representative images and spheroid diameter quantification of BPH-derived prostate organoids cultured for 1 week with sunitinib or DMSO; luminal epithelial identity confirmed by <t>KRT18</t> immunofluorescence (green) with DAPI nuclear staining (blue). Scale bars: 1.0 cm. g Flow cytometric quantification of apoptosis in BPH-derived primary luminal epithelial cells after 96 h treatment with sunitinib. h Comparison of prostate weight in normal or testosterone-induced BPH mice treated with placebo, finasteride, or sunitinib for 8 weeks. i Representative IHC staining of Ki-67 and quantification of Ki-67 positive epithelial cells in mouse prostates from the indicated groups. Scale bars: 100 μm. Data are presented as mean ± SD from at least three independent experiments or biological replicates. Statistical significance was determined by Student’s t -test; * P < 0.05, ** P < 0.01, *** P < 0.001; n.s, not significant
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Pharmacological inhibition of RTK signaling with sunitinib suppresses proliferation and induces apoptosis in BPH epithelial cells. a Growth curves of BPH-1 cells treated with sunitinib or DMSO for up to 60 h, measured by MTT assay. b Representative images and quantification of colony formation in BPH-1 cells under the sunitinib or DMSO treatments. c BrdU incorporation assays showing reduced proliferative activity in BPH-1 cells after sunitinib treatment; BrdU-positive cells were visualized by immunofluorescence (BrdU, green; DAPI, blue). d Flow cytometric analysis of apoptosis in BPH-1 cells following 96 h treatment with sunitinib, assessed by Annexin V/PI staining. e Growth curves of primary luminal epithelial cells isolated from BPH tissues (n = 3 patient-derived cultures) treated with sunitinib or DMSO. f Representative images and spheroid diameter quantification of BPH-derived prostate organoids cultured for 1 week with sunitinib or DMSO; luminal epithelial identity confirmed by <t>KRT18</t> immunofluorescence (green) with DAPI nuclear staining (blue). Scale bars: 1.0 cm. g Flow cytometric quantification of apoptosis in BPH-derived primary luminal epithelial cells after 96 h treatment with sunitinib. h Comparison of prostate weight in normal or testosterone-induced BPH mice treated with placebo, finasteride, or sunitinib for 8 weeks. i Representative IHC staining of Ki-67 and quantification of Ki-67 positive epithelial cells in mouse prostates from the indicated groups. Scale bars: 100 μm. Data are presented as mean ± SD from at least three independent experiments or biological replicates. Statistical significance was determined by Student’s t -test; * P < 0.05, ** P < 0.01, *** P < 0.001; n.s, not significant
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Image Search Results


Characterization of hAECs and hUC-MSCs. A Schematic illustration of the experimental design for comparing the effects of hAECs and hUC-MSCs on ovarian function. B , C Morphological feature and flow cytometric analysis of hAECs and hUC-MSCs. D , E Representative images of double immunofluorescence staining for OCT4 and CK18 or N-cadherin in hAECs and hUC-MSCs. F Multilineage differentiation potential of hUC-MSCs into osteoblasts, adipocytes, and chondrocytes, as assessed by Alizarin Red, Oil Red O, and Alcian Blue staining, respectively. Scale bars represent 25, 50, 100 and 200 μm

Journal: Stem Cell Research & Therapy

Article Title: Comparative evaluation of the therapeutic efficacy between human amniotic epithelial cells and human umbilical cord mesenchymal stem cells in premature ovarian insufficiency

doi: 10.1186/s13287-025-04881-7

Figure Lengend Snippet: Characterization of hAECs and hUC-MSCs. A Schematic illustration of the experimental design for comparing the effects of hAECs and hUC-MSCs on ovarian function. B , C Morphological feature and flow cytometric analysis of hAECs and hUC-MSCs. D , E Representative images of double immunofluorescence staining for OCT4 and CK18 or N-cadherin in hAECs and hUC-MSCs. F Multilineage differentiation potential of hUC-MSCs into osteoblasts, adipocytes, and chondrocytes, as assessed by Alizarin Red, Oil Red O, and Alcian Blue staining, respectively. Scale bars represent 25, 50, 100 and 200 μm

Article Snippet: After permeabilization with 0.1% Triton X-100 (Sigma-Aldrich, St. Louis, MO, USA), cell were incubated with the following primary antibodies at 4 °C for overnight: OCT4 (1:200, Boster), CK18 (1:200, Boster) and N-cadherin (1:200, Boster).

Techniques: Double Immunofluorescence Staining, Staining

Pharmacological inhibition of RTK signaling with sunitinib suppresses proliferation and induces apoptosis in BPH epithelial cells. a Growth curves of BPH-1 cells treated with sunitinib or DMSO for up to 60 h, measured by MTT assay. b Representative images and quantification of colony formation in BPH-1 cells under the sunitinib or DMSO treatments. c BrdU incorporation assays showing reduced proliferative activity in BPH-1 cells after sunitinib treatment; BrdU-positive cells were visualized by immunofluorescence (BrdU, green; DAPI, blue). d Flow cytometric analysis of apoptosis in BPH-1 cells following 96 h treatment with sunitinib, assessed by Annexin V/PI staining. e Growth curves of primary luminal epithelial cells isolated from BPH tissues (n = 3 patient-derived cultures) treated with sunitinib or DMSO. f Representative images and spheroid diameter quantification of BPH-derived prostate organoids cultured for 1 week with sunitinib or DMSO; luminal epithelial identity confirmed by KRT18 immunofluorescence (green) with DAPI nuclear staining (blue). Scale bars: 1.0 cm. g Flow cytometric quantification of apoptosis in BPH-derived primary luminal epithelial cells after 96 h treatment with sunitinib. h Comparison of prostate weight in normal or testosterone-induced BPH mice treated with placebo, finasteride, or sunitinib for 8 weeks. i Representative IHC staining of Ki-67 and quantification of Ki-67 positive epithelial cells in mouse prostates from the indicated groups. Scale bars: 100 μm. Data are presented as mean ± SD from at least three independent experiments or biological replicates. Statistical significance was determined by Student’s t -test; * P < 0.05, ** P < 0.01, *** P < 0.001; n.s, not significant

Journal: Molecular Biomedicine

Article Title: Fibroblasts promote the progression of benign prostatic hyperplasia through colony-stimulating factor 1 receptor-mediated RTK signaling in prostatic epithelial cells

doi: 10.1186/s43556-025-00360-w

Figure Lengend Snippet: Pharmacological inhibition of RTK signaling with sunitinib suppresses proliferation and induces apoptosis in BPH epithelial cells. a Growth curves of BPH-1 cells treated with sunitinib or DMSO for up to 60 h, measured by MTT assay. b Representative images and quantification of colony formation in BPH-1 cells under the sunitinib or DMSO treatments. c BrdU incorporation assays showing reduced proliferative activity in BPH-1 cells after sunitinib treatment; BrdU-positive cells were visualized by immunofluorescence (BrdU, green; DAPI, blue). d Flow cytometric analysis of apoptosis in BPH-1 cells following 96 h treatment with sunitinib, assessed by Annexin V/PI staining. e Growth curves of primary luminal epithelial cells isolated from BPH tissues (n = 3 patient-derived cultures) treated with sunitinib or DMSO. f Representative images and spheroid diameter quantification of BPH-derived prostate organoids cultured for 1 week with sunitinib or DMSO; luminal epithelial identity confirmed by KRT18 immunofluorescence (green) with DAPI nuclear staining (blue). Scale bars: 1.0 cm. g Flow cytometric quantification of apoptosis in BPH-derived primary luminal epithelial cells after 96 h treatment with sunitinib. h Comparison of prostate weight in normal or testosterone-induced BPH mice treated with placebo, finasteride, or sunitinib for 8 weeks. i Representative IHC staining of Ki-67 and quantification of Ki-67 positive epithelial cells in mouse prostates from the indicated groups. Scale bars: 100 μm. Data are presented as mean ± SD from at least three independent experiments or biological replicates. Statistical significance was determined by Student’s t -test; * P < 0.05, ** P < 0.01, *** P < 0.001; n.s, not significant

Article Snippet: Prostate epithelial identity was confirmed by immunofluorescence staining for the epithelial marker KRT18 (anti- KRT18; Cell Signaling Technology, #4548; dilution 1:800).

Techniques: Inhibition, MTT Assay, BrdU Incorporation Assay, Activity Assay, Immunofluorescence, Staining, Isolation, Derivative Assay, Cell Culture, Comparison, Immunohistochemistry