verteporfin Search Results


95
Tocris verteporfin treatment
A . Quantification of A–P axis length at 17 hpf (t-test; control n = 12, mutant n = 12; p = 0.7367), 24 hpf (t-test; control n = 10, mutant n = 11; p = 0.1232), 27 hpf (t-test; control n = 20, mutant n = 20; p = 0.0039), 30 hpf (Mann–Whitney test; control n = 16, mutant n = 19; p < 0.0001), and 36 hpf (t-test; control n = 7, mutant n = 7; p < 0.0001). The same control measurements were used in . B . Mathematical model predictions of notochord length for control and vgll4b mutant embryos at different time points. The model assumes that YAP increases progenitor addition r p and simultaneously regulates the vacuolation front speed v front , slowing the wave of vacuolation, without affecting the vacuolation rate of each notochord cell (see and in the main text). The empirical measurements shown in the graph are the same as those presented in . C . Segmentation of notochord vacuoles in control and mutant embryos at 30 hpf visualized with Bodipy staining (scale bar: 50 μm). D . Quantification of notochord vacuole area at 27 hpf (Mann–Whitney test; control n = 8, mutant n = 6; p < 0.0001), 30 hpf (t-test; control n = 8, mutant n = 7; p = 0.0083), 2 dpf (t-test; control n = 9, mutant n = 12; p = 0.0003), and 3 dpf (t-test; control n = 11, mutant n = 12; p = 0.0009). E . Schematic of <t>verteporfin</t> (YAP inhibitor) treatment strategy. F . Confocal images of the posterior notochord at 24 hpf and 30 hpf in control and verteporfin-treated embryos, showing segmented nuclei (scale bar: 50 μm). G . Quantification of posterior notochord cell density: Treatment A (t-test; control n = 10, treated n = 14; p = 0.0219); Treatment B (t-test; control n = 8, treated n = 9; p = 0.4696). H. Segmentation of notochord vacuoles in control and verteporfin-treated embryos visualized with Bodipy staining (scale bar: 50 μm). I . Quantification of vacuole area in the central notochord: Treatment A (t-test; control n = 7, treated n = 4; p = 0.00078); Treatment B (t-test; control n = 7, treated n = 7; p = 0.2406).
Verteporfin Treatment, supplied by Tocris, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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95
Tocris verteporfin
A . Quantification of A–P axis length at 17 hpf (t-test; control n = 12, mutant n = 12; p = 0.7367), 24 hpf (t-test; control n = 10, mutant n = 11; p = 0.1232), 27 hpf (t-test; control n = 20, mutant n = 20; p = 0.0039), 30 hpf (Mann–Whitney test; control n = 16, mutant n = 19; p < 0.0001), and 36 hpf (t-test; control n = 7, mutant n = 7; p < 0.0001). The same control measurements were used in . B . Mathematical model predictions of notochord length for control and vgll4b mutant embryos at different time points. The model assumes that YAP increases progenitor addition r p and simultaneously regulates the vacuolation front speed v front , slowing the wave of vacuolation, without affecting the vacuolation rate of each notochord cell (see and in the main text). The empirical measurements shown in the graph are the same as those presented in . C . Segmentation of notochord vacuoles in control and mutant embryos at 30 hpf visualized with Bodipy staining (scale bar: 50 μm). D . Quantification of notochord vacuole area at 27 hpf (Mann–Whitney test; control n = 8, mutant n = 6; p < 0.0001), 30 hpf (t-test; control n = 8, mutant n = 7; p = 0.0083), 2 dpf (t-test; control n = 9, mutant n = 12; p = 0.0003), and 3 dpf (t-test; control n = 11, mutant n = 12; p = 0.0009). E . Schematic of <t>verteporfin</t> (YAP inhibitor) treatment strategy. F . Confocal images of the posterior notochord at 24 hpf and 30 hpf in control and verteporfin-treated embryos, showing segmented nuclei (scale bar: 50 μm). G . Quantification of posterior notochord cell density: Treatment A (t-test; control n = 10, treated n = 14; p = 0.0219); Treatment B (t-test; control n = 8, treated n = 9; p = 0.4696). H. Segmentation of notochord vacuoles in control and verteporfin-treated embryos visualized with Bodipy staining (scale bar: 50 μm). I . Quantification of vacuole area in the central notochord: Treatment A (t-test; control n = 7, treated n = 4; p = 0.00078); Treatment B (t-test; control n = 7, treated n = 7; p = 0.2406).
Verteporfin, supplied by Tocris, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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95
Selleck Chemicals verteporfin
A . Quantification of A–P axis length at 17 hpf (t-test; control n = 12, mutant n = 12; p = 0.7367), 24 hpf (t-test; control n = 10, mutant n = 11; p = 0.1232), 27 hpf (t-test; control n = 20, mutant n = 20; p = 0.0039), 30 hpf (Mann–Whitney test; control n = 16, mutant n = 19; p < 0.0001), and 36 hpf (t-test; control n = 7, mutant n = 7; p < 0.0001). The same control measurements were used in . B . Mathematical model predictions of notochord length for control and vgll4b mutant embryos at different time points. The model assumes that YAP increases progenitor addition r p and simultaneously regulates the vacuolation front speed v front , slowing the wave of vacuolation, without affecting the vacuolation rate of each notochord cell (see and in the main text). The empirical measurements shown in the graph are the same as those presented in . C . Segmentation of notochord vacuoles in control and mutant embryos at 30 hpf visualized with Bodipy staining (scale bar: 50 μm). D . Quantification of notochord vacuole area at 27 hpf (Mann–Whitney test; control n = 8, mutant n = 6; p < 0.0001), 30 hpf (t-test; control n = 8, mutant n = 7; p = 0.0083), 2 dpf (t-test; control n = 9, mutant n = 12; p = 0.0003), and 3 dpf (t-test; control n = 11, mutant n = 12; p = 0.0009). E . Schematic of <t>verteporfin</t> (YAP inhibitor) treatment strategy. F . Confocal images of the posterior notochord at 24 hpf and 30 hpf in control and verteporfin-treated embryos, showing segmented nuclei (scale bar: 50 μm). G . Quantification of posterior notochord cell density: Treatment A (t-test; control n = 10, treated n = 14; p = 0.0219); Treatment B (t-test; control n = 8, treated n = 9; p = 0.4696). H. Segmentation of notochord vacuoles in control and verteporfin-treated embryos visualized with Bodipy staining (scale bar: 50 μm). I . Quantification of vacuole area in the central notochord: Treatment A (t-test; control n = 7, treated n = 4; p = 0.00078); Treatment B (t-test; control n = 7, treated n = 7; p = 0.2406).
Verteporfin, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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96
medchemexpress hy-b0146

Hy B0146, supplied by medchemexpress, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/verteporfin/pmc11196208-17-0-4?v=medchemexpress
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90
Carl Zeiss verteporfin

Verteporfin, supplied by Carl Zeiss, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
QLT Ophthalmics Inc photodynamic therapy (pdt) with verteporfin

Photodynamic Therapy (Pdt) With Verteporfin, supplied by QLT Ophthalmics Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/verteporfin/pmc03265181-14-12-13?v=QLT+Ophthalmics+Inc
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90
Becton Dickinson verteporfin
Physico-chemical and encapsulation properties of nanostructured lipid carriers (NLC).
Verteporfin, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Parkedale Pharmaceuticals Inc verteporfin visudyne
Physico-chemical and encapsulation properties of nanostructured lipid carriers (NLC).
Verteporfin Visudyne, supplied by Parkedale Pharmaceuticals Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
Mauget Inc pdt verteporfin
Physico-chemical and encapsulation properties of nanostructured lipid carriers (NLC).
Pdt Verteporfin, supplied by Mauget Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
CSNpharm Inc verteporfin
Inhibiting YAP–TEAD interaction attenuated fenofibrate-induced hepatomegaly. (A) Schematic diagram illustrating the inhibitory effect of <t>verteporfin</t> on the interaction between YAP and TEAD within the Hippo signaling cascade. (B) Experimental procedure in verteporfin-treated mice. (C) Co-IP analysis between YAP and TEAD in the liver of mice treated with either vehicle or verteporfin. (D) Ratios of liver weight to body weight ( n = 5). (E) Representative photographs of mouse livers. (F) H&E, CTNNB1, and KI67 staining. (G) Quantitative analysis of cellular size and determination of KI67 + cell proportion ( n = 3). Data are depicted as the mean ± SD values; ∗/∗∗/∗∗∗/∗∗∗∗ indicates P < 0.05/0.01/0.001/0.0001, versus the Control. Scale bar = 50 μm.
Verteporfin, supplied by CSNpharm Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Beijing Solarbio Science verteporfin
Flow cytometry analysis of apoptosis and a CCK-8 assay performed with ADS JZ SMCs. a Cells were transfected with the let-7a overexpression lentiviral vector GV280 or lentiviral null vector for 72 h and then used for flow cytometry analysis. b The percentages of apoptotic cells in the lenti-GV280 group and lenti-NC group. c <t>Verteporfin-treated</t> cells were transfected with the let-7a overexpression lentiviral vector GV280 for 72 h and then used for flow cytometry analysis. d The percentages of apoptotic cells in the lenti-GV280 + verteporfin group and verteporfin group. e OD 450 values of the lenti-GV280 group and lenti-NC group. f OD 450 values of the lenti-GV280 + verteporfin group and verteporfin group. These experiments were performed two times with three replicates in each experiment. Significance was determined by Student’s t test; **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05
Verteporfin, supplied by Beijing Solarbio Science, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
ApexBio yap inhibitor verteporfin
Loss of SPTBN1 inhibited autophagy by activating <t>YAP</t> in HCC cells. A and B , QRT-PCR. Huh-7 ( A ) and PLC/PRF/5 ( B ) cells were transiently transfected with siRNA to SPTBN1 or/and YAP for 48 hours and then analyzed. YAP siRNA reversed the expression of autophagy-related genes BECN1 and ATG4B that were downregulated by SPTBN1 knockdown (n = 3; ∗ P < .05, ∗∗ P < .01 vs siCON, # P < .05, ## P < .01 vs siSPTBN1). C and D , Western blot. The decreased ratio of LC3BII/LC3B I protein was reversed by YAP siRNA in Huh-7 ( C ) and PLC/PRF/5 ( D ) cells. Significance of the mean value difference was determined using a Student t test (∗∗ P < .01 vs siCON, ## P < .01 vs siSPTBN1). E , Analysis of autophagy level by Western blot. The decreased ratio of protein LC3BII/ LC3B I was reversed by YAP inhibitor <t>verteporfin</t> in the Huh-7 ( upper ) and PLC/PRF/5 ( lower ) HCC cells. F , The statistical analysis of Western blot in Figure E (n = 3; ∗∗ P < .01 vs siCON, # P < .05, ## P < .01 vs siSPTBN1). G , Autophagy and autophagic flux detection by fluorescence microscopy after GFP-RFP-LC3 LV transfection and HBSS induction for 24 hours. The reduced autophagy spots in response to SPTBN1 knockdown were reversed by YAP siRNA in Huh-7 ( left ) and PLC/PRF/5 ( right ) cells. White bars represent 10 μm.
Yap Inhibitor Verteporfin, supplied by ApexBio, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


A . Quantification of A–P axis length at 17 hpf (t-test; control n = 12, mutant n = 12; p = 0.7367), 24 hpf (t-test; control n = 10, mutant n = 11; p = 0.1232), 27 hpf (t-test; control n = 20, mutant n = 20; p = 0.0039), 30 hpf (Mann–Whitney test; control n = 16, mutant n = 19; p < 0.0001), and 36 hpf (t-test; control n = 7, mutant n = 7; p < 0.0001). The same control measurements were used in . B . Mathematical model predictions of notochord length for control and vgll4b mutant embryos at different time points. The model assumes that YAP increases progenitor addition r p and simultaneously regulates the vacuolation front speed v front , slowing the wave of vacuolation, without affecting the vacuolation rate of each notochord cell (see and in the main text). The empirical measurements shown in the graph are the same as those presented in . C . Segmentation of notochord vacuoles in control and mutant embryos at 30 hpf visualized with Bodipy staining (scale bar: 50 μm). D . Quantification of notochord vacuole area at 27 hpf (Mann–Whitney test; control n = 8, mutant n = 6; p < 0.0001), 30 hpf (t-test; control n = 8, mutant n = 7; p = 0.0083), 2 dpf (t-test; control n = 9, mutant n = 12; p = 0.0003), and 3 dpf (t-test; control n = 11, mutant n = 12; p = 0.0009). E . Schematic of verteporfin (YAP inhibitor) treatment strategy. F . Confocal images of the posterior notochord at 24 hpf and 30 hpf in control and verteporfin-treated embryos, showing segmented nuclei (scale bar: 50 μm). G . Quantification of posterior notochord cell density: Treatment A (t-test; control n = 10, treated n = 14; p = 0.0219); Treatment B (t-test; control n = 8, treated n = 9; p = 0.4696). H. Segmentation of notochord vacuoles in control and verteporfin-treated embryos visualized with Bodipy staining (scale bar: 50 μm). I . Quantification of vacuole area in the central notochord: Treatment A (t-test; control n = 7, treated n = 4; p = 0.00078); Treatment B (t-test; control n = 7, treated n = 7; p = 0.2406).

Journal: bioRxiv

Article Title: Long-Range Coupling of Posterior Cell Addition and Anterior Vacuolation Provides Robustness in Notochord Elongation

doi: 10.64898/2026.02.17.706348

Figure Lengend Snippet: A . Quantification of A–P axis length at 17 hpf (t-test; control n = 12, mutant n = 12; p = 0.7367), 24 hpf (t-test; control n = 10, mutant n = 11; p = 0.1232), 27 hpf (t-test; control n = 20, mutant n = 20; p = 0.0039), 30 hpf (Mann–Whitney test; control n = 16, mutant n = 19; p < 0.0001), and 36 hpf (t-test; control n = 7, mutant n = 7; p < 0.0001). The same control measurements were used in . B . Mathematical model predictions of notochord length for control and vgll4b mutant embryos at different time points. The model assumes that YAP increases progenitor addition r p and simultaneously regulates the vacuolation front speed v front , slowing the wave of vacuolation, without affecting the vacuolation rate of each notochord cell (see and in the main text). The empirical measurements shown in the graph are the same as those presented in . C . Segmentation of notochord vacuoles in control and mutant embryos at 30 hpf visualized with Bodipy staining (scale bar: 50 μm). D . Quantification of notochord vacuole area at 27 hpf (Mann–Whitney test; control n = 8, mutant n = 6; p < 0.0001), 30 hpf (t-test; control n = 8, mutant n = 7; p = 0.0083), 2 dpf (t-test; control n = 9, mutant n = 12; p = 0.0003), and 3 dpf (t-test; control n = 11, mutant n = 12; p = 0.0009). E . Schematic of verteporfin (YAP inhibitor) treatment strategy. F . Confocal images of the posterior notochord at 24 hpf and 30 hpf in control and verteporfin-treated embryos, showing segmented nuclei (scale bar: 50 μm). G . Quantification of posterior notochord cell density: Treatment A (t-test; control n = 10, treated n = 14; p = 0.0219); Treatment B (t-test; control n = 8, treated n = 9; p = 0.4696). H. Segmentation of notochord vacuoles in control and verteporfin-treated embryos visualized with Bodipy staining (scale bar: 50 μm). I . Quantification of vacuole area in the central notochord: Treatment A (t-test; control n = 7, treated n = 4; p = 0.00078); Treatment B (t-test; control n = 7, treated n = 7; p = 0.2406).

Article Snippet: For verteporfin treatment, dechorionated embryos were maintained at 28 °C in E3 medium containing either DMSO (vehicle control) or verteporfin (Tocris, 5305) dissolved in DMSO.

Techniques: Control, Mutagenesis, MANN-WHITNEY, Staining

Journal: Clinical Science (London, England : 1979)

Article Title: IGFBP7 promotes endothelial cell repair in the recovery phase of acute lung injury

doi: 10.1042/CS20240179

Figure Lengend Snippet:

Article Snippet: Verteporfin (YAP1 inhibitor) , MCE , Cat# HY-B0146.

Techniques: Recombinant, SYBR Green Assay, CCK-8 Assay, Extraction, Proliferation Assay, Immunoprecipitation

Physico-chemical and encapsulation properties of nanostructured lipid carriers (NLC).

Journal: Cancers

Article Title: Verteporfin-Loaded Lipid Nanoparticles Improve Ovarian Cancer Photodynamic Therapy In Vitro and In Vivo

doi: 10.3390/cancers11111760

Figure Lengend Snippet: Physico-chemical and encapsulation properties of nanostructured lipid carriers (NLC).

Article Snippet: Fluorescence emission of verteporfin was analyzed using flow cytometry LSRII and FCS Express software (BD Biosciences, San Jose, CA, USA).

Techniques: Concentration Assay

Verteporfin and NLC-verteporfin interact with ovarian cancer cells. Ovarian cancer SKOV3, IGROV1, and OVCAR3 cells were incubated with 1 µmol·L −1 verteporfin or NLC-verteporfin for 2 h or 24 h at 4 °C or 37 °C as indicated. ( a ) Histograms show cellular uptake assessed by flow cytometry. Black, control cells; blue, 4 °C for 2 h; green, 37 °C for 2 h; red, 37 °C for 24 h. ( b ) Median fluorescence intensity (MFI). Data are expressed as the mean ± standard deviation (SD) of three independent experiments.

Journal: Cancers

Article Title: Verteporfin-Loaded Lipid Nanoparticles Improve Ovarian Cancer Photodynamic Therapy In Vitro and In Vivo

doi: 10.3390/cancers11111760

Figure Lengend Snippet: Verteporfin and NLC-verteporfin interact with ovarian cancer cells. Ovarian cancer SKOV3, IGROV1, and OVCAR3 cells were incubated with 1 µmol·L −1 verteporfin or NLC-verteporfin for 2 h or 24 h at 4 °C or 37 °C as indicated. ( a ) Histograms show cellular uptake assessed by flow cytometry. Black, control cells; blue, 4 °C for 2 h; green, 37 °C for 2 h; red, 37 °C for 24 h. ( b ) Median fluorescence intensity (MFI). Data are expressed as the mean ± standard deviation (SD) of three independent experiments.

Article Snippet: Fluorescence emission of verteporfin was analyzed using flow cytometry LSRII and FCS Express software (BD Biosciences, San Jose, CA, USA).

Techniques: Incubation, Flow Cytometry, Fluorescence, Standard Deviation

Verteporfin and NLC-verteporfin are internalized in SKOV3 cells and spheroids. Representative confocal microscopy images of SKOV3 cells ( a ) or sections of SKOV3 spheroids ( b ), incubated with 1 µmol·L −1 verteporfin or NLC-verteporfin for 24 h. Nuclei are stained with Hoechst 33342 (in blue). Verteporfin fluorescence is observed in red. Control: untreated cells or spheroids.

Journal: Cancers

Article Title: Verteporfin-Loaded Lipid Nanoparticles Improve Ovarian Cancer Photodynamic Therapy In Vitro and In Vivo

doi: 10.3390/cancers11111760

Figure Lengend Snippet: Verteporfin and NLC-verteporfin are internalized in SKOV3 cells and spheroids. Representative confocal microscopy images of SKOV3 cells ( a ) or sections of SKOV3 spheroids ( b ), incubated with 1 µmol·L −1 verteporfin or NLC-verteporfin for 24 h. Nuclei are stained with Hoechst 33342 (in blue). Verteporfin fluorescence is observed in red. Control: untreated cells or spheroids.

Article Snippet: Fluorescence emission of verteporfin was analyzed using flow cytometry LSRII and FCS Express software (BD Biosciences, San Jose, CA, USA).

Techniques: Confocal Microscopy, Incubation, Staining, Fluorescence

Verteporfin and NLC-verteporfin mediated phototoxicity in SKOV3 and OVCAR3 cells and spheroids. SKOV3 (left panels) and OVCAR3 (right panels) cells ( a , b ) or spheroids ( c , d ) were treated with increasing concentrations of free verteporfin (in grey/black) or NLC-verteporfin (in blue) for 2 h or 24 h before NIR light exposure at 690 nm (fluency 10 J·cm −2 ). In parallel, cells or spheroids were maintained in the dark. ( a , b ) Cell viability was assessed 72 h following light exposure. Data are expressed as the mean ± SD of ≥ 3 independent experiments. ( c , d ) Cell viability in spheroids was assessed 72 h following light exposure. Data are expressed as the mean ± SD of ≥ 3 independent experiments in triplicate.

Journal: Cancers

Article Title: Verteporfin-Loaded Lipid Nanoparticles Improve Ovarian Cancer Photodynamic Therapy In Vitro and In Vivo

doi: 10.3390/cancers11111760

Figure Lengend Snippet: Verteporfin and NLC-verteporfin mediated phototoxicity in SKOV3 and OVCAR3 cells and spheroids. SKOV3 (left panels) and OVCAR3 (right panels) cells ( a , b ) or spheroids ( c , d ) were treated with increasing concentrations of free verteporfin (in grey/black) or NLC-verteporfin (in blue) for 2 h or 24 h before NIR light exposure at 690 nm (fluency 10 J·cm −2 ). In parallel, cells or spheroids were maintained in the dark. ( a , b ) Cell viability was assessed 72 h following light exposure. Data are expressed as the mean ± SD of ≥ 3 independent experiments. ( c , d ) Cell viability in spheroids was assessed 72 h following light exposure. Data are expressed as the mean ± SD of ≥ 3 independent experiments in triplicate.

Article Snippet: Fluorescence emission of verteporfin was analyzed using flow cytometry LSRII and FCS Express software (BD Biosciences, San Jose, CA, USA).

Techniques:

Sensitivity of ovarian cancer cells to verteporfin and  NLC-verteporfin.

Journal: Cancers

Article Title: Verteporfin-Loaded Lipid Nanoparticles Improve Ovarian Cancer Photodynamic Therapy In Vitro and In Vivo

doi: 10.3390/cancers11111760

Figure Lengend Snippet: Sensitivity of ovarian cancer cells to verteporfin and NLC-verteporfin.

Article Snippet: Fluorescence emission of verteporfin was analyzed using flow cytometry LSRII and FCS Express software (BD Biosciences, San Jose, CA, USA).

Techniques:

NLC circulated in the bloodstream and accumulated in subcutaneous SKOV3 tumors. ( a ) Healthy mice were injected intravenously with NLC-verteporfin (8 mg·kg −1 of verteporfin), dye-loaded NLC (LipImage TM -815), or free verteporfin (2 mg·kg −1 ). Fluorescence intensity measurements of verteporfin (for free verteporfin or NLC-verteporfin), or of LipImage TM -815 (for NLC-LipImage) were performed on blood plasma samples taken at different time points. The results are expressed as the mean ± SD ( n = 3). ( b – e ) Mice with SKOV3 subcutaneous tumors were injected intravenously with NLC-LipImage. ( b ) Representative fluorescence images (50 ms integration time) recorded using 2D-Fluorescence reflectance optical imaging (FRI) at different times after intravenous injection are shown (min-max: 4243-55869). Dotted lines show subcutaneous tumors. ( c ) Regions of interest (ROI) are defined on tumor, liver, and skin to semi-quantify the amount of photons detected per pixel. The results are expressed as the mean fluorescence ± SD in tumor, skin, and liver, and as the mean tumor/skin and tumor/liver fluorescence ratios ± SD ( n = 3). ( d ) Fluorescence images were performed on isolated organs 24 h after intravenous injection of NLC-LipImage. Representative fluorescence images of organs in injected and non-injected mice are shown (20 ms integration time; min-max: 1414-27109). ( e ) ROI are defined on the extracted organs to semi-quantify the amount of photons detected per pixel. The results are expressed as the mean ± SD in SKOV3 tumor-bearing mice ( n = 3) and non-injected mice (control). ( f ) Mice with SKOV3 subcutaneous tumors were injected intravenously with NLC-verteporfin (8 mg·kg −1 of verteporfin). Verteporfin measurements were performed by HPLC at 24 h on tumors, livers, and kidneys. The results are expressed as the mean ± SD ( n = 2).

Journal: Cancers

Article Title: Verteporfin-Loaded Lipid Nanoparticles Improve Ovarian Cancer Photodynamic Therapy In Vitro and In Vivo

doi: 10.3390/cancers11111760

Figure Lengend Snippet: NLC circulated in the bloodstream and accumulated in subcutaneous SKOV3 tumors. ( a ) Healthy mice were injected intravenously with NLC-verteporfin (8 mg·kg −1 of verteporfin), dye-loaded NLC (LipImage TM -815), or free verteporfin (2 mg·kg −1 ). Fluorescence intensity measurements of verteporfin (for free verteporfin or NLC-verteporfin), or of LipImage TM -815 (for NLC-LipImage) were performed on blood plasma samples taken at different time points. The results are expressed as the mean ± SD ( n = 3). ( b – e ) Mice with SKOV3 subcutaneous tumors were injected intravenously with NLC-LipImage. ( b ) Representative fluorescence images (50 ms integration time) recorded using 2D-Fluorescence reflectance optical imaging (FRI) at different times after intravenous injection are shown (min-max: 4243-55869). Dotted lines show subcutaneous tumors. ( c ) Regions of interest (ROI) are defined on tumor, liver, and skin to semi-quantify the amount of photons detected per pixel. The results are expressed as the mean fluorescence ± SD in tumor, skin, and liver, and as the mean tumor/skin and tumor/liver fluorescence ratios ± SD ( n = 3). ( d ) Fluorescence images were performed on isolated organs 24 h after intravenous injection of NLC-LipImage. Representative fluorescence images of organs in injected and non-injected mice are shown (20 ms integration time; min-max: 1414-27109). ( e ) ROI are defined on the extracted organs to semi-quantify the amount of photons detected per pixel. The results are expressed as the mean ± SD in SKOV3 tumor-bearing mice ( n = 3) and non-injected mice (control). ( f ) Mice with SKOV3 subcutaneous tumors were injected intravenously with NLC-verteporfin (8 mg·kg −1 of verteporfin). Verteporfin measurements were performed by HPLC at 24 h on tumors, livers, and kidneys. The results are expressed as the mean ± SD ( n = 2).

Article Snippet: Fluorescence emission of verteporfin was analyzed using flow cytometry LSRII and FCS Express software (BD Biosciences, San Jose, CA, USA).

Techniques: Injection, Fluorescence, Optical Imaging, Isolation

NLC-verteporfin improved PDT after intravenous administration in mice with ovarian cancer. ( a ) Mice with well-established SKOV3 subcutaneous tumors (125 ± 7 mm 3 ) were distributed into groups of 8 mice and treated by a single intravenous injection of free verteporfin, NLC-verteporfin or vehicle (control). Mice were maintained in the dark or submitted to a single NIR laser exposure 15 min or 24 h after injection. Non-invasive monitoring of tissue oxygenation (StO 2 ) was performed by in vivo photoacoustic imaging (Ph.ac.) on the tumors 24 h after light exposure. The tumor volume was evaluated by caliper measurements 3 times a week for 2 weeks. ( b , c ) Mice were injected with 1× PBS (control), free verteporfin (2 mg·kg −1 ), or NLC-verteporfin (2 mg·kg −1 of verteporfin), and tumors were exposed to 50 J·cm −2 light 15 min or 24 h after the injection, as indicated. Data are expressed as the relative tumor growth (% of tumor volume on the day of light exposure) ± SEM in each group ( n = 8, except in the group treated with free verteporfin and exposed to light 15 min after IV injection of verteporfin, in which 5 mice died during the experiment, as illustrated by skulls). Dotted red lines represent the tumor volume of each mouse from the group exposed to 50 J·cm −2 light, 15 min after free verteporfin injection. ( d ) Mice were intravenously injected with 1× PBS (control), or NLC-verteporfin (verteporfin 8 mg·kg −1 ), and exposed to 200 J·cm −2 light, 24 h after the injection as indicated. Data are expressed as the relative tumor growth (% of tumor volume at the day of light exposure) ± SEM in each group ( n = 8). p = 0.0003 ANOVA with Tukey post-hoc tests (**, ***, significantly different from the control group). ( e ) Hematoxylin and eosin staining on frozen tumor sections, Scale bar: 50 µm. Representative images in each group are shown.

Journal: Cancers

Article Title: Verteporfin-Loaded Lipid Nanoparticles Improve Ovarian Cancer Photodynamic Therapy In Vitro and In Vivo

doi: 10.3390/cancers11111760

Figure Lengend Snippet: NLC-verteporfin improved PDT after intravenous administration in mice with ovarian cancer. ( a ) Mice with well-established SKOV3 subcutaneous tumors (125 ± 7 mm 3 ) were distributed into groups of 8 mice and treated by a single intravenous injection of free verteporfin, NLC-verteporfin or vehicle (control). Mice were maintained in the dark or submitted to a single NIR laser exposure 15 min or 24 h after injection. Non-invasive monitoring of tissue oxygenation (StO 2 ) was performed by in vivo photoacoustic imaging (Ph.ac.) on the tumors 24 h after light exposure. The tumor volume was evaluated by caliper measurements 3 times a week for 2 weeks. ( b , c ) Mice were injected with 1× PBS (control), free verteporfin (2 mg·kg −1 ), or NLC-verteporfin (2 mg·kg −1 of verteporfin), and tumors were exposed to 50 J·cm −2 light 15 min or 24 h after the injection, as indicated. Data are expressed as the relative tumor growth (% of tumor volume on the day of light exposure) ± SEM in each group ( n = 8, except in the group treated with free verteporfin and exposed to light 15 min after IV injection of verteporfin, in which 5 mice died during the experiment, as illustrated by skulls). Dotted red lines represent the tumor volume of each mouse from the group exposed to 50 J·cm −2 light, 15 min after free verteporfin injection. ( d ) Mice were intravenously injected with 1× PBS (control), or NLC-verteporfin (verteporfin 8 mg·kg −1 ), and exposed to 200 J·cm −2 light, 24 h after the injection as indicated. Data are expressed as the relative tumor growth (% of tumor volume at the day of light exposure) ± SEM in each group ( n = 8). p = 0.0003 ANOVA with Tukey post-hoc tests (**, ***, significantly different from the control group). ( e ) Hematoxylin and eosin staining on frozen tumor sections, Scale bar: 50 µm. Representative images in each group are shown.

Article Snippet: Fluorescence emission of verteporfin was analyzed using flow cytometry LSRII and FCS Express software (BD Biosciences, San Jose, CA, USA).

Techniques: Injection, In Vivo, Imaging, IV Injection, Staining

Inhibiting YAP–TEAD interaction attenuated fenofibrate-induced hepatomegaly. (A) Schematic diagram illustrating the inhibitory effect of verteporfin on the interaction between YAP and TEAD within the Hippo signaling cascade. (B) Experimental procedure in verteporfin-treated mice. (C) Co-IP analysis between YAP and TEAD in the liver of mice treated with either vehicle or verteporfin. (D) Ratios of liver weight to body weight ( n = 5). (E) Representative photographs of mouse livers. (F) H&E, CTNNB1, and KI67 staining. (G) Quantitative analysis of cellular size and determination of KI67 + cell proportion ( n = 3). Data are depicted as the mean ± SD values; ∗/∗∗/∗∗∗/∗∗∗∗ indicates P < 0.05/0.01/0.001/0.0001, versus the Control. Scale bar = 50 μm.

Journal: Acta Pharmaceutica Sinica. B

Article Title: Fenofibrate-promoted hepatomegaly and liver regeneration are PPAR α -dependent and partially related to the YAP pathway

doi: 10.1016/j.apsb.2024.03.030

Figure Lengend Snippet: Inhibiting YAP–TEAD interaction attenuated fenofibrate-induced hepatomegaly. (A) Schematic diagram illustrating the inhibitory effect of verteporfin on the interaction between YAP and TEAD within the Hippo signaling cascade. (B) Experimental procedure in verteporfin-treated mice. (C) Co-IP analysis between YAP and TEAD in the liver of mice treated with either vehicle or verteporfin. (D) Ratios of liver weight to body weight ( n = 5). (E) Representative photographs of mouse livers. (F) H&E, CTNNB1, and KI67 staining. (G) Quantitative analysis of cellular size and determination of KI67 + cell proportion ( n = 3). Data are depicted as the mean ± SD values; ∗/∗∗/∗∗∗/∗∗∗∗ indicates P < 0.05/0.01/0.001/0.0001, versus the Control. Scale bar = 50 μm.

Article Snippet: Wild-type mice were intraperitoneally injected with 100 mg/kg/day verteporfin (CSNpharm, Cat# CSN12195, USA) or intragastrically injected with 50 mg/kg/day fenofibrate for 10 days.

Techniques: Co-Immunoprecipitation Assay, Staining, Control

Flow cytometry analysis of apoptosis and a CCK-8 assay performed with ADS JZ SMCs. a Cells were transfected with the let-7a overexpression lentiviral vector GV280 or lentiviral null vector for 72 h and then used for flow cytometry analysis. b The percentages of apoptotic cells in the lenti-GV280 group and lenti-NC group. c Verteporfin-treated cells were transfected with the let-7a overexpression lentiviral vector GV280 for 72 h and then used for flow cytometry analysis. d The percentages of apoptotic cells in the lenti-GV280 + verteporfin group and verteporfin group. e OD 450 values of the lenti-GV280 group and lenti-NC group. f OD 450 values of the lenti-GV280 + verteporfin group and verteporfin group. These experiments were performed two times with three replicates in each experiment. Significance was determined by Student’s t test; **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05

Journal: Reproductive Biology and Endocrinology : RB&E

Article Title: Upregulated microRNA let-7a accelerates apoptosis and inhibits proliferation in uterine junctional zone smooth muscle cells in adenomyosis under conditions of a normal activated hippo-YAP1 axis

doi: 10.1186/s12958-021-00753-w

Figure Lengend Snippet: Flow cytometry analysis of apoptosis and a CCK-8 assay performed with ADS JZ SMCs. a Cells were transfected with the let-7a overexpression lentiviral vector GV280 or lentiviral null vector for 72 h and then used for flow cytometry analysis. b The percentages of apoptotic cells in the lenti-GV280 group and lenti-NC group. c Verteporfin-treated cells were transfected with the let-7a overexpression lentiviral vector GV280 for 72 h and then used for flow cytometry analysis. d The percentages of apoptotic cells in the lenti-GV280 + verteporfin group and verteporfin group. e OD 450 values of the lenti-GV280 group and lenti-NC group. f OD 450 values of the lenti-GV280 + verteporfin group and verteporfin group. These experiments were performed two times with three replicates in each experiment. Significance was determined by Student’s t test; **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05

Article Snippet: Verteporfin (Beijing Solarbio Science & Technology Co., Ltd., Beijing, China) was used at a dose of 1 μM for 24 h at 37 °C to treat SMCs to block the hippo-YAP1 axis.

Techniques: Flow Cytometry, CCK-8 Assay, Transfection, Over Expression, Plasmid Preparation

The expression levels of YAP, TAZ and phospho-YAP1 in JZ SMCs in the verteporfin-ADS group and ADS group and CCK-8 assay results for the verteporfin-ADS group and negative control group. a Cells were co-cultured with 1 μM verteporfin and then used for western blotting. b The relative fold protein expression of YAP1 normalized against α-tubulin. c The relative fold protein expression of TAZ normalized against α-tubulin. d The relative fold protein expression of phospho-YAP1 normalized against α-tubulin. e Cells were treated with verteporfin, and then a CCK-8 assay was used to test the proliferative ability of ADS JZ SMCs. These experiments were performed two times with three replicates in each experiment. Significance was determined by Student’s t test; **** p < 0.0001, ** p < 0.01, * p < 0.05

Journal: Reproductive Biology and Endocrinology : RB&E

Article Title: Upregulated microRNA let-7a accelerates apoptosis and inhibits proliferation in uterine junctional zone smooth muscle cells in adenomyosis under conditions of a normal activated hippo-YAP1 axis

doi: 10.1186/s12958-021-00753-w

Figure Lengend Snippet: The expression levels of YAP, TAZ and phospho-YAP1 in JZ SMCs in the verteporfin-ADS group and ADS group and CCK-8 assay results for the verteporfin-ADS group and negative control group. a Cells were co-cultured with 1 μM verteporfin and then used for western blotting. b The relative fold protein expression of YAP1 normalized against α-tubulin. c The relative fold protein expression of TAZ normalized against α-tubulin. d The relative fold protein expression of phospho-YAP1 normalized against α-tubulin. e Cells were treated with verteporfin, and then a CCK-8 assay was used to test the proliferative ability of ADS JZ SMCs. These experiments were performed two times with three replicates in each experiment. Significance was determined by Student’s t test; **** p < 0.0001, ** p < 0.01, * p < 0.05

Article Snippet: Verteporfin (Beijing Solarbio Science & Technology Co., Ltd., Beijing, China) was used at a dose of 1 μM for 24 h at 37 °C to treat SMCs to block the hippo-YAP1 axis.

Techniques: Expressing, CCK-8 Assay, Negative Control, Cell Culture, Western Blot

Loss of SPTBN1 inhibited autophagy by activating YAP in HCC cells. A and B , QRT-PCR. Huh-7 ( A ) and PLC/PRF/5 ( B ) cells were transiently transfected with siRNA to SPTBN1 or/and YAP for 48 hours and then analyzed. YAP siRNA reversed the expression of autophagy-related genes BECN1 and ATG4B that were downregulated by SPTBN1 knockdown (n = 3; ∗ P < .05, ∗∗ P < .01 vs siCON, # P < .05, ## P < .01 vs siSPTBN1). C and D , Western blot. The decreased ratio of LC3BII/LC3B I protein was reversed by YAP siRNA in Huh-7 ( C ) and PLC/PRF/5 ( D ) cells. Significance of the mean value difference was determined using a Student t test (∗∗ P < .01 vs siCON, ## P < .01 vs siSPTBN1). E , Analysis of autophagy level by Western blot. The decreased ratio of protein LC3BII/ LC3B I was reversed by YAP inhibitor verteporfin in the Huh-7 ( upper ) and PLC/PRF/5 ( lower ) HCC cells. F , The statistical analysis of Western blot in Figure E (n = 3; ∗∗ P < .01 vs siCON, # P < .05, ## P < .01 vs siSPTBN1). G , Autophagy and autophagic flux detection by fluorescence microscopy after GFP-RFP-LC3 LV transfection and HBSS induction for 24 hours. The reduced autophagy spots in response to SPTBN1 knockdown were reversed by YAP siRNA in Huh-7 ( left ) and PLC/PRF/5 ( right ) cells. White bars represent 10 μm.

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Loss of SPTBN1 Suppresses Autophagy Via SETD7-mediated YAP Methylation in Hepatocellular Carcinoma Initiation and Development

doi: 10.1016/j.jcmgh.2021.10.012

Figure Lengend Snippet: Loss of SPTBN1 inhibited autophagy by activating YAP in HCC cells. A and B , QRT-PCR. Huh-7 ( A ) and PLC/PRF/5 ( B ) cells were transiently transfected with siRNA to SPTBN1 or/and YAP for 48 hours and then analyzed. YAP siRNA reversed the expression of autophagy-related genes BECN1 and ATG4B that were downregulated by SPTBN1 knockdown (n = 3; ∗ P < .05, ∗∗ P < .01 vs siCON, # P < .05, ## P < .01 vs siSPTBN1). C and D , Western blot. The decreased ratio of LC3BII/LC3B I protein was reversed by YAP siRNA in Huh-7 ( C ) and PLC/PRF/5 ( D ) cells. Significance of the mean value difference was determined using a Student t test (∗∗ P < .01 vs siCON, ## P < .01 vs siSPTBN1). E , Analysis of autophagy level by Western blot. The decreased ratio of protein LC3BII/ LC3B I was reversed by YAP inhibitor verteporfin in the Huh-7 ( upper ) and PLC/PRF/5 ( lower ) HCC cells. F , The statistical analysis of Western blot in Figure E (n = 3; ∗∗ P < .01 vs siCON, # P < .05, ## P < .01 vs siSPTBN1). G , Autophagy and autophagic flux detection by fluorescence microscopy after GFP-RFP-LC3 LV transfection and HBSS induction for 24 hours. The reduced autophagy spots in response to SPTBN1 knockdown were reversed by YAP siRNA in Huh-7 ( left ) and PLC/PRF/5 ( right ) cells. White bars represent 10 μm.

Article Snippet: Cells were also treated with the YAP inhibitor verteporfin (10 μM, APExBIO, Houston, TX) after SPTBN1 siRNA transfection.

Techniques: Quantitative RT-PCR, Transfection, Expressing, Knockdown, Western Blot, Fluorescence, Microscopy