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Microglial displacement facilitates the Ang-II-induced effect of disinhibition on glutaminergic neurons in the PVN. A – C Representative images of PVN neurons and nearby cells, via transmission electron microscopy. ( A ) the microglia and neuron are illustrated by pseudo colors, red for neuron and green for microglia; Scale bar, 10 μm; ( B ) GABA stained by colloidal gold particles in microglia, as indicated in pseudo color (light blue); Scale bar, 5 μm; ( C ) GABA stained by colloidal gold particles outside of the microglia. Scale bar, 1 μm. D The AAV injection sites and a representative image of the BSTM (bed nucleus of the stria terminalis, medial division), where the neuro-tracing virus was injected. Scale bar, 50 μm. E Representative images of glutamatergic PVN-RVLM projecting neurons (PSN, green), PV + presynaptic terminals (red), and microglia (cyan) in the PVN, showing a close spatial relationship among these cells. 3D reconstruction with z-stacked images by Imaris 9. Scale bar, as indicated. F Representative immunofluorescent image of NeuN nuclei (white), Iba1 (green), and VGAT + puncta (red) in the PVN prepared 30 min following Ang-II/saline injection. Yellow arrows in the main panel and orthogonal panels indicate sites of microglial bulbous tip contact with VGAT + terminals. Scale bar, 2 μm. G Percentage of Iba1 processes colocalizing with VGAT + puncta ( n = 4 mice). Data are expressed as the mean ± SEM. (vehicle+Ang-II vs vehicle+saline, ns, no significant difference, *** P <0.001, unpaired Student’s t -test). H Representative traces of miniature IPSCs (mIPSCs) in PVN-RVLM projecting neurons from sections with Ang-II bath application and without <t>TRAM34</t> pretreatment (a selective blocker of IKCa1 to inhibit microglial migration, 1 μmol/L, 30 min before Ang-II, no wash). I, J Summary of amplitude ( I ) and frequency ( J ) of mIPSCs before and after Ang-II application, in the presence of TRAM34 ( n = 5 mice/group. After vs Before, ** P <0.01, paired Student’s t -test). K Suppression ratio of Ang-II-induced reduction of mIPSC frequency, in the presence of TRAM34 (A17G vs WT, *** P <0.001, unpaired Student’s t -test; WT+TRAM34 vs WT, ††† P <0.001)
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Microglial displacement facilitates the Ang-II-induced effect of disinhibition on glutaminergic neurons in the PVN. A – C Representative images of PVN neurons and nearby cells, via transmission electron microscopy. ( A ) the microglia and neuron are illustrated by pseudo colors, red for neuron and green for microglia; Scale bar, 10 μm; ( B ) GABA stained by colloidal gold particles in microglia, as indicated in pseudo color (light blue); Scale bar, 5 μm; ( C ) GABA stained by colloidal gold particles outside of the microglia. Scale bar, 1 μm. D The AAV injection sites and a representative image of the BSTM (bed nucleus of the stria terminalis, medial division), where the neuro-tracing virus was injected. Scale bar, 50 μm. E Representative images of glutamatergic PVN-RVLM projecting neurons (PSN, green), PV + presynaptic terminals (red), and microglia (cyan) in the PVN, showing a close spatial relationship among these cells. 3D reconstruction with z-stacked images by Imaris 9. Scale bar, as indicated. F Representative immunofluorescent image of NeuN nuclei (white), Iba1 (green), and VGAT + puncta (red) in the PVN prepared 30 min following Ang-II/saline injection. Yellow arrows in the main panel and orthogonal panels indicate sites of microglial bulbous tip contact with VGAT + terminals. Scale bar, 2 μm. G Percentage of Iba1 processes colocalizing with VGAT + puncta ( n = 4 mice). Data are expressed as the mean ± SEM. (vehicle+Ang-II vs vehicle+saline, ns, no significant difference, *** P <0.001, unpaired Student’s t -test). H Representative traces of miniature IPSCs (mIPSCs) in PVN-RVLM projecting neurons from sections with Ang-II bath application and without <t>TRAM34</t> pretreatment (a selective blocker of IKCa1 to inhibit microglial migration, 1 μmol/L, 30 min before Ang-II, no wash). I, J Summary of amplitude ( I ) and frequency ( J ) of mIPSCs before and after Ang-II application, in the presence of TRAM34 ( n = 5 mice/group. After vs Before, ** P <0.01, paired Student’s t -test). K Suppression ratio of Ang-II-induced reduction of mIPSC frequency, in the presence of TRAM34 (A17G vs WT, *** P <0.001, unpaired Student’s t -test; WT+TRAM34 vs WT, ††† P <0.001)
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Microglial displacement facilitates the Ang-II-induced effect of disinhibition on glutaminergic neurons in the PVN. A – C Representative images of PVN neurons and nearby cells, via transmission electron microscopy. ( A ) the microglia and neuron are illustrated by pseudo colors, red for neuron and green for microglia; Scale bar, 10 μm; ( B ) GABA stained by colloidal gold particles in microglia, as indicated in pseudo color (light blue); Scale bar, 5 μm; ( C ) GABA stained by colloidal gold particles outside of the microglia. Scale bar, 1 μm. D The AAV injection sites and a representative image of the BSTM (bed nucleus of the stria terminalis, medial division), where the neuro-tracing virus was injected. Scale bar, 50 μm. E Representative images of glutamatergic PVN-RVLM projecting neurons (PSN, green), PV + presynaptic terminals (red), and microglia (cyan) in the PVN, showing a close spatial relationship among these cells. 3D reconstruction with z-stacked images by Imaris 9. Scale bar, as indicated. F Representative immunofluorescent image of NeuN nuclei (white), Iba1 (green), and VGAT + puncta (red) in the PVN prepared 30 min following Ang-II/saline injection. Yellow arrows in the main panel and orthogonal panels indicate sites of microglial bulbous tip contact with VGAT + terminals. Scale bar, 2 μm. G Percentage of Iba1 processes colocalizing with VGAT + puncta ( n = 4 mice). Data are expressed as the mean ± SEM. (vehicle+Ang-II vs vehicle+saline, ns, no significant difference, *** P <0.001, unpaired Student’s t -test). H Representative traces of miniature IPSCs (mIPSCs) in PVN-RVLM projecting neurons from sections with Ang-II bath application and without <t>TRAM34</t> pretreatment (a selective blocker of IKCa1 to inhibit microglial migration, 1 μmol/L, 30 min before Ang-II, no wash). I, J Summary of amplitude ( I ) and frequency ( J ) of mIPSCs before and after Ang-II application, in the presence of TRAM34 ( n = 5 mice/group. After vs Before, ** P <0.01, paired Student’s t -test). K Suppression ratio of Ang-II-induced reduction of mIPSC frequency, in the presence of TRAM34 (A17G vs WT, *** P <0.001, unpaired Student’s t -test; WT+TRAM34 vs WT, ††† P <0.001)
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Microglial displacement facilitates the Ang-II-induced effect of disinhibition on glutaminergic neurons in the PVN. A – C Representative images of PVN neurons and nearby cells, via transmission electron microscopy. ( A ) the microglia and neuron are illustrated by pseudo colors, red for neuron and green for microglia; Scale bar, 10 μm; ( B ) GABA stained by colloidal gold particles in microglia, as indicated in pseudo color (light blue); Scale bar, 5 μm; ( C ) GABA stained by colloidal gold particles outside of the microglia. Scale bar, 1 μm. D The AAV injection sites and a representative image of the BSTM (bed nucleus of the stria terminalis, medial division), where the neuro-tracing virus was injected. Scale bar, 50 μm. E Representative images of glutamatergic PVN-RVLM projecting neurons (PSN, green), PV + presynaptic terminals (red), and microglia (cyan) in the PVN, showing a close spatial relationship among these cells. 3D reconstruction with z-stacked images by Imaris 9. Scale bar, as indicated. F Representative immunofluorescent image of NeuN nuclei (white), Iba1 (green), and VGAT + puncta (red) in the PVN prepared 30 min following Ang-II/saline injection. Yellow arrows in the main panel and orthogonal panels indicate sites of microglial bulbous tip contact with VGAT + terminals. Scale bar, 2 μm. G Percentage of Iba1 processes colocalizing with VGAT + puncta ( n = 4 mice). Data are expressed as the mean ± SEM. (vehicle+Ang-II vs vehicle+saline, ns, no significant difference, *** P <0.001, unpaired Student’s t -test). H Representative traces of miniature IPSCs (mIPSCs) in PVN-RVLM projecting neurons from sections with Ang-II bath application and without <t>TRAM34</t> pretreatment (a selective blocker of IKCa1 to inhibit microglial migration, 1 μmol/L, 30 min before Ang-II, no wash). I, J Summary of amplitude ( I ) and frequency ( J ) of mIPSCs before and after Ang-II application, in the presence of TRAM34 ( n = 5 mice/group. After vs Before, ** P <0.01, paired Student’s t -test). K Suppression ratio of Ang-II-induced reduction of mIPSC frequency, in the presence of TRAM34 (A17G vs WT, *** P <0.001, unpaired Student’s t -test; WT+TRAM34 vs WT, ††† P <0.001)
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Microglial displacement facilitates the Ang-II-induced effect of disinhibition on glutaminergic neurons in the PVN. A – C Representative images of PVN neurons and nearby cells, via transmission electron microscopy. ( A ) the microglia and neuron are illustrated by pseudo colors, red for neuron and green for microglia; Scale bar, 10 μm; ( B ) GABA stained by colloidal gold particles in microglia, as indicated in pseudo color (light blue); Scale bar, 5 μm; ( C ) GABA stained by colloidal gold particles outside of the microglia. Scale bar, 1 μm. D The AAV injection sites and a representative image of the BSTM (bed nucleus of the stria terminalis, medial division), where the neuro-tracing virus was injected. Scale bar, 50 μm. E Representative images of glutamatergic PVN-RVLM projecting neurons (PSN, green), PV + presynaptic terminals (red), and microglia (cyan) in the PVN, showing a close spatial relationship among these cells. 3D reconstruction with z-stacked images by Imaris 9. Scale bar, as indicated. F Representative immunofluorescent image of NeuN nuclei (white), Iba1 (green), and VGAT + puncta (red) in the PVN prepared 30 min following Ang-II/saline injection. Yellow arrows in the main panel and orthogonal panels indicate sites of microglial bulbous tip contact with VGAT + terminals. Scale bar, 2 μm. G Percentage of Iba1 processes colocalizing with VGAT + puncta ( n = 4 mice). Data are expressed as the mean ± SEM. (vehicle+Ang-II vs vehicle+saline, ns, no significant difference, *** P <0.001, unpaired Student’s t -test). H Representative traces of miniature IPSCs (mIPSCs) in PVN-RVLM projecting neurons from sections with Ang-II bath application and without <t>TRAM34</t> pretreatment (a selective blocker of IKCa1 to inhibit microglial migration, 1 μmol/L, 30 min before Ang-II, no wash). I, J Summary of amplitude ( I ) and frequency ( J ) of mIPSCs before and after Ang-II application, in the presence of TRAM34 ( n = 5 mice/group. After vs Before, ** P <0.01, paired Student’s t -test). K Suppression ratio of Ang-II-induced reduction of mIPSC frequency, in the presence of TRAM34 (A17G vs WT, *** P <0.001, unpaired Student’s t -test; WT+TRAM34 vs WT, ††† P <0.001)
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Comparison of molecular pathological markers in luteinized thecoma associated with sclerosing peritonitis and thecoma.
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Comparison of molecular pathological markers in luteinized thecoma associated with sclerosing peritonitis and thecoma.
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Comparison of molecular pathological markers in luteinized thecoma associated with sclerosing peritonitis and thecoma.
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Comparison of molecular pathological markers in luteinized thecoma associated with sclerosing peritonitis and thecoma.
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Comparison of molecular pathological markers in luteinized thecoma associated with sclerosing peritonitis and thecoma.
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Comparison of molecular pathological markers in luteinized thecoma associated with sclerosing peritonitis and thecoma.
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Comparison of molecular pathological markers in luteinized thecoma associated with sclerosing peritonitis and thecoma.
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Image Search Results


Microglial displacement facilitates the Ang-II-induced effect of disinhibition on glutaminergic neurons in the PVN. A – C Representative images of PVN neurons and nearby cells, via transmission electron microscopy. ( A ) the microglia and neuron are illustrated by pseudo colors, red for neuron and green for microglia; Scale bar, 10 μm; ( B ) GABA stained by colloidal gold particles in microglia, as indicated in pseudo color (light blue); Scale bar, 5 μm; ( C ) GABA stained by colloidal gold particles outside of the microglia. Scale bar, 1 μm. D The AAV injection sites and a representative image of the BSTM (bed nucleus of the stria terminalis, medial division), where the neuro-tracing virus was injected. Scale bar, 50 μm. E Representative images of glutamatergic PVN-RVLM projecting neurons (PSN, green), PV + presynaptic terminals (red), and microglia (cyan) in the PVN, showing a close spatial relationship among these cells. 3D reconstruction with z-stacked images by Imaris 9. Scale bar, as indicated. F Representative immunofluorescent image of NeuN nuclei (white), Iba1 (green), and VGAT + puncta (red) in the PVN prepared 30 min following Ang-II/saline injection. Yellow arrows in the main panel and orthogonal panels indicate sites of microglial bulbous tip contact with VGAT + terminals. Scale bar, 2 μm. G Percentage of Iba1 processes colocalizing with VGAT + puncta ( n = 4 mice). Data are expressed as the mean ± SEM. (vehicle+Ang-II vs vehicle+saline, ns, no significant difference, *** P <0.001, unpaired Student’s t -test). H Representative traces of miniature IPSCs (mIPSCs) in PVN-RVLM projecting neurons from sections with Ang-II bath application and without TRAM34 pretreatment (a selective blocker of IKCa1 to inhibit microglial migration, 1 μmol/L, 30 min before Ang-II, no wash). I, J Summary of amplitude ( I ) and frequency ( J ) of mIPSCs before and after Ang-II application, in the presence of TRAM34 ( n = 5 mice/group. After vs Before, ** P <0.01, paired Student’s t -test). K Suppression ratio of Ang-II-induced reduction of mIPSC frequency, in the presence of TRAM34 (A17G vs WT, *** P <0.001, unpaired Student’s t -test; WT+TRAM34 vs WT, ††† P <0.001)

Journal: Neuroscience Bulletin

Article Title: ADAM17 Supports Disinhibition of Pre-sympathetic Glutamatergic Neurons Through Microglial Chemotaxis

doi: 10.1007/s12264-025-01471-8

Figure Lengend Snippet: Microglial displacement facilitates the Ang-II-induced effect of disinhibition on glutaminergic neurons in the PVN. A – C Representative images of PVN neurons and nearby cells, via transmission electron microscopy. ( A ) the microglia and neuron are illustrated by pseudo colors, red for neuron and green for microglia; Scale bar, 10 μm; ( B ) GABA stained by colloidal gold particles in microglia, as indicated in pseudo color (light blue); Scale bar, 5 μm; ( C ) GABA stained by colloidal gold particles outside of the microglia. Scale bar, 1 μm. D The AAV injection sites and a representative image of the BSTM (bed nucleus of the stria terminalis, medial division), where the neuro-tracing virus was injected. Scale bar, 50 μm. E Representative images of glutamatergic PVN-RVLM projecting neurons (PSN, green), PV + presynaptic terminals (red), and microglia (cyan) in the PVN, showing a close spatial relationship among these cells. 3D reconstruction with z-stacked images by Imaris 9. Scale bar, as indicated. F Representative immunofluorescent image of NeuN nuclei (white), Iba1 (green), and VGAT + puncta (red) in the PVN prepared 30 min following Ang-II/saline injection. Yellow arrows in the main panel and orthogonal panels indicate sites of microglial bulbous tip contact with VGAT + terminals. Scale bar, 2 μm. G Percentage of Iba1 processes colocalizing with VGAT + puncta ( n = 4 mice). Data are expressed as the mean ± SEM. (vehicle+Ang-II vs vehicle+saline, ns, no significant difference, *** P <0.001, unpaired Student’s t -test). H Representative traces of miniature IPSCs (mIPSCs) in PVN-RVLM projecting neurons from sections with Ang-II bath application and without TRAM34 pretreatment (a selective blocker of IKCa1 to inhibit microglial migration, 1 μmol/L, 30 min before Ang-II, no wash). I, J Summary of amplitude ( I ) and frequency ( J ) of mIPSCs before and after Ang-II application, in the presence of TRAM34 ( n = 5 mice/group. After vs Before, ** P <0.01, paired Student’s t -test). K Suppression ratio of Ang-II-induced reduction of mIPSC frequency, in the presence of TRAM34 (A17G vs WT, *** P <0.001, unpaired Student’s t -test; WT+TRAM34 vs WT, ††† P <0.001)

Article Snippet: In the inhibitor group, TRAM34 (Cat.# HY-13519, MCE, China) and AZD8797 (Cat.# 2255, Axon Medchem, The Netherlands) were given 30 min before Ang-II (Cat.# 4006473, BCHEM, USA).

Techniques: Transmission Assay, Electron Microscopy, Staining, Injection, Virus, Saline, Migration

Pharmacologically blocking the CX3CL1/CX3CR1 chemotactic pathway blunts the Ang-II-induced pressor response. A Location of Cx3cl1 mRNA expression based on the single-nuclei RNA-seq data collected from the PVN and adjacent tissue. Upper panel: mRNA location; lower panel: UMAP for individual cell clusters. B , C Schematic and image of the administration route for Ang-II or antagonists. Scale bar, 50 μm. D Representative blood pressure (BP) recording traces from awake WT mice. E Summary data of the BP increase (mean arterial pressure, ΔMAP) in awake WT mice undergoing Ang-II injection (100 ng/100 nL) into the PVN with or without injection of AZD8797 (a selective blocker of CX3CR1, 5 μmol/L per 100 nL, 30 min before Ang-II injection); and with or without injection of TRAM34 (a selective blocker of IKCa1 to inhibit microglial migration, 10 mg/kg in 100 nL, 30 min before Ang-II injection). F Representative BP recordings from anesthetized WT mice. G Summary data of BP increase (ΔMAP) in anesthetized WT mice undergoing Ang-II injection (100 ng/100 nL) into the PVN with or without injection of AZD8797 (5 μmol/L per 100nL, 30 min before Ang-II injection); and with or without injection of TRAM34 (10 mg/kg in 100 nL, 30 min before Ang-II injection). Each data point represents an individual mouse, n = 7–9 mice. Data are shown as the mean ± SEM. * P <0.05, ** P <0.01, *** P <0.001 vs Ang-II, one-way ANOVA followed by Dunnett post tests

Journal: Neuroscience Bulletin

Article Title: ADAM17 Supports Disinhibition of Pre-sympathetic Glutamatergic Neurons Through Microglial Chemotaxis

doi: 10.1007/s12264-025-01471-8

Figure Lengend Snippet: Pharmacologically blocking the CX3CL1/CX3CR1 chemotactic pathway blunts the Ang-II-induced pressor response. A Location of Cx3cl1 mRNA expression based on the single-nuclei RNA-seq data collected from the PVN and adjacent tissue. Upper panel: mRNA location; lower panel: UMAP for individual cell clusters. B , C Schematic and image of the administration route for Ang-II or antagonists. Scale bar, 50 μm. D Representative blood pressure (BP) recording traces from awake WT mice. E Summary data of the BP increase (mean arterial pressure, ΔMAP) in awake WT mice undergoing Ang-II injection (100 ng/100 nL) into the PVN with or without injection of AZD8797 (a selective blocker of CX3CR1, 5 μmol/L per 100 nL, 30 min before Ang-II injection); and with or without injection of TRAM34 (a selective blocker of IKCa1 to inhibit microglial migration, 10 mg/kg in 100 nL, 30 min before Ang-II injection). F Representative BP recordings from anesthetized WT mice. G Summary data of BP increase (ΔMAP) in anesthetized WT mice undergoing Ang-II injection (100 ng/100 nL) into the PVN with or without injection of AZD8797 (5 μmol/L per 100nL, 30 min before Ang-II injection); and with or without injection of TRAM34 (10 mg/kg in 100 nL, 30 min before Ang-II injection). Each data point represents an individual mouse, n = 7–9 mice. Data are shown as the mean ± SEM. * P <0.05, ** P <0.01, *** P <0.001 vs Ang-II, one-way ANOVA followed by Dunnett post tests

Article Snippet: In the inhibitor group, TRAM34 (Cat.# HY-13519, MCE, China) and AZD8797 (Cat.# 2255, Axon Medchem, The Netherlands) were given 30 min before Ang-II (Cat.# 4006473, BCHEM, USA).

Techniques: Blocking Assay, Expressing, RNA Sequencing, Injection, Migration

Comparison of molecular pathological markers in luteinized thecoma associated with sclerosing peritonitis and thecoma.

Journal: Medicine

Article Title: Pathological discrimination between luteinized thecoma associated with sclerosing peritonitis and thecoma

doi: 10.1097/MD.0000000000033911

Figure Lengend Snippet: Comparison of molecular pathological markers in luteinized thecoma associated with sclerosing peritonitis and thecoma.

Article Snippet: The tissue sections were stained for MGAT5B (1:200; catalog number 16993; Proteintech, Wuhan, China), NCOA3 (1:50, catalog number 20032, Proteintech), Vimentin (1:200, catalog number 10366, Proteintech), Catenin beta-1 (β-Catenin; 1:200, catalog number 17565, Proteintech), receptor tyrosine-protein kinase erbB-2 (HER2; 1:600, catalog number 18299, Proteintech), proliferation marker protein Ki-67 (MKI67; 1:5000, catalog number 27309, Proteintech), estrogen receptor (ESR; 1:200, catalog number 21244, Proteintech), progesterone receptor (PGR; 1:200, catalog number 25871, Proteintech), CD99 antigen (CD99; 1:200; catalog number abs136282; Absin, Shanghai, China), Wilms tumor protein (WT1; 1:200, catalog number abs135851, Absin), and hematoxylin-eosin as follows.

Techniques: Comparison

Molecular pathological markers show significant ascendant expression in LTSP. (A–F) Immunohistochemical staining of alpha-1,6-mannosylglycoprotein 6-beta- n -acetylglucosaminyltransferase B (MGAT5B), nuclear receptor coactivator 3 (NCOA3) and proliferation marker protein Ki-67 (MKI67) are respectively (A, C, E) diffusely positive in the luteinized cells but (B, D, F) weak to moderate in the thecoma cells. (G) Statistical analysis of the 3 markers. Data are expressed as mean ± SD. n = 9 to 11 sections per marker (G, LTSP); n = 81 to 85 sections per marker (G, Thecoma). *** P < .001 ( t test). Scale bar, 500 μm. AOD = average optical density, LTSP = luteinized thecoma associated with sclerosing peritonitis.

Journal: Medicine

Article Title: Pathological discrimination between luteinized thecoma associated with sclerosing peritonitis and thecoma

doi: 10.1097/MD.0000000000033911

Figure Lengend Snippet: Molecular pathological markers show significant ascendant expression in LTSP. (A–F) Immunohistochemical staining of alpha-1,6-mannosylglycoprotein 6-beta- n -acetylglucosaminyltransferase B (MGAT5B), nuclear receptor coactivator 3 (NCOA3) and proliferation marker protein Ki-67 (MKI67) are respectively (A, C, E) diffusely positive in the luteinized cells but (B, D, F) weak to moderate in the thecoma cells. (G) Statistical analysis of the 3 markers. Data are expressed as mean ± SD. n = 9 to 11 sections per marker (G, LTSP); n = 81 to 85 sections per marker (G, Thecoma). *** P < .001 ( t test). Scale bar, 500 μm. AOD = average optical density, LTSP = luteinized thecoma associated with sclerosing peritonitis.

Article Snippet: The tissue sections were stained for MGAT5B (1:200; catalog number 16993; Proteintech, Wuhan, China), NCOA3 (1:50, catalog number 20032, Proteintech), Vimentin (1:200, catalog number 10366, Proteintech), Catenin beta-1 (β-Catenin; 1:200, catalog number 17565, Proteintech), receptor tyrosine-protein kinase erbB-2 (HER2; 1:600, catalog number 18299, Proteintech), proliferation marker protein Ki-67 (MKI67; 1:5000, catalog number 27309, Proteintech), estrogen receptor (ESR; 1:200, catalog number 21244, Proteintech), progesterone receptor (PGR; 1:200, catalog number 25871, Proteintech), CD99 antigen (CD99; 1:200; catalog number abs136282; Absin, Shanghai, China), Wilms tumor protein (WT1; 1:200, catalog number abs135851, Absin), and hematoxylin-eosin as follows.

Techniques: Expressing, Immunohistochemical staining, Staining, Marker

MGAT5B-NCOA3 fusion gene in LTSP of the ovary. Schematic representation of the MGAT5B-NCOA3 fusion transcript including the exons and bases sequence involved. The breakpoint of the 5′ and 3′ partner genes are represented as red dotted lines. LTSP = luteinized thecoma associated with sclerosing peritonitis, MGAT5B = alpha-1,6-mannosylglycoprotein 6-beta- n -acetylglucosaminyltransferase B, NCOA3 = nuclear receptor coactivator 3.

Journal: Medicine

Article Title: Pathological discrimination between luteinized thecoma associated with sclerosing peritonitis and thecoma

doi: 10.1097/MD.0000000000033911

Figure Lengend Snippet: MGAT5B-NCOA3 fusion gene in LTSP of the ovary. Schematic representation of the MGAT5B-NCOA3 fusion transcript including the exons and bases sequence involved. The breakpoint of the 5′ and 3′ partner genes are represented as red dotted lines. LTSP = luteinized thecoma associated with sclerosing peritonitis, MGAT5B = alpha-1,6-mannosylglycoprotein 6-beta- n -acetylglucosaminyltransferase B, NCOA3 = nuclear receptor coactivator 3.

Article Snippet: The tissue sections were stained for MGAT5B (1:200; catalog number 16993; Proteintech, Wuhan, China), NCOA3 (1:50, catalog number 20032, Proteintech), Vimentin (1:200, catalog number 10366, Proteintech), Catenin beta-1 (β-Catenin; 1:200, catalog number 17565, Proteintech), receptor tyrosine-protein kinase erbB-2 (HER2; 1:600, catalog number 18299, Proteintech), proliferation marker protein Ki-67 (MKI67; 1:5000, catalog number 27309, Proteintech), estrogen receptor (ESR; 1:200, catalog number 21244, Proteintech), progesterone receptor (PGR; 1:200, catalog number 25871, Proteintech), CD99 antigen (CD99; 1:200; catalog number abs136282; Absin, Shanghai, China), Wilms tumor protein (WT1; 1:200, catalog number abs135851, Absin), and hematoxylin-eosin as follows.

Techniques: Sequencing

MGAT5B-NCOA3 fusion gene is most common in LTSP. (A–C) MGAT5B-NCOA3 fusion gene is most common in (A) luteinized cells, but (B) rare in thecoma cells and (C) normal fimbriae tubae cells as assessed by FISH. FISH showing fusion signals for MGAT5B-NCOA3 with the overlapping yellow fluorescent signal (white arrows: orange, NCOA3; green, MGAT5B; yellow, fusion area). (D) Statistical analysis of positive incidence. Data are expressed as mean ± SD percentage. n = 7 cases (D, LTSP); n = 5 cases (D, Thecoma); n = 2 cases (D, Control). *** P < .001 (one-way analysis of variance and post hoc test). Scale bar, 250 μm. FISH = fluorescence in situ hybridization, LTSP = luteinized thecoma associated with sclerosing peritonitis, MGAT5B = alpha-1,6-mannosylglycoprotein 6-beta- n -acetylglucosaminyltransferase B, NCOA3 = nuclear receptor coactivator 3, ns = no significance.

Journal: Medicine

Article Title: Pathological discrimination between luteinized thecoma associated with sclerosing peritonitis and thecoma

doi: 10.1097/MD.0000000000033911

Figure Lengend Snippet: MGAT5B-NCOA3 fusion gene is most common in LTSP. (A–C) MGAT5B-NCOA3 fusion gene is most common in (A) luteinized cells, but (B) rare in thecoma cells and (C) normal fimbriae tubae cells as assessed by FISH. FISH showing fusion signals for MGAT5B-NCOA3 with the overlapping yellow fluorescent signal (white arrows: orange, NCOA3; green, MGAT5B; yellow, fusion area). (D) Statistical analysis of positive incidence. Data are expressed as mean ± SD percentage. n = 7 cases (D, LTSP); n = 5 cases (D, Thecoma); n = 2 cases (D, Control). *** P < .001 (one-way analysis of variance and post hoc test). Scale bar, 250 μm. FISH = fluorescence in situ hybridization, LTSP = luteinized thecoma associated with sclerosing peritonitis, MGAT5B = alpha-1,6-mannosylglycoprotein 6-beta- n -acetylglucosaminyltransferase B, NCOA3 = nuclear receptor coactivator 3, ns = no significance.

Article Snippet: The tissue sections were stained for MGAT5B (1:200; catalog number 16993; Proteintech, Wuhan, China), NCOA3 (1:50, catalog number 20032, Proteintech), Vimentin (1:200, catalog number 10366, Proteintech), Catenin beta-1 (β-Catenin; 1:200, catalog number 17565, Proteintech), receptor tyrosine-protein kinase erbB-2 (HER2; 1:600, catalog number 18299, Proteintech), proliferation marker protein Ki-67 (MKI67; 1:5000, catalog number 27309, Proteintech), estrogen receptor (ESR; 1:200, catalog number 21244, Proteintech), progesterone receptor (PGR; 1:200, catalog number 25871, Proteintech), CD99 antigen (CD99; 1:200; catalog number abs136282; Absin, Shanghai, China), Wilms tumor protein (WT1; 1:200, catalog number abs135851, Absin), and hematoxylin-eosin as follows.

Techniques: Control, Fluorescence, In Situ Hybridization