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a , Immunofluorescence of NeuN and PGE2 receptors in the cerebral cortex showing neuronal expression of Ptger1, <t>Ptger2,</t> Ptger3 and Ptger4 in the adult mouse brain. Scale bar: 50 μm. Same staining was repeated independently in more than 3 mice with similar results. b , Immunofluorescence showing expression of Ptger1, Ptger2, Ptger3 and Ptger4 in primary neuronal cultures (3 weeks in vitro). Ptger2 is mainly located in the neuronal cell body; Ptger1, Ptger3 and Ptger4 are located in both the neuronal cell body and neuronal processes. Scale bar: 50 μm. Same staining was repeated independently in more than 3 batches of primary neuron preparations with similar results.
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Image Search Results


a , Immunofluorescence of NeuN and PGE2 receptors in the cerebral cortex showing neuronal expression of Ptger1, Ptger2, Ptger3 and Ptger4 in the adult mouse brain. Scale bar: 50 μm. Same staining was repeated independently in more than 3 mice with similar results. b , Immunofluorescence showing expression of Ptger1, Ptger2, Ptger3 and Ptger4 in primary neuronal cultures (3 weeks in vitro). Ptger2 is mainly located in the neuronal cell body; Ptger1, Ptger3 and Ptger4 are located in both the neuronal cell body and neuronal processes. Scale bar: 50 μm. Same staining was repeated independently in more than 3 batches of primary neuron preparations with similar results.

Journal: Nature Neuroscience

Article Title: NG2 glia protect against prion neurotoxicity by inhibiting microglia-to-neuron prostaglandin E2 signaling

doi: 10.1038/s41593-024-01663-x

Figure Lengend Snippet: a , Immunofluorescence of NeuN and PGE2 receptors in the cerebral cortex showing neuronal expression of Ptger1, Ptger2, Ptger3 and Ptger4 in the adult mouse brain. Scale bar: 50 μm. Same staining was repeated independently in more than 3 mice with similar results. b , Immunofluorescence showing expression of Ptger1, Ptger2, Ptger3 and Ptger4 in primary neuronal cultures (3 weeks in vitro). Ptger2 is mainly located in the neuronal cell body; Ptger1, Ptger3 and Ptger4 are located in both the neuronal cell body and neuronal processes. Scale bar: 50 μm. Same staining was repeated independently in more than 3 batches of primary neuron preparations with similar results.

Article Snippet: Lenti-vectors used for expressing human PGE2 receptors EP1 (pLenti-PTGER1-mGFP-P2A-Puro, cat. no. RC208597L4), EP2 (pLenti-PTGER2-mGFP-P2A-Puro, cat. no. RC210883L4), EP3 (pLenti-PTGER3-mGFP-P2A-Puro, cat. no. RC220173L4) and EP4 (pLenti-PTGER4-mGFP-P2A-Puro, cat. no. RC210932L4) were purchased from OriGene Technologies.

Techniques: Immunofluorescence, Expressing, Staining, In Vitro

a , b , Live-cell imaging ( a ) and quantitative analysis ( b ) of chronically prion-infected HovS cells expressing control (Ctrl) transgene or one of the four PGE2 receptors (Ptger1–4). Effects of PGE2 treatment on prion-induced cell toxicity were measured with the ratio of GFP signals under the PGE2 condition against the DMSO condition; n = 4 independent experiments. Data are presented as mean ± s.e.m. One-way ANOVA with Benjamini–Hochberg FDR adjustment for multiple comparisons: P < 0.0001 (Ptger1 versus Ctrl); P = 0.2246 (Ptger2 versus Ctrl); P = 0.3351 (Ptger3 versus Ctrl); P < 0.0001 (Ptger4 versus Ctrl). c , Immunofluorescence of NeuN, Map2 and Tau showing cellular damage of prion-infected primary neurons treated with different concentrations of Ptger4 agonist L902688. d , Quantification of neuronal density as well as Map2-positive and Tau positive areas shown in c ; n = 6 independent experiments. Data are presented as mean ± s.e.m. One-way ANOVA with Benjamini–Hochberg FDR adjustment for multiple comparisons. NeuN: P = 0.0150 (1 μM versus 0 μM); P < 0.0001 (5 μM versus 0 μM); P < 0.0001 (10 μM versus 0 μM). Map2: P = 0.0020 (1 μM versus 0 μM); P < 0.0001 (5 μM versus 0 μM); P < 0.0001 (10 μM versus 0 μM). Tau: P = 0.0005 (1 μM versus 0 μM); P < 0.0001 (5 μM versus 0 μM); P < 0.0001 (10 μM versus 0 μM). e , f , NeuN immunofluorescence ( e ) and quantification ( f ) showing concentration-dependent enhancement of prion-induced neurodegeneration in L902688-treated Tga20 COCS; n = 12 slices per condition for NBH; prion: 15 slices for 0 μM and 1 μM; 14 slices for 5 μM. Data are presented as mean ± s.e.m. One-way ANOVA with Benjamini–Hochberg FDR adjustment for multiple comparisons: P = 0.0810 (NBH + 0 μM versus NBH + 1 μM); P < 0.0001 (NBH + 0 μM versus NBH + 5 μM); P < 0.0001 (NBH + 0 μM versus prion + 0 μM); P < 0.0001 (prion + 0 μM versus prion + 1 μM); P < 0.0001 (prion + 0 μM versus prion + 5 μM).

Journal: Nature Neuroscience

Article Title: NG2 glia protect against prion neurotoxicity by inhibiting microglia-to-neuron prostaglandin E2 signaling

doi: 10.1038/s41593-024-01663-x

Figure Lengend Snippet: a , b , Live-cell imaging ( a ) and quantitative analysis ( b ) of chronically prion-infected HovS cells expressing control (Ctrl) transgene or one of the four PGE2 receptors (Ptger1–4). Effects of PGE2 treatment on prion-induced cell toxicity were measured with the ratio of GFP signals under the PGE2 condition against the DMSO condition; n = 4 independent experiments. Data are presented as mean ± s.e.m. One-way ANOVA with Benjamini–Hochberg FDR adjustment for multiple comparisons: P < 0.0001 (Ptger1 versus Ctrl); P = 0.2246 (Ptger2 versus Ctrl); P = 0.3351 (Ptger3 versus Ctrl); P < 0.0001 (Ptger4 versus Ctrl). c , Immunofluorescence of NeuN, Map2 and Tau showing cellular damage of prion-infected primary neurons treated with different concentrations of Ptger4 agonist L902688. d , Quantification of neuronal density as well as Map2-positive and Tau positive areas shown in c ; n = 6 independent experiments. Data are presented as mean ± s.e.m. One-way ANOVA with Benjamini–Hochberg FDR adjustment for multiple comparisons. NeuN: P = 0.0150 (1 μM versus 0 μM); P < 0.0001 (5 μM versus 0 μM); P < 0.0001 (10 μM versus 0 μM). Map2: P = 0.0020 (1 μM versus 0 μM); P < 0.0001 (5 μM versus 0 μM); P < 0.0001 (10 μM versus 0 μM). Tau: P = 0.0005 (1 μM versus 0 μM); P < 0.0001 (5 μM versus 0 μM); P < 0.0001 (10 μM versus 0 μM). e , f , NeuN immunofluorescence ( e ) and quantification ( f ) showing concentration-dependent enhancement of prion-induced neurodegeneration in L902688-treated Tga20 COCS; n = 12 slices per condition for NBH; prion: 15 slices for 0 μM and 1 μM; 14 slices for 5 μM. Data are presented as mean ± s.e.m. One-way ANOVA with Benjamini–Hochberg FDR adjustment for multiple comparisons: P = 0.0810 (NBH + 0 μM versus NBH + 1 μM); P < 0.0001 (NBH + 0 μM versus NBH + 5 μM); P < 0.0001 (NBH + 0 μM versus prion + 0 μM); P < 0.0001 (prion + 0 μM versus prion + 1 μM); P < 0.0001 (prion + 0 μM versus prion + 5 μM).

Article Snippet: Lenti-vectors used for expressing human PGE2 receptors EP1 (pLenti-PTGER1-mGFP-P2A-Puro, cat. no. RC208597L4), EP2 (pLenti-PTGER2-mGFP-P2A-Puro, cat. no. RC210883L4), EP3 (pLenti-PTGER3-mGFP-P2A-Puro, cat. no. RC220173L4) and EP4 (pLenti-PTGER4-mGFP-P2A-Puro, cat. no. RC210932L4) were purchased from OriGene Technologies.

Techniques: Live Cell Imaging, Infection, Expressing, Control, Immunofluorescence, Concentration Assay

Journal: Cell Reports Medicine

Article Title: Surface CD52, CD84, and PTGER2 mark mature PMN-MDSCs from cancer patients and G-CSF-treated donors

doi: 10.1016/j.xcrm.2023.101380

Figure Lengend Snippet:

Article Snippet: anti-human PTGER2-FITC (polyclonal) – Lab 1/2 , biorbyt , Cat# orb7558; RRID: AB_10938289.

Techniques: Recombinant, Enzyme-linked Immunosorbent Assay, Staining, Cell Isolation, Amplification, Multiplexing, Expressing, Software