Structured Review

Cayman Chemical ep2
EP1-3, but not EP4, mediates the effects of Ca 2+ on phosphorylating tau. (A–H) N2a cells were treated with PGE 2 (500 nM) in the absence or presence of EP1-4 inhibitors (SC51322, antagonist of EP1; PF-04418948, antagonist of <t>EP2;</t> DG-041, antagonist of <t>EP3;</t> and CJ-42794, antagonist of EP4) for 24 h ( n = 6). The expression of phosphorylated tau and p35/25 and the total protein expression level of tau were determined by western blotting using β-actin as an internal control. The data represent the means ± S.E. of independent experiments. ∗ p
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Images

1) Product Images from "Calcium Ions Stimulate the Hyperphosphorylation of Tau by Activating Microsomal Prostaglandin E Synthase 1"

Article Title: Calcium Ions Stimulate the Hyperphosphorylation of Tau by Activating Microsomal Prostaglandin E Synthase 1

Journal: Frontiers in Aging Neuroscience

doi: 10.3389/fnagi.2019.00108

EP1-3, but not EP4, mediates the effects of Ca 2+ on phosphorylating tau. (A–H) N2a cells were treated with PGE 2 (500 nM) in the absence or presence of EP1-4 inhibitors (SC51322, antagonist of EP1; PF-04418948, antagonist of EP2; DG-041, antagonist of EP3; and CJ-42794, antagonist of EP4) for 24 h ( n = 6). The expression of phosphorylated tau and p35/25 and the total protein expression level of tau were determined by western blotting using β-actin as an internal control. The data represent the means ± S.E. of independent experiments. ∗ p
Figure Legend Snippet: EP1-3, but not EP4, mediates the effects of Ca 2+ on phosphorylating tau. (A–H) N2a cells were treated with PGE 2 (500 nM) in the absence or presence of EP1-4 inhibitors (SC51322, antagonist of EP1; PF-04418948, antagonist of EP2; DG-041, antagonist of EP3; and CJ-42794, antagonist of EP4) for 24 h ( n = 6). The expression of phosphorylated tau and p35/25 and the total protein expression level of tau were determined by western blotting using β-actin as an internal control. The data represent the means ± S.E. of independent experiments. ∗ p

Techniques Used: Expressing, Western Blot

2) Product Images from "Dectin-1/2–induced autocrine PGE2 signaling licenses dendritic cells to prime Th2 responses"

Article Title: Dectin-1/2–induced autocrine PGE2 signaling licenses dendritic cells to prime Th2 responses

Journal: PLoS Biology

doi: 10.1371/journal.pbio.2005504

Proposed model of S . mansoni –driven Th2 polarization. S . mansoni egg antigens, but not ω-1, interact with Dectin-1 and Dectin-2 expressed by DCs to promote 2 intracellular pathways in moDCs in an Syk-dependent manner: ERK-cPLA 2 -COX and ROS activity that culminate in PGE 2 and PGE 2 isomer synthesis, respectively. Both PGE 2 and its isomers can then bind to EP2 and EP4 in an autocrine loop to trigger OX40L expression, which endows the DCs with the capacity to prime a Th2 response. ω-1, omega-1; COX, cyclooxygenase; cPLA 2 , cytosolic phospholipase A 2 ; DC, dendritic cell; EP2, prostaglandin E 2 receptor 2; ERK, extracellular signal-regulated kinase; moDC, monocyte-derived DC; OX40L, OX40 ligand; PGE 2 , prostaglandin E 2 ; ROS, reactive oxygen species; Syk, spleen tyrosine kinase; Th2, T helper 2.
Figure Legend Snippet: Proposed model of S . mansoni –driven Th2 polarization. S . mansoni egg antigens, but not ω-1, interact with Dectin-1 and Dectin-2 expressed by DCs to promote 2 intracellular pathways in moDCs in an Syk-dependent manner: ERK-cPLA 2 -COX and ROS activity that culminate in PGE 2 and PGE 2 isomer synthesis, respectively. Both PGE 2 and its isomers can then bind to EP2 and EP4 in an autocrine loop to trigger OX40L expression, which endows the DCs with the capacity to prime a Th2 response. ω-1, omega-1; COX, cyclooxygenase; cPLA 2 , cytosolic phospholipase A 2 ; DC, dendritic cell; EP2, prostaglandin E 2 receptor 2; ERK, extracellular signal-regulated kinase; moDC, monocyte-derived DC; OX40L, OX40 ligand; PGE 2 , prostaglandin E 2 ; ROS, reactive oxygen species; Syk, spleen tyrosine kinase; Th2, T helper 2.

Techniques Used: Activity Assay, Expressing, Derivative Assay

ω-1–independent Th2 polarization by SEA is dependent on PGE 2 synthesis by moDCs. (A–C) T-cell polarization assay as described in Fig 1B . (A) Neutralizing anti-PGE 2 antibody was added during stimulation of moDCs with indicated reagents or (B) during DC–T cell coculture. (C) EP2 and EP4 receptor inhibitors (EP2-I and EP4-I) were added during stimulation of moDCs with indicated stimuli. (A–C) Left: representative flow cytometry plots are shown of intracellular staining of CD4 + T cells for IL-4 and IFN-γ. Numbers in plots represent frequencies of cells in indicated quadrants. Right: these data were used to calculate the fold change in frequency of IL-4 + and IFN-γ + T cells polarized by moDCs stimulated with indicated stimuli relative to the cytokine production by T cells polarized by LPS-stimulated moDCs, for which the values were set to 1. Bars represent mean ± SEM of at least 4 independent experiments. Significance was calculated based on the ratio of IL-4 over IFN-γ between conditions. * P
Figure Legend Snippet: ω-1–independent Th2 polarization by SEA is dependent on PGE 2 synthesis by moDCs. (A–C) T-cell polarization assay as described in Fig 1B . (A) Neutralizing anti-PGE 2 antibody was added during stimulation of moDCs with indicated reagents or (B) during DC–T cell coculture. (C) EP2 and EP4 receptor inhibitors (EP2-I and EP4-I) were added during stimulation of moDCs with indicated stimuli. (A–C) Left: representative flow cytometry plots are shown of intracellular staining of CD4 + T cells for IL-4 and IFN-γ. Numbers in plots represent frequencies of cells in indicated quadrants. Right: these data were used to calculate the fold change in frequency of IL-4 + and IFN-γ + T cells polarized by moDCs stimulated with indicated stimuli relative to the cytokine production by T cells polarized by LPS-stimulated moDCs, for which the values were set to 1. Bars represent mean ± SEM of at least 4 independent experiments. Significance was calculated based on the ratio of IL-4 over IFN-γ between conditions. * P

Techniques Used: Flow Cytometry, Cytometry, Staining

3) Product Images from "Dectin-1/2–induced autocrine PGE2 signaling licenses dendritic cells to prime Th2 responses"

Article Title: Dectin-1/2–induced autocrine PGE2 signaling licenses dendritic cells to prime Th2 responses

Journal: PLoS Biology

doi: 10.1371/journal.pbio.2005504

Proposed model of S . mansoni –driven Th2 polarization. S . mansoni egg antigens, but not ω-1, interact with Dectin-1 and Dectin-2 expressed by DCs to promote 2 intracellular pathways in moDCs in an Syk-dependent manner: ERK-cPLA 2 -COX and ROS activity that culminate in PGE 2 and PGE 2 isomer synthesis, respectively. Both PGE 2 and its isomers can then bind to EP2 and EP4 in an autocrine loop to trigger OX40L expression, which endows the DCs with the capacity to prime a Th2 response. ω-1, omega-1; COX, cyclooxygenase; cPLA 2 , cytosolic phospholipase A 2 ; DC, dendritic cell; EP2, prostaglandin E 2 receptor 2; ERK, extracellular signal-regulated kinase; moDC, monocyte-derived DC; OX40L, OX40 ligand; PGE 2 , prostaglandin E 2 ; ROS, reactive oxygen species; Syk, spleen tyrosine kinase; Th2, T helper 2.
Figure Legend Snippet: Proposed model of S . mansoni –driven Th2 polarization. S . mansoni egg antigens, but not ω-1, interact with Dectin-1 and Dectin-2 expressed by DCs to promote 2 intracellular pathways in moDCs in an Syk-dependent manner: ERK-cPLA 2 -COX and ROS activity that culminate in PGE 2 and PGE 2 isomer synthesis, respectively. Both PGE 2 and its isomers can then bind to EP2 and EP4 in an autocrine loop to trigger OX40L expression, which endows the DCs with the capacity to prime a Th2 response. ω-1, omega-1; COX, cyclooxygenase; cPLA 2 , cytosolic phospholipase A 2 ; DC, dendritic cell; EP2, prostaglandin E 2 receptor 2; ERK, extracellular signal-regulated kinase; moDC, monocyte-derived DC; OX40L, OX40 ligand; PGE 2 , prostaglandin E 2 ; ROS, reactive oxygen species; Syk, spleen tyrosine kinase; Th2, T helper 2.

Techniques Used: Activity Assay, Expressing, Derivative Assay

4) Product Images from "Dectin-1/2–induced autocrine PGE2 signaling licenses dendritic cells to prime Th2 responses"

Article Title: Dectin-1/2–induced autocrine PGE2 signaling licenses dendritic cells to prime Th2 responses

Journal: PLoS Biology

doi: 10.1371/journal.pbio.2005504

Proposed model of S . mansoni –driven Th2 polarization. S . mansoni egg antigens, but not ω-1, interact with Dectin-1 and Dectin-2 expressed by DCs to promote 2 intracellular pathways in moDCs in an Syk-dependent manner: ERK-cPLA 2 -COX and ROS activity that culminate in PGE 2 and PGE 2 isomer synthesis, respectively. Both PGE 2 and its isomers can then bind to EP2 and EP4 in an autocrine loop to trigger OX40L expression, which endows the DCs with the capacity to prime a Th2 response. ω-1, omega-1; COX, cyclooxygenase; cPLA 2 , cytosolic phospholipase A 2 ; DC, dendritic cell; EP2, prostaglandin E 2 receptor 2; ERK, extracellular signal-regulated kinase; moDC, monocyte-derived DC; OX40L, OX40 ligand; PGE 2 , prostaglandin E 2 ; ROS, reactive oxygen species; Syk, spleen tyrosine kinase; Th2, T helper 2.
Figure Legend Snippet: Proposed model of S . mansoni –driven Th2 polarization. S . mansoni egg antigens, but not ω-1, interact with Dectin-1 and Dectin-2 expressed by DCs to promote 2 intracellular pathways in moDCs in an Syk-dependent manner: ERK-cPLA 2 -COX and ROS activity that culminate in PGE 2 and PGE 2 isomer synthesis, respectively. Both PGE 2 and its isomers can then bind to EP2 and EP4 in an autocrine loop to trigger OX40L expression, which endows the DCs with the capacity to prime a Th2 response. ω-1, omega-1; COX, cyclooxygenase; cPLA 2 , cytosolic phospholipase A 2 ; DC, dendritic cell; EP2, prostaglandin E 2 receptor 2; ERK, extracellular signal-regulated kinase; moDC, monocyte-derived DC; OX40L, OX40 ligand; PGE 2 , prostaglandin E 2 ; ROS, reactive oxygen species; Syk, spleen tyrosine kinase; Th2, T helper 2.

Techniques Used: Activity Assay, Expressing, Derivative Assay

ω-1–independent Th2 polarization by SEA is dependent on PGE 2 synthesis by moDCs. (A–C) T-cell polarization assay as described in Fig 1B . (A) Neutralizing anti-PGE 2 antibody was added during stimulation of moDCs with indicated reagents or (B) during DC–T cell coculture. (C) EP2 and EP4 receptor inhibitors (EP2-I and EP4-I) were added during stimulation of moDCs with indicated stimuli. (A–C) Left: representative flow cytometry plots are shown of intracellular staining of CD4 + T cells for IL-4 and IFN-γ. Numbers in plots represent frequencies of cells in indicated quadrants. Right: these data were used to calculate the fold change in frequency of IL-4 + and IFN-γ + T cells polarized by moDCs stimulated with indicated stimuli relative to the cytokine production by T cells polarized by LPS-stimulated moDCs, for which the values were set to 1. Bars represent mean ± SEM of at least 4 independent experiments. Significance was calculated based on the ratio of IL-4 over IFN-γ between conditions. * P
Figure Legend Snippet: ω-1–independent Th2 polarization by SEA is dependent on PGE 2 synthesis by moDCs. (A–C) T-cell polarization assay as described in Fig 1B . (A) Neutralizing anti-PGE 2 antibody was added during stimulation of moDCs with indicated reagents or (B) during DC–T cell coculture. (C) EP2 and EP4 receptor inhibitors (EP2-I and EP4-I) were added during stimulation of moDCs with indicated stimuli. (A–C) Left: representative flow cytometry plots are shown of intracellular staining of CD4 + T cells for IL-4 and IFN-γ. Numbers in plots represent frequencies of cells in indicated quadrants. Right: these data were used to calculate the fold change in frequency of IL-4 + and IFN-γ + T cells polarized by moDCs stimulated with indicated stimuli relative to the cytokine production by T cells polarized by LPS-stimulated moDCs, for which the values were set to 1. Bars represent mean ± SEM of at least 4 independent experiments. Significance was calculated based on the ratio of IL-4 over IFN-γ between conditions. * P

Techniques Used: Flow Cytometry, Cytometry, Staining

5) Product Images from "Dectin-1/2–induced autocrine PGE2 signaling licenses dendritic cells to prime Th2 responses"

Article Title: Dectin-1/2–induced autocrine PGE2 signaling licenses dendritic cells to prime Th2 responses

Journal: PLoS Biology

doi: 10.1371/journal.pbio.2005504

Proposed model of S . mansoni –driven Th2 polarization. S . mansoni egg antigens, but not ω-1, interact with Dectin-1 and Dectin-2 expressed by DCs to promote 2 intracellular pathways in moDCs in an Syk-dependent manner: ERK-cPLA 2 -COX and ROS activity that culminate in PGE 2 and PGE 2 isomer synthesis, respectively. Both PGE 2 and its isomers can then bind to EP2 and EP4 in an autocrine loop to trigger OX40L expression, which endows the DCs with the capacity to prime a Th2 response. ω-1, omega-1; COX, cyclooxygenase; cPLA 2 , cytosolic phospholipase A 2 ; DC, dendritic cell; EP2, prostaglandin E 2 receptor 2; ERK, extracellular signal-regulated kinase; moDC, monocyte-derived DC; OX40L, OX40 ligand; PGE 2 , prostaglandin E 2 ; ROS, reactive oxygen species; Syk, spleen tyrosine kinase; Th2, T helper 2.
Figure Legend Snippet: Proposed model of S . mansoni –driven Th2 polarization. S . mansoni egg antigens, but not ω-1, interact with Dectin-1 and Dectin-2 expressed by DCs to promote 2 intracellular pathways in moDCs in an Syk-dependent manner: ERK-cPLA 2 -COX and ROS activity that culminate in PGE 2 and PGE 2 isomer synthesis, respectively. Both PGE 2 and its isomers can then bind to EP2 and EP4 in an autocrine loop to trigger OX40L expression, which endows the DCs with the capacity to prime a Th2 response. ω-1, omega-1; COX, cyclooxygenase; cPLA 2 , cytosolic phospholipase A 2 ; DC, dendritic cell; EP2, prostaglandin E 2 receptor 2; ERK, extracellular signal-regulated kinase; moDC, monocyte-derived DC; OX40L, OX40 ligand; PGE 2 , prostaglandin E 2 ; ROS, reactive oxygen species; Syk, spleen tyrosine kinase; Th2, T helper 2.

Techniques Used: Activity Assay, Expressing, Derivative Assay

6) Product Images from "Prostaglandin receptors induce urothelial tumourigenesis as well as bladder cancer progression and cisplatin resistance presumably via modulating PTEN expression"

Article Title: Prostaglandin receptors induce urothelial tumourigenesis as well as bladder cancer progression and cisplatin resistance presumably via modulating PTEN expression

Journal: British Journal of Cancer

doi: 10.1038/bjc.2017.393

Effects of EP2/EP4 antagonists and celecoxib on BC cell viability and migration. ( A ) MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay in 647V, 5637, and UMUC3 cells cultured with ethanol (mock), AH6809 (10 μ M ), ONO-AE3-208 (10 μ M ), or celecoxib (10 μ M ) for 72 h. Cell viability is presented relative to that of mock treatment in each line. ( B ) Wound healing assay in 647V, 5637, and UMUC3 cells. The cells grown to confluence were gently scratched and the wound area was measured after 24-h culture with ethanol (mock), AH6809 (10 μ M ), ONO-AE3-208 (10 μ M ), or celecoxib (10 μ M ). The migration determined by the rate of cells filling the wound area is presented relative to that of mock treatment in each line. Each value represents the mean (±s.d.) from at least three independent determinations. * P
Figure Legend Snippet: Effects of EP2/EP4 antagonists and celecoxib on BC cell viability and migration. ( A ) MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay in 647V, 5637, and UMUC3 cells cultured with ethanol (mock), AH6809 (10 μ M ), ONO-AE3-208 (10 μ M ), or celecoxib (10 μ M ) for 72 h. Cell viability is presented relative to that of mock treatment in each line. ( B ) Wound healing assay in 647V, 5637, and UMUC3 cells. The cells grown to confluence were gently scratched and the wound area was measured after 24-h culture with ethanol (mock), AH6809 (10 μ M ), ONO-AE3-208 (10 μ M ), or celecoxib (10 μ M ). The migration determined by the rate of cells filling the wound area is presented relative to that of mock treatment in each line. Each value represents the mean (±s.d.) from at least three independent determinations. * P

Techniques Used: Migration, MTT Assay, Cell Culture, Wound Healing Assay

Effects of EP2/EP4 antagonists/agonists and celecoxib on the cytotoxicity of CDDP in BC cells. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay in 647V and 5637 cells cultured with ethanol (mock) vs AH6809 (1 μ M ; A ), ONO-AE3-208 (1 μ M ; B ), celecoxib (1 μ M ; C ), butaprost (1 μ M ; D ), or CAY10598 (1 μ M ; E ), and different concentrations (0–50 μ M ) of CDDP for 72 h. Cell viability is presented relative to that of each line/treatment without CDDP. Each value represents the mean (±s.d.) from at least three independent determinations. * P
Figure Legend Snippet: Effects of EP2/EP4 antagonists/agonists and celecoxib on the cytotoxicity of CDDP in BC cells. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay in 647V and 5637 cells cultured with ethanol (mock) vs AH6809 (1 μ M ; A ), ONO-AE3-208 (1 μ M ; B ), celecoxib (1 μ M ; C ), butaprost (1 μ M ; D ), or CAY10598 (1 μ M ; E ), and different concentrations (0–50 μ M ) of CDDP for 72 h. Cell viability is presented relative to that of each line/treatment without CDDP. Each value represents the mean (±s.d.) from at least three independent determinations. * P

Techniques Used: MTT Assay, Cell Culture

Immunohistochemistry of EP2, EP3, and EP4 in BC specimens. ( A ) Expression of EP2, EP3, and EP4 in BC (original magnification: × 200). Kaplan–Meier analyses for ( B ) progression-free survival in 78 patients with non-muscle-invasive tumour and ( C ) cancer-specific survival in 51 patients with muscle-invasive tumour, according to the levels of EP2/EP3/EP4 expression.
Figure Legend Snippet: Immunohistochemistry of EP2, EP3, and EP4 in BC specimens. ( A ) Expression of EP2, EP3, and EP4 in BC (original magnification: × 200). Kaplan–Meier analyses for ( B ) progression-free survival in 78 patients with non-muscle-invasive tumour and ( C ) cancer-specific survival in 51 patients with muscle-invasive tumour, according to the levels of EP2/EP3/EP4 expression.

Techniques Used: Immunohistochemistry, Expressing

Effects of EP2/EP4 antagonists and celecoxib on neoplastic transformation of urothelial cells. ( A ) SVHUC cells exposed to MCA, subsequently cultured for 6 weeks with ethanol (mock) or celecoxib (1 μ M ), suspended, and mixed with Matrigel (1 × 10 6 cells/100 μl) were subcutaneously implanted into the flank of 6-week-old male NOD-SCID mice ( n =11 in each group). The end point for this study was tumour formation without further drug treatment (exceeding 10 mm 3 in its estimated volume (by the following formula: (short diameter) 2 × (longest diameter) × 0.5) or 4 mm in greatest dimension). ( B ) Western blotting of EP2, EP4, COX-2, and PTEN using proteins extracted from SVHUC cells without MCA exposure and MCA-exposed SVHUC cells subsequently cultured for 6 weeks with ethanol or celecoxib (1 μ M ). Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) served as a loading control. Densitometry values for specific bands standardised by GAPDH that are relative to the value of mock treatment are included below the lanes. ( C ) Quantitative RT–PCR of EP2 , EP4 , and PTEN in SVHUC cells without MCA exposure and MCA-exposed SVHUC cells subsequently cultured for 6 weeks with ethanol or celecoxib (1 μ M ) were subjected to RNA extraction and subsequent real-time RT–PCR. Expression of EP2 , EP4 , or PTEN gene was normalised to that of GAPDH . Transcription amount is presented relative to that of control cells without MCA. SVHUC cells exposed to MCA and subsequently treated with ethanol (mock), AH6809 (1 μ M ), ONO-AE3-208 (1 μ M ), or celecoxib (1 μ M ) for 6 weeks were seeded for MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay ( D ; cultured for 72 h) or colony formation assay ( E ; cultured for 2 weeks). During these assays, AH6809, ONO-AE3-208, or celecoxib was not treated. Cell viability or the number of the colonies (⩾20 cells) is presented relative to that in mock-treated cells. Each value represents the mean (±s.d.) from at least three independent determinations. * P
Figure Legend Snippet: Effects of EP2/EP4 antagonists and celecoxib on neoplastic transformation of urothelial cells. ( A ) SVHUC cells exposed to MCA, subsequently cultured for 6 weeks with ethanol (mock) or celecoxib (1 μ M ), suspended, and mixed with Matrigel (1 × 10 6 cells/100 μl) were subcutaneously implanted into the flank of 6-week-old male NOD-SCID mice ( n =11 in each group). The end point for this study was tumour formation without further drug treatment (exceeding 10 mm 3 in its estimated volume (by the following formula: (short diameter) 2 × (longest diameter) × 0.5) or 4 mm in greatest dimension). ( B ) Western blotting of EP2, EP4, COX-2, and PTEN using proteins extracted from SVHUC cells without MCA exposure and MCA-exposed SVHUC cells subsequently cultured for 6 weeks with ethanol or celecoxib (1 μ M ). Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) served as a loading control. Densitometry values for specific bands standardised by GAPDH that are relative to the value of mock treatment are included below the lanes. ( C ) Quantitative RT–PCR of EP2 , EP4 , and PTEN in SVHUC cells without MCA exposure and MCA-exposed SVHUC cells subsequently cultured for 6 weeks with ethanol or celecoxib (1 μ M ) were subjected to RNA extraction and subsequent real-time RT–PCR. Expression of EP2 , EP4 , or PTEN gene was normalised to that of GAPDH . Transcription amount is presented relative to that of control cells without MCA. SVHUC cells exposed to MCA and subsequently treated with ethanol (mock), AH6809 (1 μ M ), ONO-AE3-208 (1 μ M ), or celecoxib (1 μ M ) for 6 weeks were seeded for MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay ( D ; cultured for 72 h) or colony formation assay ( E ; cultured for 2 weeks). During these assays, AH6809, ONO-AE3-208, or celecoxib was not treated. Cell viability or the number of the colonies (⩾20 cells) is presented relative to that in mock-treated cells. Each value represents the mean (±s.d.) from at least three independent determinations. * P

Techniques Used: Transformation Assay, Cell Culture, Mouse Assay, Western Blot, Quantitative RT-PCR, RNA Extraction, Expressing, MTT Assay, Colony Assay

7) Product Images from "Inhibition of STAT3- and MAPK-dependent PGE2 synthesis ameliorates phagocytosis of fibrillar β-amyloid peptide (1-42) via EP2 receptor in EMF-stimulated N9 microglial cells"

Article Title: Inhibition of STAT3- and MAPK-dependent PGE2 synthesis ameliorates phagocytosis of fibrillar β-amyloid peptide (1-42) via EP2 receptor in EMF-stimulated N9 microglial cells

Journal: Journal of Neuroinflammation

doi: 10.1186/s12974-016-0762-9

Schematic diagram illustrating the proposed immunomodulatory phagocytosis of fAβ 42 via PGE 2 -related signaling mechanism in EMF-stimulated N9 microglial cells. External electromagnetic emission as a physical stimulation directly triggers an initial activation of microglia. Activation of JAK2-STAT3 and MAPKs signaling occurs in parallel with microglial activation, leading to PGE 2 synthesis via COX-2-mPGES-1 system. Finally, PGE 2 decreased microglial phagocytosis through EP2 receptor. Preventing phosphorylation of JAK2-STAT3 and MAPKs, inhibiting COX-2 activity, or abolishing EP2 activity efficiently ameliorated microglial phagocytosis during EMF stimulation
Figure Legend Snippet: Schematic diagram illustrating the proposed immunomodulatory phagocytosis of fAβ 42 via PGE 2 -related signaling mechanism in EMF-stimulated N9 microglial cells. External electromagnetic emission as a physical stimulation directly triggers an initial activation of microglia. Activation of JAK2-STAT3 and MAPKs signaling occurs in parallel with microglial activation, leading to PGE 2 synthesis via COX-2-mPGES-1 system. Finally, PGE 2 decreased microglial phagocytosis through EP2 receptor. Preventing phosphorylation of JAK2-STAT3 and MAPKs, inhibiting COX-2 activity, or abolishing EP2 activity efficiently ameliorated microglial phagocytosis during EMF stimulation

Techniques Used: Activation Assay, Activity Assay

Involvement of EP2 activity in the restoration of impaired phagocytosis of 647-fAβ 42 in EMF-stimulated N9 cells. N9 cells were pretreated with or without PG receptor EP1 antagonist GW848687X (5 μM), EP2 antagonist AH6809 (10 μM), EP3 antagonist L-798106 (10 μM), and EP4 antagonist GW627368X (10 μM). a Normalized average fluorescence intensity of 647-fAβ 42 ingested per group 12 h after EMF exposure estimated using a flow cytometer and a confocal microscope. * P
Figure Legend Snippet: Involvement of EP2 activity in the restoration of impaired phagocytosis of 647-fAβ 42 in EMF-stimulated N9 cells. N9 cells were pretreated with or without PG receptor EP1 antagonist GW848687X (5 μM), EP2 antagonist AH6809 (10 μM), EP3 antagonist L-798106 (10 μM), and EP4 antagonist GW627368X (10 μM). a Normalized average fluorescence intensity of 647-fAβ 42 ingested per group 12 h after EMF exposure estimated using a flow cytometer and a confocal microscope. * P

Techniques Used: Activity Assay, Fluorescence, Flow Cytometry, Cytometry, Microscopy

Involvement of COX-2, JAK2, STAT3, and MAPKs in the regulation of the expression of EP2 in EMF-stimulated N9 cells. N9 cells were pretreated with or without celecoxib (25 μM), AG490 (25 μM), S3I-201 (30 μM), SB203580 (10 μM), PD98059 (30 μM), SP600125 (5 μM), and AH6809 (10 μM) for 30 min and then exposed to 2.45-GHz EMF or sham exposed for 20 min. Relative mRNA ( a ) and protein ( b ) levels of EP2 in N9 cells pretreated with or without the mentioned pharmacologic compounds of interest 12 h after EMF exposure. * P
Figure Legend Snippet: Involvement of COX-2, JAK2, STAT3, and MAPKs in the regulation of the expression of EP2 in EMF-stimulated N9 cells. N9 cells were pretreated with or without celecoxib (25 μM), AG490 (25 μM), S3I-201 (30 μM), SB203580 (10 μM), PD98059 (30 μM), SP600125 (5 μM), and AH6809 (10 μM) for 30 min and then exposed to 2.45-GHz EMF or sham exposed for 20 min. Relative mRNA ( a ) and protein ( b ) levels of EP2 in N9 cells pretreated with or without the mentioned pharmacologic compounds of interest 12 h after EMF exposure. * P

Techniques Used: Expressing

8) Product Images from "PGE2 maintains self-renewal of human adult stem cells via EP2-mediated autocrine signaling and its production is regulated by cell-to-cell contact"

Article Title: PGE2 maintains self-renewal of human adult stem cells via EP2-mediated autocrine signaling and its production is regulated by cell-to-cell contact

Journal: Scientific Reports

doi: 10.1038/srep26298

EP2 receptor has a crucial role in hMSC self-renewal. ( a ) EP receptor expression in hUCB-MSCs and hAD-MSCs was assessed by Western blot analysis. HMO6, a human microglia cell line, was used as a positive control. In the presence of selective blockers for EPs, ( b ) cell growth rates were examined by BrdU assay and ( c ) results of repeated experiments are presented. Selective blockers for EP1: SC-51089, EP2: AH-6809, EP3: L-798106, and EP4: L-161,982. ( d ) After celecoxib treatment, cells were treated with selective agonists for EP2 or EP3, and proliferation was measured with a BrdU assay kit. Gel electrophoresis was conducted under the same experimental conditions, and images of blots were cropped. Selective agonist for EP2: Butaprost, EP3: Sulprostone. * P
Figure Legend Snippet: EP2 receptor has a crucial role in hMSC self-renewal. ( a ) EP receptor expression in hUCB-MSCs and hAD-MSCs was assessed by Western blot analysis. HMO6, a human microglia cell line, was used as a positive control. In the presence of selective blockers for EPs, ( b ) cell growth rates were examined by BrdU assay and ( c ) results of repeated experiments are presented. Selective blockers for EP1: SC-51089, EP2: AH-6809, EP3: L-798106, and EP4: L-161,982. ( d ) After celecoxib treatment, cells were treated with selective agonists for EP2 or EP3, and proliferation was measured with a BrdU assay kit. Gel electrophoresis was conducted under the same experimental conditions, and images of blots were cropped. Selective agonist for EP2: Butaprost, EP3: Sulprostone. * P

Techniques Used: Expressing, Western Blot, Positive Control, BrdU Staining, Nucleic Acid Electrophoresis

9) Product Images from "PGE2 maintains self-renewal of human adult stem cells via EP2-mediated autocrine signaling and its production is regulated by cell-to-cell contact"

Article Title: PGE2 maintains self-renewal of human adult stem cells via EP2-mediated autocrine signaling and its production is regulated by cell-to-cell contact

Journal: Scientific Reports

doi: 10.1038/srep26298

EP2 receptor has a crucial role in hMSC self-renewal. ( a ) EP receptor expression in hUCB-MSCs and hAD-MSCs was assessed by Western blot analysis. HMO6, a human microglia cell line, was used as a positive control. In the presence of selective blockers for EPs, ( b ) cell growth rates were examined by BrdU assay and ( c ) results of repeated experiments are presented. Selective blockers for EP1: SC-51089, EP2: AH-6809, EP3: L-798106, and EP4: L-161,982. ( d ) After celecoxib treatment, cells were treated with selective agonists for EP2 or EP3, and proliferation was measured with a BrdU assay kit. Gel electrophoresis was conducted under the same experimental conditions, and images of blots were cropped. Selective agonist for EP2: Butaprost, EP3: Sulprostone. * P
Figure Legend Snippet: EP2 receptor has a crucial role in hMSC self-renewal. ( a ) EP receptor expression in hUCB-MSCs and hAD-MSCs was assessed by Western blot analysis. HMO6, a human microglia cell line, was used as a positive control. In the presence of selective blockers for EPs, ( b ) cell growth rates were examined by BrdU assay and ( c ) results of repeated experiments are presented. Selective blockers for EP1: SC-51089, EP2: AH-6809, EP3: L-798106, and EP4: L-161,982. ( d ) After celecoxib treatment, cells were treated with selective agonists for EP2 or EP3, and proliferation was measured with a BrdU assay kit. Gel electrophoresis was conducted under the same experimental conditions, and images of blots were cropped. Selective agonist for EP2: Butaprost, EP3: Sulprostone. * P

Techniques Used: Expressing, Western Blot, Positive Control, BrdU Staining, Nucleic Acid Electrophoresis

10) Product Images from "The role of the prostaglandin E2 receptors in vulnerability of oligodendrocyte precursor cells to death"

Article Title: The role of the prostaglandin E2 receptors in vulnerability of oligodendrocyte precursor cells to death

Journal: Journal of Neuroinflammation

doi: 10.1186/s12974-015-0323-7

The EP2 agonist butaprost (But) protects OPCs from KA-induced toxicity. OPC survival was assessed 48 h following treatment of OPCs with KA in the presence or absence of butaprost (500 nM). This graph represents the combined data from four independent experiments. Significant protection (Student t -test) was observed for Butaprost
Figure Legend Snippet: The EP2 agonist butaprost (But) protects OPCs from KA-induced toxicity. OPC survival was assessed 48 h following treatment of OPCs with KA in the presence or absence of butaprost (500 nM). This graph represents the combined data from four independent experiments. Significant protection (Student t -test) was observed for Butaprost

Techniques Used:

Expression of EP receptors in purified oligodendrocytes. Purified OPC cultures were stained with the oligodendrocyte marker Olig 1 (green) and EP1 through EP4 (red) as indicated. Co-expression appears yellow, and examples are indicated with arrows . The asterisk indicates an example where immunoreactivity for EP2 is present predominantly in the cell processes. The bar in the lower corner is 20 μm
Figure Legend Snippet: Expression of EP receptors in purified oligodendrocytes. Purified OPC cultures were stained with the oligodendrocyte marker Olig 1 (green) and EP1 through EP4 (red) as indicated. Co-expression appears yellow, and examples are indicated with arrows . The asterisk indicates an example where immunoreactivity for EP2 is present predominantly in the cell processes. The bar in the lower corner is 20 μm

Techniques Used: Expressing, Purification, Staining, Marker

11) Product Images from "EP2-PKA signaling is suppressed by triptolide in lipopolysaccharide-induced microglia activation"

Article Title: EP2-PKA signaling is suppressed by triptolide in lipopolysaccharide-induced microglia activation

Journal: Journal of Neuroinflammation

doi: 10.1186/s12974-015-0275-y

EP2 signaling pathway regulates NO release in primary rat microglial cells. (A) EP2 expression in primary rat microglial cells. Immunofluorescent staining of EP2 and CD11b, as well as the nuclear stain DAPI are shown (scale bar, 25 μm). (B) cAMP accumulation in rat microglia cells left untreated or treated with butaprost (10 μM) or AH6809 (10 μM) for 3 h ( n = 3). (C) Butaprost stimulated NO production in resting microglia. Primary rat microglial cells were stimulated with different concentrations of butaprost (0, 0.1, 1, 10 μM) for 24 h. At the end of the incubation period, the supernatants were collected for NO measurements. (D) AH6809 suppressed NO production in LPS-activated microglia. Primary rat microglial cells were unstimulated or stimulated with LPS (0.01 μg/mL) in the presence or absence of AH6809 (0.1, 1, 10 μM) for 24 h. At the end of the incubation period, the supernatants were collected for NO measurements. *** P
Figure Legend Snippet: EP2 signaling pathway regulates NO release in primary rat microglial cells. (A) EP2 expression in primary rat microglial cells. Immunofluorescent staining of EP2 and CD11b, as well as the nuclear stain DAPI are shown (scale bar, 25 μm). (B) cAMP accumulation in rat microglia cells left untreated or treated with butaprost (10 μM) or AH6809 (10 μM) for 3 h ( n = 3). (C) Butaprost stimulated NO production in resting microglia. Primary rat microglial cells were stimulated with different concentrations of butaprost (0, 0.1, 1, 10 μM) for 24 h. At the end of the incubation period, the supernatants were collected for NO measurements. (D) AH6809 suppressed NO production in LPS-activated microglia. Primary rat microglial cells were unstimulated or stimulated with LPS (0.01 μg/mL) in the presence or absence of AH6809 (0.1, 1, 10 μM) for 24 h. At the end of the incubation period, the supernatants were collected for NO measurements. *** P

Techniques Used: Expressing, Staining, Incubation

Triptolide regulates EP2 expression in LPS - stimulated microglia. (A) Rat primary microglia cells were stimulated with LPS (0.01 μg/mL) for 0, 1, 3, 6, 12, and 24 h. The cells were lysed for EP2 expression by real-time PCR analysis. (B) Rat primary microglia cells were stimulated with LPS (0.01 μg/mL) in the presence or absence of triptolide (50 nM) for 6 h. The cells were lysed for EP2 expression by real-time PCR analysis. (C) Primary rat microglial cells were stimulated with LPS (0.01 μg/mL) in the presence or absence of triptolide (50 nM) for 24 h. The cells were lysed for EP2 expression by Western blot. (D) The protein levels were quantified relative to GAPDH levels and normalized to the naïve group (untreated cells). ** P
Figure Legend Snippet: Triptolide regulates EP2 expression in LPS - stimulated microglia. (A) Rat primary microglia cells were stimulated with LPS (0.01 μg/mL) for 0, 1, 3, 6, 12, and 24 h. The cells were lysed for EP2 expression by real-time PCR analysis. (B) Rat primary microglia cells were stimulated with LPS (0.01 μg/mL) in the presence or absence of triptolide (50 nM) for 6 h. The cells were lysed for EP2 expression by real-time PCR analysis. (C) Primary rat microglial cells were stimulated with LPS (0.01 μg/mL) in the presence or absence of triptolide (50 nM) for 24 h. The cells were lysed for EP2 expression by Western blot. (D) The protein levels were quantified relative to GAPDH levels and normalized to the naïve group (untreated cells). ** P

Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Western Blot

EP2 - PKA pathway is important in LPS - stimulated NO production and triptolide inhibition. (A) Primary rat microglial cells were treated with LPS (0.01 μg/mL), LPS plus AH6809 (10 μM), LPS plus triptolide (50 nM), LPS plus triptolide plus AH6809, and LPS plus triptolide plus butaprost (0.1 μM) for 24 h. At the end of the incubation period, the supernatants were collected for NO measurements. (B) Primary rat microglial cells were treated with LPS (0.01 μg/mL), LPS plus triptolide (50 nM), LPS plus triptolide plus butaprost (0.1 μM), LPS plus triptolide plus 8-CPT (10 μM), or LPS plus triptolide plus 6Bnz (10 μM) for 24 h. At the end of the incubation period, the supernatants were collected for NO measurements. (C) BV2 cells were treated with LPS (0.01 μg/mL), LPS plus triptolide (50 nM), LPS plus triptolide plus 6Bnz (10 μM), and LPS plus triptolide plus 6Bnz (10 μM) plus KT5720 (1 μM) for 24 h. At the end of the incubation period, the supernatants were collected for NO measurements. * P
Figure Legend Snippet: EP2 - PKA pathway is important in LPS - stimulated NO production and triptolide inhibition. (A) Primary rat microglial cells were treated with LPS (0.01 μg/mL), LPS plus AH6809 (10 μM), LPS plus triptolide (50 nM), LPS plus triptolide plus AH6809, and LPS plus triptolide plus butaprost (0.1 μM) for 24 h. At the end of the incubation period, the supernatants were collected for NO measurements. (B) Primary rat microglial cells were treated with LPS (0.01 μg/mL), LPS plus triptolide (50 nM), LPS plus triptolide plus butaprost (0.1 μM), LPS plus triptolide plus 8-CPT (10 μM), or LPS plus triptolide plus 6Bnz (10 μM) for 24 h. At the end of the incubation period, the supernatants were collected for NO measurements. (C) BV2 cells were treated with LPS (0.01 μg/mL), LPS plus triptolide (50 nM), LPS plus triptolide plus 6Bnz (10 μM), and LPS plus triptolide plus 6Bnz (10 μM) plus KT5720 (1 μM) for 24 h. At the end of the incubation period, the supernatants were collected for NO measurements. * P

Techniques Used: Inhibition, Incubation, Cycling Probe Technology

12) Product Images from "Prostaglandin receptors EP1-4 as a potential marker for clinical outcome in urothelial bladder cancer"

Article Title: Prostaglandin receptors EP1-4 as a potential marker for clinical outcome in urothelial bladder cancer

Journal: American Journal of Cancer Research

doi:

Levels of cytoplasmic as well as nuclear staining of EP1, EP2 and EP3 are different in NU tissue and BCA tissue
Figure Legend Snippet: Levels of cytoplasmic as well as nuclear staining of EP1, EP2 and EP3 are different in NU tissue and BCA tissue

Techniques Used: Staining, BIA-KA

13) Product Images from "Role of Prostaglandin Receptor EP2 in the Regulations of Cancer Cell Proliferation, Invasion, and Inflammation"

Article Title: Role of Prostaglandin Receptor EP2 in the Regulations of Cancer Cell Proliferation, Invasion, and Inflammation

Journal: The Journal of Pharmacology and Experimental Therapeutics

doi: 10.1124/jpet.112.200444

Effects of EP2 receptor activation and inhibition on cancer cell proliferation and invasion. (A) EP2 activation by its natural ligand, PGE 2 , promoted PC3 cell growth, measured by MTT cell proliferation assay; growth was attenuated by treatment with compound
Figure Legend Snippet: Effects of EP2 receptor activation and inhibition on cancer cell proliferation and invasion. (A) EP2 activation by its natural ligand, PGE 2 , promoted PC3 cell growth, measured by MTT cell proliferation assay; growth was attenuated by treatment with compound

Techniques Used: Activation Assay, Inhibition, MTT Assay, Proliferation Assay

COX-2 and prostaglandin receptor EP2 signaling in cancer cells. (A) Chemical structure of EP2 antagonist TG4-155 (SID 17,515,129). (B) The Schild K B values of TG4-155 were compared for inhibition of eight human prostanoid receptors. Schild K B values:
Figure Legend Snippet: COX-2 and prostaglandin receptor EP2 signaling in cancer cells. (A) Chemical structure of EP2 antagonist TG4-155 (SID 17,515,129). (B) The Schild K B values of TG4-155 were compared for inhibition of eight human prostanoid receptors. Schild K B values:

Techniques Used: Inhibition

Pharmacological Inhibition of Prostaglandin Receptor EP2 in Cancer Cells.
Figure Legend Snippet: Pharmacological Inhibition of Prostaglandin Receptor EP2 in Cancer Cells.

Techniques Used: Inhibition

EP2 receptor activation induces inflammatory cytokines in cancer cells. (A) PC3 cells were incubated with 1 µ M butaprost for 0, 2, and 8 hours, and the levels of four proinflammatory cytokines, IL-1 β , IL-6, IFN- γ , and TNF- α
Figure Legend Snippet: EP2 receptor activation induces inflammatory cytokines in cancer cells. (A) PC3 cells were incubated with 1 µ M butaprost for 0, 2, and 8 hours, and the levels of four proinflammatory cytokines, IL-1 β , IL-6, IFN- γ , and TNF- α

Techniques Used: Activation Assay, Incubation

EP2 receptor mediates cancer cell activities possibly via an inflammatory mechanism. (A) Low cytotoxicity of EP2 antagonist TG4-155. Cytotoxicity of TG4-155 was tested in C6G cells with the CellTiter-Glo luminescent cell viability assay. TG4-155 did not
Figure Legend Snippet: EP2 receptor mediates cancer cell activities possibly via an inflammatory mechanism. (A) Low cytotoxicity of EP2 antagonist TG4-155. Cytotoxicity of TG4-155 was tested in C6G cells with the CellTiter-Glo luminescent cell viability assay. TG4-155 did not

Techniques Used: Cell Viability Assay

14) Product Images from "EP4 and EP2 receptor activation of protein kinase A by prostaglandin E2 impairs macrophage phagocytosis of Clostridium sordellii"

Article Title: EP4 and EP2 receptor activation of protein kinase A by prostaglandin E2 impairs macrophage phagocytosis of Clostridium sordellii

Journal: American journal of reproductive immunology (New York, N.Y. : 1989)

doi: 10.1111/aji.12153

EP2 and EP4 receptors mediate PGE 2 -induced intracellular cAMP increase and phagocytosis inhibition in THP-1 cells
Figure Legend Snippet: EP2 and EP4 receptors mediate PGE 2 -induced intracellular cAMP increase and phagocytosis inhibition in THP-1 cells

Techniques Used: Inhibition

15) Product Images from "Concurrent targeting of EP1/EP4 receptors and COX-2 induces synergistic apoptosis in KSHV and EBV associated non-Hodgkin lymphoma cell lines"

Article Title: Concurrent targeting of EP1/EP4 receptors and COX-2 induces synergistic apoptosis in KSHV and EBV associated non-Hodgkin lymphoma cell lines

Journal: Translational research : the journal of laboratory and clinical medicine

doi: 10.1016/j.trsl.2013.02.008

EP receptors in non-Hodgkin lymphoma cell lines and de novo KSHV infected HMVEC-d cells (a) Total lysates from 5×10 5 BJAB, Akata/EBV−, BCBL-1, BC-3, Akata/EBV+, and JSC-1 cells were immunoblotted for EP1, EP2, EP3, and EP4. Data represents three independent experiments. Tubulin was used as loading control. (b) In parallel experiments, supernatants from the indicated cells were collected to measure the amount of PGE2 secreted by each cell line. (c) The indicated cell lines were stained for EP1, EP2, EP3, and EP4 receptors by immunofluorescence. (d) Mean fluorescent intensity (MFI) of EP1, EP2, EP3, and EP4 receptors in HMVEC-d cells infected with KSHV measured by FACS. Indicated are the MFI for the respective receptor at each time point. The data is representative of three independent experiments.
Figure Legend Snippet: EP receptors in non-Hodgkin lymphoma cell lines and de novo KSHV infected HMVEC-d cells (a) Total lysates from 5×10 5 BJAB, Akata/EBV−, BCBL-1, BC-3, Akata/EBV+, and JSC-1 cells were immunoblotted for EP1, EP2, EP3, and EP4. Data represents three independent experiments. Tubulin was used as loading control. (b) In parallel experiments, supernatants from the indicated cells were collected to measure the amount of PGE2 secreted by each cell line. (c) The indicated cell lines were stained for EP1, EP2, EP3, and EP4 receptors by immunofluorescence. (d) Mean fluorescent intensity (MFI) of EP1, EP2, EP3, and EP4 receptors in HMVEC-d cells infected with KSHV measured by FACS. Indicated are the MFI for the respective receptor at each time point. The data is representative of three independent experiments.

Techniques Used: Infection, Staining, Immunofluorescence, FACS

16) Product Images from "Altered Prostanoid Signaling Contributes to Increased Skin Tumorigenesis in Tpl2 Knockout Mice"

Article Title: Altered Prostanoid Signaling Contributes to Increased Skin Tumorigenesis in Tpl2 Knockout Mice

Journal: PLoS ONE

doi: 10.1371/journal.pone.0056212

Western blotting of prostanoid receptor expression in wildtype and Tpl2 −/− mouse keratinocytes. Wildtype or Tpl2 −/− keratinocytes received DMSO only (labeled C) or TPA (10 ng/ml) for 1, 3, 6, 12, or 24 hours. Western blotting analysis was used to determine the levels of EP1, EP2, EP3, EP4, and β -actin. Bands were quantified through densitometry (Image J) and normalized to β -actin.
Figure Legend Snippet: Western blotting of prostanoid receptor expression in wildtype and Tpl2 −/− mouse keratinocytes. Wildtype or Tpl2 −/− keratinocytes received DMSO only (labeled C) or TPA (10 ng/ml) for 1, 3, 6, 12, or 24 hours. Western blotting analysis was used to determine the levels of EP1, EP2, EP3, EP4, and β -actin. Bands were quantified through densitometry (Image J) and normalized to β -actin.

Techniques Used: Western Blot, Expressing, Labeling

EP2 and EP4 receptor expression is heightened in epidermis and papillomas from Tpl2 −/− mice. Shaved wildtype and Tpl2 −/− mice were treated with TPA (10 µg) for 0, 4, 8, 12, or 24 hours and analyzed for expression of EP2 ( Figure 4A ) or EP4 ( Figure 4C ). Additionally, papillomas from wildtype and Tpl2 −/− mice were analyzed for expression of EP2 ( Figure 4B ). Magnification = 10X.
Figure Legend Snippet: EP2 and EP4 receptor expression is heightened in epidermis and papillomas from Tpl2 −/− mice. Shaved wildtype and Tpl2 −/− mice were treated with TPA (10 µg) for 0, 4, 8, 12, or 24 hours and analyzed for expression of EP2 ( Figure 4A ) or EP4 ( Figure 4C ). Additionally, papillomas from wildtype and Tpl2 −/− mice were analyzed for expression of EP2 ( Figure 4B ). Magnification = 10X.

Techniques Used: Expressing, Mouse Assay

Proposed model describing how loss of Tpl2 results in increased inflammation and tumorigenesis. Tpl2 is normally held in complex with p105 NF-κB, preventing proteolysis and activation of the NF-κB and MAPK signaling pathways. Without Tpl2, NF-κB activity increases (see reference 19), resulting in increased production of NF-κB target genes such as COX-2. COX-2 activation results in the conversion of arachidonic acid to PGE 2 , which then can bind to one of four G-protein linked receptors (EP1–EP4). EP2 and EP4 receptor activation causes the formation of cAMP from ATP. cAMP can then bind to cAMP response genes such as CREB and PKA. The end result is an increase in inflammatory and cell survival proteins, ultimately contributing to both tumorigenesis and inflammation.
Figure Legend Snippet: Proposed model describing how loss of Tpl2 results in increased inflammation and tumorigenesis. Tpl2 is normally held in complex with p105 NF-κB, preventing proteolysis and activation of the NF-κB and MAPK signaling pathways. Without Tpl2, NF-κB activity increases (see reference 19), resulting in increased production of NF-κB target genes such as COX-2. COX-2 activation results in the conversion of arachidonic acid to PGE 2 , which then can bind to one of four G-protein linked receptors (EP1–EP4). EP2 and EP4 receptor activation causes the formation of cAMP from ATP. cAMP can then bind to cAMP response genes such as CREB and PKA. The end result is an increase in inflammatory and cell survival proteins, ultimately contributing to both tumorigenesis and inflammation.

Techniques Used: Activation Assay, Activity Assay

17) Product Images from "Altered Prostanoid Signaling Contributes to Increased Skin Tumorigenesis in Tpl2 Knockout Mice"

Article Title: Altered Prostanoid Signaling Contributes to Increased Skin Tumorigenesis in Tpl2 Knockout Mice

Journal: PLoS ONE

doi: 10.1371/journal.pone.0056212

Western blotting of prostanoid receptor expression in wildtype and Tpl2 −/− mouse keratinocytes. Wildtype or Tpl2 −/− keratinocytes received DMSO only (labeled C) or TPA (10 ng/ml) for 1, 3, 6, 12, or 24 hours. Western blotting analysis was used to determine the levels of EP1, EP2, EP3, EP4, and β -actin. Bands were quantified through densitometry (Image J) and normalized to β -actin.
Figure Legend Snippet: Western blotting of prostanoid receptor expression in wildtype and Tpl2 −/− mouse keratinocytes. Wildtype or Tpl2 −/− keratinocytes received DMSO only (labeled C) or TPA (10 ng/ml) for 1, 3, 6, 12, or 24 hours. Western blotting analysis was used to determine the levels of EP1, EP2, EP3, EP4, and β -actin. Bands were quantified through densitometry (Image J) and normalized to β -actin.

Techniques Used: Western Blot, Expressing, Labeling

EP2 and EP4 receptor expression is heightened in epidermis and papillomas from Tpl2 −/− mice. Shaved wildtype and Tpl2 −/− mice were treated with TPA (10 µg) for 0, 4, 8, 12, or 24 hours and analyzed for expression of EP2 ( Figure 4A ) or EP4 ( Figure 4C ). Additionally, papillomas from wildtype and Tpl2 −/− mice were analyzed for expression of EP2 ( Figure 4B ). Magnification = 10X.
Figure Legend Snippet: EP2 and EP4 receptor expression is heightened in epidermis and papillomas from Tpl2 −/− mice. Shaved wildtype and Tpl2 −/− mice were treated with TPA (10 µg) for 0, 4, 8, 12, or 24 hours and analyzed for expression of EP2 ( Figure 4A ) or EP4 ( Figure 4C ). Additionally, papillomas from wildtype and Tpl2 −/− mice were analyzed for expression of EP2 ( Figure 4B ). Magnification = 10X.

Techniques Used: Expressing, Mouse Assay

Proposed model describing how loss of Tpl2 results in increased inflammation and tumorigenesis. Tpl2 is normally held in complex with p105 NF-κB, preventing proteolysis and activation of the NF-κB and MAPK signaling pathways. Without Tpl2, NF-κB activity increases (see reference 19), resulting in increased production of NF-κB target genes such as COX-2. COX-2 activation results in the conversion of arachidonic acid to PGE 2 , which then can bind to one of four G-protein linked receptors (EP1–EP4). EP2 and EP4 receptor activation causes the formation of cAMP from ATP. cAMP can then bind to cAMP response genes such as CREB and PKA. The end result is an increase in inflammatory and cell survival proteins, ultimately contributing to both tumorigenesis and inflammation.
Figure Legend Snippet: Proposed model describing how loss of Tpl2 results in increased inflammation and tumorigenesis. Tpl2 is normally held in complex with p105 NF-κB, preventing proteolysis and activation of the NF-κB and MAPK signaling pathways. Without Tpl2, NF-κB activity increases (see reference 19), resulting in increased production of NF-κB target genes such as COX-2. COX-2 activation results in the conversion of arachidonic acid to PGE 2 , which then can bind to one of four G-protein linked receptors (EP1–EP4). EP2 and EP4 receptor activation causes the formation of cAMP from ATP. cAMP can then bind to cAMP response genes such as CREB and PKA. The end result is an increase in inflammatory and cell survival proteins, ultimately contributing to both tumorigenesis and inflammation.

Techniques Used: Activation Assay, Activity Assay

18) Product Images from "Selective Inhibition of Prostaglandin E2 Receptors EP2 and EP4 Inhibits Adhesion of Human Endometriotic Epithelial and Stromal Cells Through Suppression of Integrin-Mediated Mechanisms 1"

Article Title: Selective Inhibition of Prostaglandin E2 Receptors EP2 and EP4 Inhibits Adhesion of Human Endometriotic Epithelial and Stromal Cells Through Suppression of Integrin-Mediated Mechanisms 1

Journal: Biology of Reproduction

doi: 10.1095/biolreprod.112.100883

Selective inhibition of EP2 and EP4 decreased the expression of integrin proteins in human endometriotic epithelial and stromal cells. A ) Western blot analysis of integrin α- and β-subunit proteins in endometriotic epithelial cells 12Z
Figure Legend Snippet: Selective inhibition of EP2 and EP4 decreased the expression of integrin proteins in human endometriotic epithelial and stromal cells. A ) Western blot analysis of integrin α- and β-subunit proteins in endometriotic epithelial cells 12Z

Techniques Used: Inhibition, Expressing, Western Blot

Mechanisms through which EP2- and EP4-mediated PGE 2 signaling promotes and loss of function of EP2 and EP4 inhibits adhesion of human endometriotic epithelial and stromal cells on ECM substrates. 1 ) PGE 2 binds EP2 and EP4 receptors. 2 ) Activation of EP2/EP4
Figure Legend Snippet: Mechanisms through which EP2- and EP4-mediated PGE 2 signaling promotes and loss of function of EP2 and EP4 inhibits adhesion of human endometriotic epithelial and stromal cells on ECM substrates. 1 ) PGE 2 binds EP2 and EP4 receptors. 2 ) Activation of EP2/EP4

Techniques Used: Activation Assay

Selective inhibition of EP2 and EP4 decreased their direct interaction with β1- and β3-subunits of integrin receptors and FAK and talin proteins in human endometriotic epithelial and stromal cells. A ) Immunoprecipitation (IP)/Western blot
Figure Legend Snippet: Selective inhibition of EP2 and EP4 decreased their direct interaction with β1- and β3-subunits of integrin receptors and FAK and talin proteins in human endometriotic epithelial and stromal cells. A ) Immunoprecipitation (IP)/Western blot

Techniques Used: Inhibition, Immunoprecipitation, Western Blot

EP2 and EP4 interact with β-subunit of integrin receptors through Src/ β-arrestin 1 complex in human endometriotic epithelial and stromal cells. A ) Immunoprecipitation (IP)/Western blot analysis. Total Src protein was immunoprecipitated
Figure Legend Snippet: EP2 and EP4 interact with β-subunit of integrin receptors through Src/ β-arrestin 1 complex in human endometriotic epithelial and stromal cells. A ) Immunoprecipitation (IP)/Western blot analysis. Total Src protein was immunoprecipitated

Techniques Used: Immunoprecipitation, Western Blot

Selective inhibition of EP2 and EP4 decreased the expression of talin and FAK proteins in human endometriotic epithelial and stromal cells. Densitometry of Western blot analysis of talin ( A ) and FAK ( B ) proteins in endometriotic epithelial cells 12Z and
Figure Legend Snippet: Selective inhibition of EP2 and EP4 decreased the expression of talin and FAK proteins in human endometriotic epithelial and stromal cells. Densitometry of Western blot analysis of talin ( A ) and FAK ( B ) proteins in endometriotic epithelial cells 12Z and

Techniques Used: Inhibition, Expressing, Western Blot

EP2 and EP4 interact with p-FAK, P-ERK1/2, and P-AKT through Src/ β-arrestin 1 complex in human endometriotic epithelial and stromal cells. A ) Immunoprecipitation (IP)/Western blot analysis. Total Src protein was immunoprecipitated, and its interactions
Figure Legend Snippet: EP2 and EP4 interact with p-FAK, P-ERK1/2, and P-AKT through Src/ β-arrestin 1 complex in human endometriotic epithelial and stromal cells. A ) Immunoprecipitation (IP)/Western blot analysis. Total Src protein was immunoprecipitated, and its interactions

Techniques Used: Immunoprecipitation, Western Blot

Knockdown of EP2 and EP4 decreased adhesion of human endometriotic epithelial and stromal cells. Effects of knockdown of EP2 and EP4 genes on adhesion of endometriotic epithelial cells 12Z ( Panel-1 , A – F ) and endometriotic stromal cell 22B ( Panel-2
Figure Legend Snippet: Knockdown of EP2 and EP4 decreased adhesion of human endometriotic epithelial and stromal cells. Effects of knockdown of EP2 and EP4 genes on adhesion of endometriotic epithelial cells 12Z ( Panel-1 , A – F ) and endometriotic stromal cell 22B ( Panel-2

Techniques Used:

Selective inhibition of EP2 and EP4 decreased adhesion of human endometriotic epithelial and stromal cells. Effects of pharmacological inhibition of EP2 and EP4 on the temporal adhesion of endometriotic epithelial cells 12Z ( A – F ) and endometriotic
Figure Legend Snippet: Selective inhibition of EP2 and EP4 decreased adhesion of human endometriotic epithelial and stromal cells. Effects of pharmacological inhibition of EP2 and EP4 on the temporal adhesion of endometriotic epithelial cells 12Z ( A – F ) and endometriotic

Techniques Used: Inhibition

19) Product Images from "Autocrine Prostaglandin E2 Signaling Promotes Tumor Cell Survival and Proliferation in Childhood Neuroblastoma"

Article Title: Autocrine Prostaglandin E2 Signaling Promotes Tumor Cell Survival and Proliferation in Childhood Neuroblastoma

Journal: PLoS ONE

doi: 10.1371/journal.pone.0029331

Neuroblastoma expresses all four PGE 2 receptors. (A) Immunohistochemistry showing specific expression of EP1-4 in tumor cells of a primary human neuroblastoma. (B) Antibody specific blocking peptides were used to control for non-specific binding. Magnification ×400. (C) RT-PCR detecting EP1-4 mRNA in human neuroblastoma cell lines. The myelocytic cell line, U-937, was used as positive control. β-actin was used to ensure equal cDNA load. (D) Western blot detecting bands at 42, 52, 52 and 65 kDa corresponding to EP1, EP2, EP3 and EP4, respectively, in protein extracts from human neuroblastoma cell lines. U-937 cells were used as a positive control. β-actin was used to ensure equal protein loading. The western blots are representative of two independent experiments. (E) Immunofluorescence staining identifying EP1 and EP4 receptor expression in the cellular membrane, in the cytoplasm, and in the nuclear membrane of neuroblastoma cells. EP2 and EP3 were detected in the cellular membrane and in the cytoplasm. Cells were double stained with DAPI to visualize cell nucleus. Magnification ×400.
Figure Legend Snippet: Neuroblastoma expresses all four PGE 2 receptors. (A) Immunohistochemistry showing specific expression of EP1-4 in tumor cells of a primary human neuroblastoma. (B) Antibody specific blocking peptides were used to control for non-specific binding. Magnification ×400. (C) RT-PCR detecting EP1-4 mRNA in human neuroblastoma cell lines. The myelocytic cell line, U-937, was used as positive control. β-actin was used to ensure equal cDNA load. (D) Western blot detecting bands at 42, 52, 52 and 65 kDa corresponding to EP1, EP2, EP3 and EP4, respectively, in protein extracts from human neuroblastoma cell lines. U-937 cells were used as a positive control. β-actin was used to ensure equal protein loading. The western blots are representative of two independent experiments. (E) Immunofluorescence staining identifying EP1 and EP4 receptor expression in the cellular membrane, in the cytoplasm, and in the nuclear membrane of neuroblastoma cells. EP2 and EP3 were detected in the cellular membrane and in the cytoplasm. Cells were double stained with DAPI to visualize cell nucleus. Magnification ×400.

Techniques Used: Immunohistochemistry, Expressing, Blocking Assay, Binding Assay, Reverse Transcription Polymerase Chain Reaction, Positive Control, Western Blot, Immunofluorescence, Staining

20) Product Images from "The cyclooxygenase-2 pathway via the PGE2 EP2 receptor contributes to oligodendrocytes apoptosis in cuprizone-induced demyelination"

Article Title: The cyclooxygenase-2 pathway via the PGE2 EP2 receptor contributes to oligodendrocytes apoptosis in cuprizone-induced demyelination

Journal: Journal of Neurochemistry

doi: 10.1111/j.1471-4159.2011.07363.x

The EP2 receptor antagonist AH6809 reduces demyelination, motor dysfunction and caspase-3 activity after cuprizone exposure
Figure Legend Snippet: The EP2 receptor antagonist AH6809 reduces demyelination, motor dysfunction and caspase-3 activity after cuprizone exposure

Techniques Used: Activity Assay

21) Product Images from "PGE2 receptor EP2 mediates the antagonistic effect of COX-2 on TGF-? signaling during mammary tumorigenesis"

Article Title: PGE2 receptor EP2 mediates the antagonistic effect of COX-2 on TGF-? signaling during mammary tumorigenesis

Journal: The FASEB Journal

doi: 10.1096/fj.09-141341

TGF-β induces EP2 expression in normal and malignant MECs. A ) Quiescent NMuMG cells were stimulated with TGF-β1 (5 ng/ml) for 36 h. Detergent-solubilized whole-cell extracts were immunoblotted with antibodies against COX-2, EPs 1-4, and
Figure Legend Snippet: TGF-β induces EP2 expression in normal and malignant MECs. A ) Quiescent NMuMG cells were stimulated with TGF-β1 (5 ng/ml) for 36 h. Detergent-solubilized whole-cell extracts were immunoblotted with antibodies against COX-2, EPs 1-4, and

Techniques Used: Expressing

Altered EP2 expression affects oncogenic TGF-β signaling in malignant MECs. A ) Top panel: detergent-solubilized whole-cell extracts prepared from control ( i.e. , empty vector; Neo) or EP2-expressing 4T1 cells were immunoblotted with antibodies
Figure Legend Snippet: Altered EP2 expression affects oncogenic TGF-β signaling in malignant MECs. A ) Top panel: detergent-solubilized whole-cell extracts prepared from control ( i.e. , empty vector; Neo) or EP2-expressing 4T1 cells were immunoblotted with antibodies

Techniques Used: Expressing, Plasmid Preparation

EP2 deficiency abrogates the oncogenic TGF-β signaling in 4T1 cells. A ) 4T1 cells were infected with lentivirus particles encoding for either a scrambled shRNA (Scram) or a murine EP2 shRNA (EP2sh). The extent of EP2 depletion was monitored by
Figure Legend Snippet: EP2 deficiency abrogates the oncogenic TGF-β signaling in 4T1 cells. A ) 4T1 cells were infected with lentivirus particles encoding for either a scrambled shRNA (Scram) or a murine EP2 shRNA (EP2sh). The extent of EP2 depletion was monitored by

Techniques Used: Infection, shRNA

Altered EP2 expression affects oncogenic TGF-β signaling in malignant MECs. A ) NMuMG cells were infected with lentivirus particles encoding for either a scrambled shRNA (Scram) or a murine EP2 shRNA (EP2sh). Extent of EP2 depletion was monitored
Figure Legend Snippet: Altered EP2 expression affects oncogenic TGF-β signaling in malignant MECs. A ) NMuMG cells were infected with lentivirus particles encoding for either a scrambled shRNA (Scram) or a murine EP2 shRNA (EP2sh). Extent of EP2 depletion was monitored

Techniques Used: Expressing, Infection, shRNA

EP2 expression alters oncogenic TGF-β signaling in NMuMG cells. A ) Top panel: detergent-solubilized whole-cell extracts prepared from control ( i.e. , empty vector; Neo) or EP2-expressing NMuMG cells were immunoblotted with antibodies against EP2
Figure Legend Snippet: EP2 expression alters oncogenic TGF-β signaling in NMuMG cells. A ) Top panel: detergent-solubilized whole-cell extracts prepared from control ( i.e. , empty vector; Neo) or EP2-expressing NMuMG cells were immunoblotted with antibodies against EP2

Techniques Used: Expressing, Plasmid Preparation

EP2 deficiency inhibits mammary tumor growth and pulmonary metastasis induced by TGF-β. A , B ) Control (Scram) or EP2-deficient 4T1 cells were injected into the mammary fat pads of Balb/C mice. At 10 d postinjection, tumor volumes were measured
Figure Legend Snippet: EP2 deficiency inhibits mammary tumor growth and pulmonary metastasis induced by TGF-β. A , B ) Control (Scram) or EP2-deficient 4T1 cells were injected into the mammary fat pads of Balb/C mice. At 10 d postinjection, tumor volumes were measured

Techniques Used: Injection, Mouse Assay

22) Product Images from "PGE2 receptor EP2 mediates the antagonistic effect of COX-2 on TGF-? signaling during mammary tumorigenesis"

Article Title: PGE2 receptor EP2 mediates the antagonistic effect of COX-2 on TGF-? signaling during mammary tumorigenesis

Journal: The FASEB Journal

doi: 10.1096/fj.09-141341

TGF-β induces EP2 expression in normal and malignant MECs. A ) Quiescent NMuMG cells were stimulated with TGF-β1 (5 ng/ml) for 36 h. Detergent-solubilized whole-cell extracts were immunoblotted with antibodies against COX-2, EPs 1-4, and
Figure Legend Snippet: TGF-β induces EP2 expression in normal and malignant MECs. A ) Quiescent NMuMG cells were stimulated with TGF-β1 (5 ng/ml) for 36 h. Detergent-solubilized whole-cell extracts were immunoblotted with antibodies against COX-2, EPs 1-4, and

Techniques Used: Expressing

Altered EP2 expression affects oncogenic TGF-β signaling in malignant MECs. A ) Top panel: detergent-solubilized whole-cell extracts prepared from control ( i.e. , empty vector; Neo) or EP2-expressing 4T1 cells were immunoblotted with antibodies
Figure Legend Snippet: Altered EP2 expression affects oncogenic TGF-β signaling in malignant MECs. A ) Top panel: detergent-solubilized whole-cell extracts prepared from control ( i.e. , empty vector; Neo) or EP2-expressing 4T1 cells were immunoblotted with antibodies

Techniques Used: Expressing, Plasmid Preparation

EP2 deficiency abrogates the oncogenic TGF-β signaling in 4T1 cells. A ) 4T1 cells were infected with lentivirus particles encoding for either a scrambled shRNA (Scram) or a murine EP2 shRNA (EP2sh). The extent of EP2 depletion was monitored by
Figure Legend Snippet: EP2 deficiency abrogates the oncogenic TGF-β signaling in 4T1 cells. A ) 4T1 cells were infected with lentivirus particles encoding for either a scrambled shRNA (Scram) or a murine EP2 shRNA (EP2sh). The extent of EP2 depletion was monitored by

Techniques Used: Infection, shRNA

Altered EP2 expression affects oncogenic TGF-β signaling in malignant MECs. A ) NMuMG cells were infected with lentivirus particles encoding for either a scrambled shRNA (Scram) or a murine EP2 shRNA (EP2sh). Extent of EP2 depletion was monitored
Figure Legend Snippet: Altered EP2 expression affects oncogenic TGF-β signaling in malignant MECs. A ) NMuMG cells were infected with lentivirus particles encoding for either a scrambled shRNA (Scram) or a murine EP2 shRNA (EP2sh). Extent of EP2 depletion was monitored

Techniques Used: Expressing, Infection, shRNA

EP2 expression alters oncogenic TGF-β signaling in NMuMG cells. A ) Top panel: detergent-solubilized whole-cell extracts prepared from control ( i.e. , empty vector; Neo) or EP2-expressing NMuMG cells were immunoblotted with antibodies against EP2
Figure Legend Snippet: EP2 expression alters oncogenic TGF-β signaling in NMuMG cells. A ) Top panel: detergent-solubilized whole-cell extracts prepared from control ( i.e. , empty vector; Neo) or EP2-expressing NMuMG cells were immunoblotted with antibodies against EP2

Techniques Used: Expressing, Plasmid Preparation

EP2 deficiency inhibits mammary tumor growth and pulmonary metastasis induced by TGF-β. A , B ) Control (Scram) or EP2-deficient 4T1 cells were injected into the mammary fat pads of Balb/C mice. At 10 d postinjection, tumor volumes were measured
Figure Legend Snippet: EP2 deficiency inhibits mammary tumor growth and pulmonary metastasis induced by TGF-β. A , B ) Control (Scram) or EP2-deficient 4T1 cells were injected into the mammary fat pads of Balb/C mice. At 10 d postinjection, tumor volumes were measured

Techniques Used: Injection, Mouse Assay

23) Product Images from "Anti-inflammatory Role of Microsomal Prostaglandin E Synthase-1 in a Model of Neuroinflammation *"

Article Title: Anti-inflammatory Role of Microsomal Prostaglandin E Synthase-1 in a Model of Neuroinflammation *

Journal: The Journal of Biological Chemistry

doi: 10.1074/jbc.M110.157362

LPS priming induces EP2 and EP4 expression in spinal microglia and/or invading macrophages. A , mRNA levels of EP2 and EP4 were determined by real-time RT-PCR in L4–5 spinal segments of wild-type mice receiving 27-h and 3-h prior preparation of either ACSF twice or ACSF and LPS twice or LPS twice. Protein homogenates of six animals were pooled. B , same as A except that EP2 expression is shown by Western blot analysis. In the lower panel the densitometric analysis of expression in 3–4 mice is shown. Student's t test: **, p ≤ 0.01. C and D , immunohistochemical analysis of spinal cord tissue sections from naïve and LPS-primed mice. EP2 ( B ) and EP4 ( C ) expression shown in red were costained with CD11b for microglia and/or macrophages ( green ). Shown are representative regions from spinal cord white matter. Scale bars , 20 μm.
Figure Legend Snippet: LPS priming induces EP2 and EP4 expression in spinal microglia and/or invading macrophages. A , mRNA levels of EP2 and EP4 were determined by real-time RT-PCR in L4–5 spinal segments of wild-type mice receiving 27-h and 3-h prior preparation of either ACSF twice or ACSF and LPS twice or LPS twice. Protein homogenates of six animals were pooled. B , same as A except that EP2 expression is shown by Western blot analysis. In the lower panel the densitometric analysis of expression in 3–4 mice is shown. Student's t test: **, p ≤ 0.01. C and D , immunohistochemical analysis of spinal cord tissue sections from naïve and LPS-primed mice. EP2 ( B ) and EP4 ( C ) expression shown in red were costained with CD11b for microglia and/or macrophages ( green ). Shown are representative regions from spinal cord white matter. Scale bars , 20 μm.

Techniques Used: Expressing, Quantitative RT-PCR, Mouse Assay, Western Blot, Immunohistochemistry

Schematic summary of the results showing the consequences of mPGES-1 mediated PGE 2 synthesis for LPS-induced neuroinflammation. A , single intrathecal LPS injection, which simulates acute neuroinflammation, activates microglial toll-like receptor-4, causing a marked increase of cytokine release ( i.e. TNFα and IL-1β). Via activation of their receptors they induce in microglia, neurons, or endothelial cells an up-regulation of COX-2 and mPGES-1 resulting in a selective synthesis of PGE 2 . Through neuronal EP2, PGE 2 induces deleterious effects including neurodegeneration, excitotoxicity, or sensitization. B , if LPS was injected sequentially (24 h and 3 h before preparation), a situation of chronic neuroinflammation is mimicked. As a consequence, EP2 and EP4 are up-regulated in microglia enabling PGE 2 to act via an additional pathway in microglia with a function as anti-inflammatory negative feedback regulator. As a proximate cause of this pathway, innate immune responses including cytokine and prostanoid synthesis induced by a second LPS injection are attenuated, promoting the resolution of neuroinflammation.
Figure Legend Snippet: Schematic summary of the results showing the consequences of mPGES-1 mediated PGE 2 synthesis for LPS-induced neuroinflammation. A , single intrathecal LPS injection, which simulates acute neuroinflammation, activates microglial toll-like receptor-4, causing a marked increase of cytokine release ( i.e. TNFα and IL-1β). Via activation of their receptors they induce in microglia, neurons, or endothelial cells an up-regulation of COX-2 and mPGES-1 resulting in a selective synthesis of PGE 2 . Through neuronal EP2, PGE 2 induces deleterious effects including neurodegeneration, excitotoxicity, or sensitization. B , if LPS was injected sequentially (24 h and 3 h before preparation), a situation of chronic neuroinflammation is mimicked. As a consequence, EP2 and EP4 are up-regulated in microglia enabling PGE 2 to act via an additional pathway in microglia with a function as anti-inflammatory negative feedback regulator. As a proximate cause of this pathway, innate immune responses including cytokine and prostanoid synthesis induced by a second LPS injection are attenuated, promoting the resolution of neuroinflammation.

Techniques Used: Injection, Activation Assay, Activated Clotting Time Assay

24) Product Images from "Mechanisms Mediating the Synergistic Anticancer Effects of Combined ?-Tocotrienol and Celecoxib Treatment"

Article Title: Mechanisms Mediating the Synergistic Anticancer Effects of Combined ?-Tocotrienol and Celecoxib Treatment

Journal: Journal of bioanalysis & biomedicine

doi: 10.4172/1948-593X.1000036

Western blot analysis of γ-tocotrienol and celecoxib treatment on EP2 and EP4 receptors in neoplastic +SA mammary epithelial cells. Cells were initially plated at a density of 1×10 6 cells/100 mm culture dishes, divided into different treatment groups, and then maintained on their respective control or treatment media for a 4-day treatment period. Afterwards, cells were isolated and prepared for Western blot analysis. Samples were analyzed for relative levels of the proteins. Scanning densitometric analysis was performed for each blot to visualize the relative levels of proteins. Integrated optical density of each band was normalized with their corresponding β-actin and control treatment bands and then shown in bar graphs. Vertical bars indicate the fold-change in protein levels in various treatment groups as compared with their respective controls.
Figure Legend Snippet: Western blot analysis of γ-tocotrienol and celecoxib treatment on EP2 and EP4 receptors in neoplastic +SA mammary epithelial cells. Cells were initially plated at a density of 1×10 6 cells/100 mm culture dishes, divided into different treatment groups, and then maintained on their respective control or treatment media for a 4-day treatment period. Afterwards, cells were isolated and prepared for Western blot analysis. Samples were analyzed for relative levels of the proteins. Scanning densitometric analysis was performed for each blot to visualize the relative levels of proteins. Integrated optical density of each band was normalized with their corresponding β-actin and control treatment bands and then shown in bar graphs. Vertical bars indicate the fold-change in protein levels in various treatment groups as compared with their respective controls.

Techniques Used: Western Blot, Isolation

25) Product Images from "The Prostaglandin E2 Receptor, EP2, Stimulates Keratinocyte Proliferation in Mouse Skin by G Protein-dependent and ?-Arrestin1-dependent Signaling Pathways *"

Article Title: The Prostaglandin E2 Receptor, EP2, Stimulates Keratinocyte Proliferation in Mouse Skin by G Protein-dependent and ?-Arrestin1-dependent Signaling Pathways *

Journal: The Journal of Biological Chemistry

doi: 10.1074/jbc.M110.117689

EP2 activation increased epidermal proliferation. A , BrdU incorporation into epidermal keratinocytes. Six-week-old female CD-1 mice were treated with acetone, butaprost (50 or 100 nmol), or PGE 2 (120 nmol) for 24 h, and BrdU was injected i.p. 1 h before sacrifice. The skin sections were immunostained with an antibody against BrdU. Skin sections are shown at a magnification of 200×. B , number of BrdU-stained cells in the skin of butaprost- and PGE 2 -treated mice. *, p
Figure Legend Snippet: EP2 activation increased epidermal proliferation. A , BrdU incorporation into epidermal keratinocytes. Six-week-old female CD-1 mice were treated with acetone, butaprost (50 or 100 nmol), or PGE 2 (120 nmol) for 24 h, and BrdU was injected i.p. 1 h before sacrifice. The skin sections were immunostained with an antibody against BrdU. Skin sections are shown at a magnification of 200×. B , number of BrdU-stained cells in the skin of butaprost- and PGE 2 -treated mice. *, p

Techniques Used: Activation Assay, BrdU Incorporation Assay, Mouse Assay, Injection, Staining

Proposed EP2-mediated signaling pathways that contributed to keratinocyte replication and mouse skin papilloma formation. EP2 stimulation by butaprost activated PKA and its downstream effectors, p-GSK3β, p-CREB, and p-ERK1/2. Butaprost also activated EGFR and its downstream effectors, p-ERK1/2, p-STAT3, and p-Akt. EGFR activation involves Src activation via an EP2-β-arrestin1-Src complex. Activation of the PKA and EGFR pathways induced cell proliferation, thereby contributing to skin tumor formation.
Figure Legend Snippet: Proposed EP2-mediated signaling pathways that contributed to keratinocyte replication and mouse skin papilloma formation. EP2 stimulation by butaprost activated PKA and its downstream effectors, p-GSK3β, p-CREB, and p-ERK1/2. Butaprost also activated EGFR and its downstream effectors, p-ERK1/2, p-STAT3, and p-Akt. EGFR activation involves Src activation via an EP2-β-arrestin1-Src complex. Activation of the PKA and EGFR pathways induced cell proliferation, thereby contributing to skin tumor formation.

Techniques Used: Activation Assay

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    Cayman Chemical pf 04418948
    PGE 2 regulates epithelial CFTR-dependent fluid secretion and mucociliary transport. ( A ) Human tracheal epithelial organoids cultured for 21 days in the absence or presence of daily stimulation with 1 μg/mL PGE 2 , or with PGE 2 + <t>EP2</t> <t>inhibitor</t> (EP2 inh ) or PGE 2 + EP4 inhibitor (EP4 inh ). Original magnification, 20×; scale bar, 100 μm. representative of at least 2–3 wells per experiment in at least 4 independent experiments with different tracheal and sinus epithelial donors. ( B ) Diameter of organoids in A . Each dot represents 1 of 200 randomly selected organoids per well × 3 replicate wells per condition. Line indicates median diameter. **** P
    Pf 04418948, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pf 04418948/product/Cayman Chemical
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    pf 04418948 - by Bioz Stars, 2022-11
    94/100 stars
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    94
    Cayman Chemical ep2 receptor polyclonal antibody
    PGE 2 regulates epithelial CFTR-dependent fluid secretion and mucociliary transport. ( A ) Human tracheal epithelial organoids cultured for 21 days in the absence or presence of daily stimulation with 1 μg/mL PGE 2 , or with PGE 2 + <t>EP2</t> <t>inhibitor</t> (EP2 inh ) or PGE 2 + EP4 inhibitor (EP4 inh ). Original magnification, 20×; scale bar, 100 μm. representative of at least 2–3 wells per experiment in at least 4 independent experiments with different tracheal and sinus epithelial donors. ( B ) Diameter of organoids in A . Each dot represents 1 of 200 randomly selected organoids per well × 3 replicate wells per condition. Line indicates median diameter. **** P
    Ep2 Receptor Polyclonal Antibody, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 94/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ep2 receptor polyclonal antibody/product/Cayman Chemical
    Average 94 stars, based on 8 article reviews
    Price from $9.99 to $1999.99
    ep2 receptor polyclonal antibody - by Bioz Stars, 2022-11
    94/100 stars
      Buy from Supplier

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    PGE 2 regulates epithelial CFTR-dependent fluid secretion and mucociliary transport. ( A ) Human tracheal epithelial organoids cultured for 21 days in the absence or presence of daily stimulation with 1 μg/mL PGE 2 , or with PGE 2 + EP2 inhibitor (EP2 inh ) or PGE 2 + EP4 inhibitor (EP4 inh ). Original magnification, 20×; scale bar, 100 μm. representative of at least 2–3 wells per experiment in at least 4 independent experiments with different tracheal and sinus epithelial donors. ( B ) Diameter of organoids in A . Each dot represents 1 of 200 randomly selected organoids per well × 3 replicate wells per condition. Line indicates median diameter. **** P

    Journal: JCI Insight

    Article Title: IL-13–programmed airway tuft cells produce PGE2, which promotes CFTR-dependent mucociliary function

    doi: 10.1172/jci.insight.159832

    Figure Lengend Snippet: PGE 2 regulates epithelial CFTR-dependent fluid secretion and mucociliary transport. ( A ) Human tracheal epithelial organoids cultured for 21 days in the absence or presence of daily stimulation with 1 μg/mL PGE 2 , or with PGE 2 + EP2 inhibitor (EP2 inh ) or PGE 2 + EP4 inhibitor (EP4 inh ). Original magnification, 20×; scale bar, 100 μm. representative of at least 2–3 wells per experiment in at least 4 independent experiments with different tracheal and sinus epithelial donors. ( B ) Diameter of organoids in A . Each dot represents 1 of 200 randomly selected organoids per well × 3 replicate wells per condition. Line indicates median diameter. **** P

    Article Snippet: Cells were stimulated with PGE2 (Sigma, 1 μg/mL) daily, EP2 inhibitor (PF-04418948, Cayman Chemical, 10 μM), EP4 inhibitor (L-161,982, Cayman Chemical, 10 μM), or CFTR inhibitor 172 (Sigma, 10 μM).

    Techniques: Cell Culture