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93
ATCC nci bl2171
Nci Bl2171, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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85
R&D Systems human recombinant cyt c
Human Recombinant Cyt C, supplied by R&D Systems, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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93
DSMZ rhizobia strain bradyrhizobium sp
Rhizobia Strain Bradyrhizobium Sp, supplied by DSMZ, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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94
Eldex Laboratories optos 1sip
Optos 1sip, supplied by Eldex Laboratories, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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92
Tocris epac1 r ce3f4
The P2Y 11 receptor-mediated release of sTNFR2, but not of VEGF, is controlled by the cAMP effector binding protein <t>Epac1.</t> A P2Y 11 receptor signaling upregulates the expression of suppressor of cytokine signaling 3 (SOCS3). M2 macrophages were cultured for 6 h in the presence of the P2Y 11 receptor agonist ATPγS (20 µM) either alone or in combination with the PDE4 inhibitor rolipram (10 µM), and the copy numbers of SOCS3 mRNA were determined using NanoString technology. NF340 (20 µM) was used to confirm that agonist-mediated changes were specific to P2Y 11 receptor stimulation. *** p < 0.001, **** p < 0.0001. B Graphical illustration showing that SOCS3 is a target gene of Epac1. C , D M2 macrophages were treated for 24 h with the P2Y 11 receptor agonist ATPγS (20 µM) either alone or in combination with IL-1α (2 ng·ml −1 ) or IL-1β (2 ng·ml −1 ) in the presence or absence of the PDE4-selective inhibitor rolipram (10 µM). In addition, all treatments were carried out in the presence or absence of the selective Epac1 inhibitor <t>(R)-CE3F4</t> (20 µM). sTNFR2 ( C ) and VEGF ( D ) levels were measured in cell culture supernatants (n = 3). ** p < 0.01, *** p < 0.001, **** p < 0.0001
Epac1 R Ce3f4, supplied by Tocris, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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The P2Y 11 receptor-mediated release of sTNFR2, but not of VEGF, is controlled by the cAMP effector binding protein Epac1. A P2Y 11 receptor signaling upregulates the expression of suppressor of cytokine signaling 3 (SOCS3). M2 macrophages were cultured for 6 h in the presence of the P2Y 11 receptor agonist ATPγS (20 µM) either alone or in combination with the PDE4 inhibitor rolipram (10 µM), and the copy numbers of SOCS3 mRNA were determined using NanoString technology. NF340 (20 µM) was used to confirm that agonist-mediated changes were specific to P2Y 11 receptor stimulation. *** p < 0.001, **** p < 0.0001. B Graphical illustration showing that SOCS3 is a target gene of Epac1. C , D M2 macrophages were treated for 24 h with the P2Y 11 receptor agonist ATPγS (20 µM) either alone or in combination with IL-1α (2 ng·ml −1 ) or IL-1β (2 ng·ml −1 ) in the presence or absence of the PDE4-selective inhibitor rolipram (10 µM). In addition, all treatments were carried out in the presence or absence of the selective Epac1 inhibitor (R)-CE3F4 (20 µM). sTNFR2 ( C ) and VEGF ( D ) levels were measured in cell culture supernatants (n = 3). ** p < 0.01, *** p < 0.001, **** p < 0.0001

Journal: Cellular and Molecular Life Sciences

Article Title: The P2Y 11 receptor of human M2 macrophages activates canonical and IL-1 receptor signaling to translate the extracellular danger signal ATP into anti-inflammatory and pro-angiogenic responses

doi: 10.1007/s00018-022-04548-z

Figure Lengend Snippet: The P2Y 11 receptor-mediated release of sTNFR2, but not of VEGF, is controlled by the cAMP effector binding protein Epac1. A P2Y 11 receptor signaling upregulates the expression of suppressor of cytokine signaling 3 (SOCS3). M2 macrophages were cultured for 6 h in the presence of the P2Y 11 receptor agonist ATPγS (20 µM) either alone or in combination with the PDE4 inhibitor rolipram (10 µM), and the copy numbers of SOCS3 mRNA were determined using NanoString technology. NF340 (20 µM) was used to confirm that agonist-mediated changes were specific to P2Y 11 receptor stimulation. *** p < 0.001, **** p < 0.0001. B Graphical illustration showing that SOCS3 is a target gene of Epac1. C , D M2 macrophages were treated for 24 h with the P2Y 11 receptor agonist ATPγS (20 µM) either alone or in combination with IL-1α (2 ng·ml −1 ) or IL-1β (2 ng·ml −1 ) in the presence or absence of the PDE4-selective inhibitor rolipram (10 µM). In addition, all treatments were carried out in the presence or absence of the selective Epac1 inhibitor (R)-CE3F4 (20 µM). sTNFR2 ( C ) and VEGF ( D ) levels were measured in cell culture supernatants (n = 3). ** p < 0.01, *** p < 0.001, **** p < 0.0001

Article Snippet: Further reagents utilized in this study include the PDE4-selective inhibitor rolipram (10 µM) (Sigma-Aldrich), BAPTA-AM (10 µM) (Sigma-Aldrich), calphostin C (250 nM) (Tocris), recombinant IL-1α and IL-1β (0.5–2 ng·ml −1 ) (R&D Systems, Minneapolis, MN, USA), the TACE/ADAM17 inhibitor TAPI-1 (20 µM) (Tocris), the selective inhibitor of Epac1 (R)-CE3F4 (20 µM) (Tocris), and the humanized anti-VEGF monoclonal antibody bevacizumab (0.5 µg ml −1 ) (Selleckchem, Houston, TX, USA).

Techniques: Binding Assay, Expressing, Cell Culture

The Epac1 inhibitor-mediated enhancement of the P2Y 11 -driven release of sTNFR2 depends on TACE/ADAM17. A–D M2 macrophages were treated for 24 h with the P2Y 11 receptor agonist ATPγS (20 µM) either alone ( A , C ) or in combination with the selective Epac1 inhibitor (R)-CE3F4 (20 µM) ( B , D ), in the presence or absence of IL-1α (2 ng·ml −1 ) ( A , B ) or IL-1β (2 ng·ml −1 ) ( C , D ), with or without the PDE4-selective inhibitor rolipram (10 µM) ( A–D ). TAPI-1 (20 µM) was used to verify an involvement of TACE/ADAM17 in the shedding of sTNFR2. sTNFR2 levels were determined in cell culture supernatants using CBA. NF340 (20 µM) was used to confirm that agonist-mediated responses were specific to P2Y 11 receptor stimulation ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Journal: Cellular and Molecular Life Sciences

Article Title: The P2Y 11 receptor of human M2 macrophages activates canonical and IL-1 receptor signaling to translate the extracellular danger signal ATP into anti-inflammatory and pro-angiogenic responses

doi: 10.1007/s00018-022-04548-z

Figure Lengend Snippet: The Epac1 inhibitor-mediated enhancement of the P2Y 11 -driven release of sTNFR2 depends on TACE/ADAM17. A–D M2 macrophages were treated for 24 h with the P2Y 11 receptor agonist ATPγS (20 µM) either alone ( A , C ) or in combination with the selective Epac1 inhibitor (R)-CE3F4 (20 µM) ( B , D ), in the presence or absence of IL-1α (2 ng·ml −1 ) ( A , B ) or IL-1β (2 ng·ml −1 ) ( C , D ), with or without the PDE4-selective inhibitor rolipram (10 µM) ( A–D ). TAPI-1 (20 µM) was used to verify an involvement of TACE/ADAM17 in the shedding of sTNFR2. sTNFR2 levels were determined in cell culture supernatants using CBA. NF340 (20 µM) was used to confirm that agonist-mediated responses were specific to P2Y 11 receptor stimulation ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Article Snippet: Further reagents utilized in this study include the PDE4-selective inhibitor rolipram (10 µM) (Sigma-Aldrich), BAPTA-AM (10 µM) (Sigma-Aldrich), calphostin C (250 nM) (Tocris), recombinant IL-1α and IL-1β (0.5–2 ng·ml −1 ) (R&D Systems, Minneapolis, MN, USA), the TACE/ADAM17 inhibitor TAPI-1 (20 µM) (Tocris), the selective inhibitor of Epac1 (R)-CE3F4 (20 µM) (Tocris), and the humanized anti-VEGF monoclonal antibody bevacizumab (0.5 µg ml −1 ) (Selleckchem, Houston, TX, USA).

Techniques: Cell Culture

The P2Y 11 /IL-1R-mediated secretion of CCL20 strongly depends on PKC signaling as well as on cAMP and Ca 2+ , while Epac1 inhibition enhances the P2Y 11 /IL-1R-mediated secretion of CCL20, an effect which is abolished when intracellular cAMP levels are raised by PDE4 inhibition. A M2 macrophages were treated for 24 h with the P2Y 11 receptor agonist ATPγS (20 µM) either alone or in combination with IL-1β (2 ng·ml −1 ), in the presence or absence of the PDE4-selective inhibitor rolipram (10 µM). In addition, all treatments were conducted with or without the Ca 2+ chelator BAPTA-AM (10 µM) or the protein kinase C inhibitor calphostin C (250 nM). CCL20 levels were measured in cell culture supernatants ( n = 3). B M2 macrophages were treated for 24 h with the P2Y 11 receptor agonist ATPγS (20 µM) either alone or in combination with IL-1α (2 ng·ml −1 ) or IL-1β (2 ng·ml −1 ), in the presence or absence of the PDE4-selective inhibitor rolipram (10 µM). In addition, all treatments were performed with or without the selective Epac1 inhibitor (R)-CE3F4 (20 µM). CCL20 levels were determined in cell culture supernatants ( n = 3). ** p < 0.01, **** p < 0.0001, #### p < 0.0001

Journal: Cellular and Molecular Life Sciences

Article Title: The P2Y 11 receptor of human M2 macrophages activates canonical and IL-1 receptor signaling to translate the extracellular danger signal ATP into anti-inflammatory and pro-angiogenic responses

doi: 10.1007/s00018-022-04548-z

Figure Lengend Snippet: The P2Y 11 /IL-1R-mediated secretion of CCL20 strongly depends on PKC signaling as well as on cAMP and Ca 2+ , while Epac1 inhibition enhances the P2Y 11 /IL-1R-mediated secretion of CCL20, an effect which is abolished when intracellular cAMP levels are raised by PDE4 inhibition. A M2 macrophages were treated for 24 h with the P2Y 11 receptor agonist ATPγS (20 µM) either alone or in combination with IL-1β (2 ng·ml −1 ), in the presence or absence of the PDE4-selective inhibitor rolipram (10 µM). In addition, all treatments were conducted with or without the Ca 2+ chelator BAPTA-AM (10 µM) or the protein kinase C inhibitor calphostin C (250 nM). CCL20 levels were measured in cell culture supernatants ( n = 3). B M2 macrophages were treated for 24 h with the P2Y 11 receptor agonist ATPγS (20 µM) either alone or in combination with IL-1α (2 ng·ml −1 ) or IL-1β (2 ng·ml −1 ), in the presence or absence of the PDE4-selective inhibitor rolipram (10 µM). In addition, all treatments were performed with or without the selective Epac1 inhibitor (R)-CE3F4 (20 µM). CCL20 levels were determined in cell culture supernatants ( n = 3). ** p < 0.01, **** p < 0.0001, #### p < 0.0001

Article Snippet: Further reagents utilized in this study include the PDE4-selective inhibitor rolipram (10 µM) (Sigma-Aldrich), BAPTA-AM (10 µM) (Sigma-Aldrich), calphostin C (250 nM) (Tocris), recombinant IL-1α and IL-1β (0.5–2 ng·ml −1 ) (R&D Systems, Minneapolis, MN, USA), the TACE/ADAM17 inhibitor TAPI-1 (20 µM) (Tocris), the selective inhibitor of Epac1 (R)-CE3F4 (20 µM) (Tocris), and the humanized anti-VEGF monoclonal antibody bevacizumab (0.5 µg ml −1 ) (Selleckchem, Houston, TX, USA).

Techniques: Inhibition, Cell Culture

Graphical summary of P2Y 11 anti-inflammatory and pro-angiogenic signaling in human M2 macrophages. 1 Canonical signaling: the ATP receptor P2Y 11 couples to PLC (via G q ) to induce Ca 2+ and PKC signaling as well as to AC (via G s ) to induce cAMP signaling. 2 P2Y 11 signaling is self-sustaining as it causes the downregulation of both, the ecto-ATPase CD39 (ENTPD1) and the pro-inflammatory ATP receptor P2X 7 . Anti-inflammatory effects of P2Y 11 signaling include the deactivation of genes encoding TLRs and inflammasome components (NLRP3, CASP1, PYCARD). 3 P2Y 11 /IL-1R crosstalk: P2Y 11 -induced upregulation of IL-1R renders M2 macrophages highly sensitive to the effects of exogenous IL-1 cytokines, which enhance the P2Y 11 -driven secretory response (VEGF, CCL20) by activation of the IL-1R signaling cascade. P2Y 11 /IL-1R crosstalk also causes the ADAM17-mediated release of sTNFR2. 4 Strong or excessive cAMP signaling can result in Epac1-dependent induction of SOCS3, which is known to attenuate IL-1R signaling through targeting of the TRAF6/TAK1 complex. Epac1 inhibitor (R)-CE3F4 enhanced the P2Y 11 /IL-1R-driven release of soluble TNFR2 (sTNFR2) and CCL20, with little effects on VEGF, suggesting that an Epac1/SOCS3 axis can control P2Y 11 /IL-1R signaling and ADAM17 pathways. 5 The potentiation of most P2Y 11 effects by rolipram-induced PDE4 inhibition emphasizes the importance of cAMP signaling in the P2Y 11 -mediated polarization of anti-inflammatory and pro-angiogenic M2 macrophages

Journal: Cellular and Molecular Life Sciences

Article Title: The P2Y 11 receptor of human M2 macrophages activates canonical and IL-1 receptor signaling to translate the extracellular danger signal ATP into anti-inflammatory and pro-angiogenic responses

doi: 10.1007/s00018-022-04548-z

Figure Lengend Snippet: Graphical summary of P2Y 11 anti-inflammatory and pro-angiogenic signaling in human M2 macrophages. 1 Canonical signaling: the ATP receptor P2Y 11 couples to PLC (via G q ) to induce Ca 2+ and PKC signaling as well as to AC (via G s ) to induce cAMP signaling. 2 P2Y 11 signaling is self-sustaining as it causes the downregulation of both, the ecto-ATPase CD39 (ENTPD1) and the pro-inflammatory ATP receptor P2X 7 . Anti-inflammatory effects of P2Y 11 signaling include the deactivation of genes encoding TLRs and inflammasome components (NLRP3, CASP1, PYCARD). 3 P2Y 11 /IL-1R crosstalk: P2Y 11 -induced upregulation of IL-1R renders M2 macrophages highly sensitive to the effects of exogenous IL-1 cytokines, which enhance the P2Y 11 -driven secretory response (VEGF, CCL20) by activation of the IL-1R signaling cascade. P2Y 11 /IL-1R crosstalk also causes the ADAM17-mediated release of sTNFR2. 4 Strong or excessive cAMP signaling can result in Epac1-dependent induction of SOCS3, which is known to attenuate IL-1R signaling through targeting of the TRAF6/TAK1 complex. Epac1 inhibitor (R)-CE3F4 enhanced the P2Y 11 /IL-1R-driven release of soluble TNFR2 (sTNFR2) and CCL20, with little effects on VEGF, suggesting that an Epac1/SOCS3 axis can control P2Y 11 /IL-1R signaling and ADAM17 pathways. 5 The potentiation of most P2Y 11 effects by rolipram-induced PDE4 inhibition emphasizes the importance of cAMP signaling in the P2Y 11 -mediated polarization of anti-inflammatory and pro-angiogenic M2 macrophages

Article Snippet: Further reagents utilized in this study include the PDE4-selective inhibitor rolipram (10 µM) (Sigma-Aldrich), BAPTA-AM (10 µM) (Sigma-Aldrich), calphostin C (250 nM) (Tocris), recombinant IL-1α and IL-1β (0.5–2 ng·ml −1 ) (R&D Systems, Minneapolis, MN, USA), the TACE/ADAM17 inhibitor TAPI-1 (20 µM) (Tocris), the selective inhibitor of Epac1 (R)-CE3F4 (20 µM) (Tocris), and the humanized anti-VEGF monoclonal antibody bevacizumab (0.5 µg ml −1 ) (Selleckchem, Houston, TX, USA).

Techniques: Activation Assay, Control, Inhibition