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vpc32183 inhibitor  (Avanti Polar)


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    Avanti Polar vpc32183 inhibitor
    Inhibition of PA-stimulated myoblast proliferation and Akt and ERK1/2 phosphorylation by the lysoPA (LPA) receptor antagonist <t>VPC32183.</t> Myoblasts were serum-starved in DMEM supplemented with 0.1% BSA for 24 h. ( A ) The cells were preincubated for 30 min with 5 μM VPC32183 and were then challenged with 15 μM PA or 15 μM LPA for 16 h, as indicated. [ 3 H]Thymidine incorporation was measured as described in the Materials and Methods section. Results are expressed relative to the control value without agonist and are the mean ± SEM of 3 independent experiments performed in triplicate. (* p < 0.05, control versus PA or LPA-treated cells, # p < 0.05; PA or LPA-treated cells versus PA or LPA-treated cells in the presence of VPC32183). ( B ) Cells were treated as in panel A. Cell proliferation was determined by staining the myoblasts with crystal violet as described in the Materials and Methods section. Results are expressed relative to the control value without agonist and are the mean ± SEM of 3 independent experiments performed. Control versus PA-treated cells; ** p < 0.01, control versus LPA-treated cells; # p < 0.05; PA- or LPA-treated cells versus PA- or LPA-treated cells in the presence of VPC32183). ( C ) Cells were preincubated with 5 μM VPC32183 for 30 min and then treated with 15 μM PA for 5 min. Cell lysates were analyzed by western blotting as described in the Materials and Methods section. Phosphorylation of Akt and ERK1/2 was determined using specific antibodies against phospho-Akt (P-Akt) or phospho-ERK1/2 (P-ERK1/2). Equal loading of protein was monitored using specific antibodies to total Akt and total ERK1/2. Panel C shows a representative blot of three independent experiments. ( D , E ) Results of scanning densitometry of the exposed films. Data are expressed as arbitrary units of intensity relative to the control siRNA values in the absence of agonist or inhibitor (Ctrl) and are the mean ± SEM of 3 replicate experiments. (* p < 0.05; ** p < 0.01; control versus PA-treated cells, # p < 0.05, ### p < 0.001; PA-treated cells versus PA-treated cells in the presence of VPC32183, as indicated).
    Vpc32183 Inhibitor, supplied by Avanti Polar, used in various techniques. Bioz Stars score: 92/100, based on 55 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Phosphatidic Acid Stimulates Myoblast Proliferation through Interaction with LPA1 and LPA2 Receptors"

    Article Title: Phosphatidic Acid Stimulates Myoblast Proliferation through Interaction with LPA1 and LPA2 Receptors

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms22031452

    Inhibition of PA-stimulated myoblast proliferation and Akt and ERK1/2 phosphorylation by the lysoPA (LPA) receptor antagonist VPC32183. Myoblasts were serum-starved in DMEM supplemented with 0.1% BSA for 24 h. ( A ) The cells were preincubated for 30 min with 5 μM VPC32183 and were then challenged with 15 μM PA or 15 μM LPA for 16 h, as indicated. [ 3 H]Thymidine incorporation was measured as described in the Materials and Methods section. Results are expressed relative to the control value without agonist and are the mean ± SEM of 3 independent experiments performed in triplicate. (* p < 0.05, control versus PA or LPA-treated cells, # p < 0.05; PA or LPA-treated cells versus PA or LPA-treated cells in the presence of VPC32183). ( B ) Cells were treated as in panel A. Cell proliferation was determined by staining the myoblasts with crystal violet as described in the Materials and Methods section. Results are expressed relative to the control value without agonist and are the mean ± SEM of 3 independent experiments performed. Control versus PA-treated cells; ** p < 0.01, control versus LPA-treated cells; # p < 0.05; PA- or LPA-treated cells versus PA- or LPA-treated cells in the presence of VPC32183). ( C ) Cells were preincubated with 5 μM VPC32183 for 30 min and then treated with 15 μM PA for 5 min. Cell lysates were analyzed by western blotting as described in the Materials and Methods section. Phosphorylation of Akt and ERK1/2 was determined using specific antibodies against phospho-Akt (P-Akt) or phospho-ERK1/2 (P-ERK1/2). Equal loading of protein was monitored using specific antibodies to total Akt and total ERK1/2. Panel C shows a representative blot of three independent experiments. ( D , E ) Results of scanning densitometry of the exposed films. Data are expressed as arbitrary units of intensity relative to the control siRNA values in the absence of agonist or inhibitor (Ctrl) and are the mean ± SEM of 3 replicate experiments. (* p < 0.05; ** p < 0.01; control versus PA-treated cells, # p < 0.05, ### p < 0.001; PA-treated cells versus PA-treated cells in the presence of VPC32183, as indicated).
    Figure Legend Snippet: Inhibition of PA-stimulated myoblast proliferation and Akt and ERK1/2 phosphorylation by the lysoPA (LPA) receptor antagonist VPC32183. Myoblasts were serum-starved in DMEM supplemented with 0.1% BSA for 24 h. ( A ) The cells were preincubated for 30 min with 5 μM VPC32183 and were then challenged with 15 μM PA or 15 μM LPA for 16 h, as indicated. [ 3 H]Thymidine incorporation was measured as described in the Materials and Methods section. Results are expressed relative to the control value without agonist and are the mean ± SEM of 3 independent experiments performed in triplicate. (* p < 0.05, control versus PA or LPA-treated cells, # p < 0.05; PA or LPA-treated cells versus PA or LPA-treated cells in the presence of VPC32183). ( B ) Cells were treated as in panel A. Cell proliferation was determined by staining the myoblasts with crystal violet as described in the Materials and Methods section. Results are expressed relative to the control value without agonist and are the mean ± SEM of 3 independent experiments performed. Control versus PA-treated cells; ** p < 0.01, control versus LPA-treated cells; # p < 0.05; PA- or LPA-treated cells versus PA- or LPA-treated cells in the presence of VPC32183). ( C ) Cells were preincubated with 5 μM VPC32183 for 30 min and then treated with 15 μM PA for 5 min. Cell lysates were analyzed by western blotting as described in the Materials and Methods section. Phosphorylation of Akt and ERK1/2 was determined using specific antibodies against phospho-Akt (P-Akt) or phospho-ERK1/2 (P-ERK1/2). Equal loading of protein was monitored using specific antibodies to total Akt and total ERK1/2. Panel C shows a representative blot of three independent experiments. ( D , E ) Results of scanning densitometry of the exposed films. Data are expressed as arbitrary units of intensity relative to the control siRNA values in the absence of agonist or inhibitor (Ctrl) and are the mean ± SEM of 3 replicate experiments. (* p < 0.05; ** p < 0.01; control versus PA-treated cells, # p < 0.05, ### p < 0.001; PA-treated cells versus PA-treated cells in the presence of VPC32183, as indicated).

    Techniques Used: Inhibition, Staining, Western Blot



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    Avanti Polar vpc32183 inhibitor
    Inhibition of PA-stimulated myoblast proliferation and Akt and ERK1/2 phosphorylation by the lysoPA (LPA) receptor antagonist <t>VPC32183.</t> Myoblasts were serum-starved in DMEM supplemented with 0.1% BSA for 24 h. ( A ) The cells were preincubated for 30 min with 5 μM VPC32183 and were then challenged with 15 μM PA or 15 μM LPA for 16 h, as indicated. [ 3 H]Thymidine incorporation was measured as described in the Materials and Methods section. Results are expressed relative to the control value without agonist and are the mean ± SEM of 3 independent experiments performed in triplicate. (* p < 0.05, control versus PA or LPA-treated cells, # p < 0.05; PA or LPA-treated cells versus PA or LPA-treated cells in the presence of VPC32183). ( B ) Cells were treated as in panel A. Cell proliferation was determined by staining the myoblasts with crystal violet as described in the Materials and Methods section. Results are expressed relative to the control value without agonist and are the mean ± SEM of 3 independent experiments performed. Control versus PA-treated cells; ** p < 0.01, control versus LPA-treated cells; # p < 0.05; PA- or LPA-treated cells versus PA- or LPA-treated cells in the presence of VPC32183). ( C ) Cells were preincubated with 5 μM VPC32183 for 30 min and then treated with 15 μM PA for 5 min. Cell lysates were analyzed by western blotting as described in the Materials and Methods section. Phosphorylation of Akt and ERK1/2 was determined using specific antibodies against phospho-Akt (P-Akt) or phospho-ERK1/2 (P-ERK1/2). Equal loading of protein was monitored using specific antibodies to total Akt and total ERK1/2. Panel C shows a representative blot of three independent experiments. ( D , E ) Results of scanning densitometry of the exposed films. Data are expressed as arbitrary units of intensity relative to the control siRNA values in the absence of agonist or inhibitor (Ctrl) and are the mean ± SEM of 3 replicate experiments. (* p < 0.05; ** p < 0.01; control versus PA-treated cells, # p < 0.05, ### p < 0.001; PA-treated cells versus PA-treated cells in the presence of VPC32183, as indicated).
    Vpc32183 Inhibitor, supplied by Avanti Polar, 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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    Figure 5 PKC, particularly PKCε, but not PKA or Rho, involves in LPA-induced potentiation of TRPV1 currents. Both <t>LPA1</t> antagonist <t>VPC32183</t> (1 μM, n = 15, p > 0.05) and PKC inhibitor BIM (1 μM, n = 13, p > 0.05) inhibit potentiation of TRPV1 currents induced by LPA in all of the neurons recorded (A and B). C: After PKA inhibitor H89 (1 μM) was delivered, no effect on LPA-induced potentiation of TRPV1 currents (n = 8, p < 0.001) was observed. D: LPA could still enhance TRPV1 currents in 14 out of 23 neurons tested (p < 0.001) after intracellular delivery of Rho inhibitor BoTXC3 (5 pg/μl). E: Intracellular delivery of PKCε inhibitor εV1-2 (200 μM) completely blocked LPA-induced potentiation of TRPV1 currents (n = 15, p > 0.05). F: Histogram showing summary.
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    PKC, particularly PKCε, but not PKA or Rho, involves in LPA-induced potentiation of TRPV1 currents . Both <t>LPA</t> <t>1</t> antagonist <t>VPC32183</t> (1 μM, n = 15, p > 0.05) and PKC inhibitor BIM (1 μM, n = 13, p > 0.05) inhibit potentiation of TRPV1 currents induced by LPA in all of the neurons recorded ( A and B ). C: After PKA inhibitor H89 (1 μM) was delivered, no effect on LPA-induced potentiation of TRPV1 currents (n = 8, p < 0.001) was observed. D: LPA could still enhance TRPV1 currents in 14 out of 23 neurons tested ( p < 0.001) after intracellular delivery of Rho inhibitor BoTXC3 (5 pg/μl). E: Intracellular delivery of PKCε inhibitor εV 1-2 (200 μM) completely blocked LPA-induced potentiation of TRPV1 currents (n = 15, p > 0.05). F: Histogram showing summary.
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    Image Search Results


    Inhibition of PA-stimulated myoblast proliferation and Akt and ERK1/2 phosphorylation by the lysoPA (LPA) receptor antagonist VPC32183. Myoblasts were serum-starved in DMEM supplemented with 0.1% BSA for 24 h. ( A ) The cells were preincubated for 30 min with 5 μM VPC32183 and were then challenged with 15 μM PA or 15 μM LPA for 16 h, as indicated. [ 3 H]Thymidine incorporation was measured as described in the Materials and Methods section. Results are expressed relative to the control value without agonist and are the mean ± SEM of 3 independent experiments performed in triplicate. (* p < 0.05, control versus PA or LPA-treated cells, # p < 0.05; PA or LPA-treated cells versus PA or LPA-treated cells in the presence of VPC32183). ( B ) Cells were treated as in panel A. Cell proliferation was determined by staining the myoblasts with crystal violet as described in the Materials and Methods section. Results are expressed relative to the control value without agonist and are the mean ± SEM of 3 independent experiments performed. Control versus PA-treated cells; ** p < 0.01, control versus LPA-treated cells; # p < 0.05; PA- or LPA-treated cells versus PA- or LPA-treated cells in the presence of VPC32183). ( C ) Cells were preincubated with 5 μM VPC32183 for 30 min and then treated with 15 μM PA for 5 min. Cell lysates were analyzed by western blotting as described in the Materials and Methods section. Phosphorylation of Akt and ERK1/2 was determined using specific antibodies against phospho-Akt (P-Akt) or phospho-ERK1/2 (P-ERK1/2). Equal loading of protein was monitored using specific antibodies to total Akt and total ERK1/2. Panel C shows a representative blot of three independent experiments. ( D , E ) Results of scanning densitometry of the exposed films. Data are expressed as arbitrary units of intensity relative to the control siRNA values in the absence of agonist or inhibitor (Ctrl) and are the mean ± SEM of 3 replicate experiments. (* p < 0.05; ** p < 0.01; control versus PA-treated cells, # p < 0.05, ### p < 0.001; PA-treated cells versus PA-treated cells in the presence of VPC32183, as indicated).

    Journal: International Journal of Molecular Sciences

    Article Title: Phosphatidic Acid Stimulates Myoblast Proliferation through Interaction with LPA1 and LPA2 Receptors

    doi: 10.3390/ijms22031452

    Figure Lengend Snippet: Inhibition of PA-stimulated myoblast proliferation and Akt and ERK1/2 phosphorylation by the lysoPA (LPA) receptor antagonist VPC32183. Myoblasts were serum-starved in DMEM supplemented with 0.1% BSA for 24 h. ( A ) The cells were preincubated for 30 min with 5 μM VPC32183 and were then challenged with 15 μM PA or 15 μM LPA for 16 h, as indicated. [ 3 H]Thymidine incorporation was measured as described in the Materials and Methods section. Results are expressed relative to the control value without agonist and are the mean ± SEM of 3 independent experiments performed in triplicate. (* p < 0.05, control versus PA or LPA-treated cells, # p < 0.05; PA or LPA-treated cells versus PA or LPA-treated cells in the presence of VPC32183). ( B ) Cells were treated as in panel A. Cell proliferation was determined by staining the myoblasts with crystal violet as described in the Materials and Methods section. Results are expressed relative to the control value without agonist and are the mean ± SEM of 3 independent experiments performed. Control versus PA-treated cells; ** p < 0.01, control versus LPA-treated cells; # p < 0.05; PA- or LPA-treated cells versus PA- or LPA-treated cells in the presence of VPC32183). ( C ) Cells were preincubated with 5 μM VPC32183 for 30 min and then treated with 15 μM PA for 5 min. Cell lysates were analyzed by western blotting as described in the Materials and Methods section. Phosphorylation of Akt and ERK1/2 was determined using specific antibodies against phospho-Akt (P-Akt) or phospho-ERK1/2 (P-ERK1/2). Equal loading of protein was monitored using specific antibodies to total Akt and total ERK1/2. Panel C shows a representative blot of three independent experiments. ( D , E ) Results of scanning densitometry of the exposed films. Data are expressed as arbitrary units of intensity relative to the control siRNA values in the absence of agonist or inhibitor (Ctrl) and are the mean ± SEM of 3 replicate experiments. (* p < 0.05; ** p < 0.01; control versus PA-treated cells, # p < 0.05, ### p < 0.001; PA-treated cells versus PA-treated cells in the presence of VPC32183, as indicated).

    Article Snippet: Sphingosine-1-phosphate, N-palmitoyl-ceramide-1-phosphate (C1P), 1,2-dipalmitoyl- sn -glycerol-3-phosphate (16:0-PA), 1-palmitoyl-2-oleoyl- sn -glycerol-3-phosphate (16:0-18:1-PA) and the VPC32183 inhibitor were supplied by Avanti Polar Lipids (Alabaster, AL, USA).

    Techniques: Inhibition, Staining, Western Blot

    Figure 5 PKC, particularly PKCε, but not PKA or Rho, involves in LPA-induced potentiation of TRPV1 currents. Both LPA1 antagonist VPC32183 (1 μM, n = 15, p > 0.05) and PKC inhibitor BIM (1 μM, n = 13, p > 0.05) inhibit potentiation of TRPV1 currents induced by LPA in all of the neurons recorded (A and B). C: After PKA inhibitor H89 (1 μM) was delivered, no effect on LPA-induced potentiation of TRPV1 currents (n = 8, p < 0.001) was observed. D: LPA could still enhance TRPV1 currents in 14 out of 23 neurons tested (p < 0.001) after intracellular delivery of Rho inhibitor BoTXC3 (5 pg/μl). E: Intracellular delivery of PKCε inhibitor εV1-2 (200 μM) completely blocked LPA-induced potentiation of TRPV1 currents (n = 15, p > 0.05). F: Histogram showing summary.

    Journal: Molecular pain

    Article Title: Involvement of lysophosphatidic acid in bone cancer pain by potentiation of TRPV1 via PKCε pathway in dorsal root ganglion neurons.

    doi: 10.1186/1744-8069-6-85

    Figure Lengend Snippet: Figure 5 PKC, particularly PKCε, but not PKA or Rho, involves in LPA-induced potentiation of TRPV1 currents. Both LPA1 antagonist VPC32183 (1 μM, n = 15, p > 0.05) and PKC inhibitor BIM (1 μM, n = 13, p > 0.05) inhibit potentiation of TRPV1 currents induced by LPA in all of the neurons recorded (A and B). C: After PKA inhibitor H89 (1 μM) was delivered, no effect on LPA-induced potentiation of TRPV1 currents (n = 8, p < 0.001) was observed. D: LPA could still enhance TRPV1 currents in 14 out of 23 neurons tested (p < 0.001) after intracellular delivery of Rho inhibitor BoTXC3 (5 pg/μl). E: Intracellular delivery of PKCε inhibitor εV1-2 (200 μM) completely blocked LPA-induced potentiation of TRPV1 currents (n = 15, p > 0.05). F: Histogram showing summary.

    Article Snippet: All the drugs for patch-clamp recording and intrathecal injection were purchased from Sigma, except that the LPA1 inhibitor VPC32183 was from Avanti Polar Lipids and PKC inhibitor V1-2 was from Biomol (Plymouth Meeting, PA).

    Techniques:

    Figure 6 LPA1 receptor antagonist VPC32183 attenuates mechanical allodynia and thermal hyperalgesia in bone cancer rats. Injections of VPC32183 (i.t., 0.6 mM, 30 μl) or saline (30 μl) were made before cancer cell injection (D0), and D2, D4, D7, D9 after cancer cells injection. A: Alleviation of bone cancer-induced mechanical allodynia by LPA1 antagonist. Ipsilateral PWTs to stimuli of von Frey filaments were standardized with baseline. PWTs of Saline + Cancer rats decreased gradually 5 days after operation, significantly lower than that of Saline + Saline rats at D5 (p < 0.01), D7 (p < 0.01), D9 (p < 0.001), D11 (p < 0.001), D13 (p < 0.001) and D16 (p < 0.05). Compared with saline injection, administration of LPA1 antagonist VPC32183 increased PWTs at D7 (p < 0.05), D9 (p < 0.01) and D11 (p < 0.05) after cancer cell injection. B: Ipsilateral PWLs to radiant heating were increased by VPC32183 at D9 (p < 0.01) and D11 (p < 0.01) after cancer cell injection. #: (Saline + Cancer) vs. (Saline + Saline); *: (VPC32183 + Cancer) vs. (Saline + Cancer).

    Journal: Molecular pain

    Article Title: Involvement of lysophosphatidic acid in bone cancer pain by potentiation of TRPV1 via PKCε pathway in dorsal root ganglion neurons.

    doi: 10.1186/1744-8069-6-85

    Figure Lengend Snippet: Figure 6 LPA1 receptor antagonist VPC32183 attenuates mechanical allodynia and thermal hyperalgesia in bone cancer rats. Injections of VPC32183 (i.t., 0.6 mM, 30 μl) or saline (30 μl) were made before cancer cell injection (D0), and D2, D4, D7, D9 after cancer cells injection. A: Alleviation of bone cancer-induced mechanical allodynia by LPA1 antagonist. Ipsilateral PWTs to stimuli of von Frey filaments were standardized with baseline. PWTs of Saline + Cancer rats decreased gradually 5 days after operation, significantly lower than that of Saline + Saline rats at D5 (p < 0.01), D7 (p < 0.01), D9 (p < 0.001), D11 (p < 0.001), D13 (p < 0.001) and D16 (p < 0.05). Compared with saline injection, administration of LPA1 antagonist VPC32183 increased PWTs at D7 (p < 0.05), D9 (p < 0.01) and D11 (p < 0.05) after cancer cell injection. B: Ipsilateral PWLs to radiant heating were increased by VPC32183 at D9 (p < 0.01) and D11 (p < 0.01) after cancer cell injection. #: (Saline + Cancer) vs. (Saline + Saline); *: (VPC32183 + Cancer) vs. (Saline + Cancer).

    Article Snippet: All the drugs for patch-clamp recording and intrathecal injection were purchased from Sigma, except that the LPA1 inhibitor VPC32183 was from Avanti Polar Lipids and PKC inhibitor V1-2 was from Biomol (Plymouth Meeting, PA).

    Techniques: Saline, Injection

    PKC, particularly PKCε, but not PKA or Rho, involves in LPA-induced potentiation of TRPV1 currents . Both LPA 1 antagonist VPC32183 (1 μM, n = 15, p > 0.05) and PKC inhibitor BIM (1 μM, n = 13, p > 0.05) inhibit potentiation of TRPV1 currents induced by LPA in all of the neurons recorded ( A and B ). C: After PKA inhibitor H89 (1 μM) was delivered, no effect on LPA-induced potentiation of TRPV1 currents (n = 8, p < 0.001) was observed. D: LPA could still enhance TRPV1 currents in 14 out of 23 neurons tested ( p < 0.001) after intracellular delivery of Rho inhibitor BoTXC3 (5 pg/μl). E: Intracellular delivery of PKCε inhibitor εV 1-2 (200 μM) completely blocked LPA-induced potentiation of TRPV1 currents (n = 15, p > 0.05). F: Histogram showing summary.

    Journal: Molecular Pain

    Article Title: Involvement of lysophosphatidic acid in bone cancer pain by potentiation of TRPV1 via PKCϵ pathway in dorsal root ganglion neurons

    doi: 10.1186/1744-8069-6-85

    Figure Lengend Snippet: PKC, particularly PKCε, but not PKA or Rho, involves in LPA-induced potentiation of TRPV1 currents . Both LPA 1 antagonist VPC32183 (1 μM, n = 15, p > 0.05) and PKC inhibitor BIM (1 μM, n = 13, p > 0.05) inhibit potentiation of TRPV1 currents induced by LPA in all of the neurons recorded ( A and B ). C: After PKA inhibitor H89 (1 μM) was delivered, no effect on LPA-induced potentiation of TRPV1 currents (n = 8, p < 0.001) was observed. D: LPA could still enhance TRPV1 currents in 14 out of 23 neurons tested ( p < 0.001) after intracellular delivery of Rho inhibitor BoTXC3 (5 pg/μl). E: Intracellular delivery of PKCε inhibitor εV 1-2 (200 μM) completely blocked LPA-induced potentiation of TRPV1 currents (n = 15, p > 0.05). F: Histogram showing summary.

    Article Snippet: All the drugs for patch-clamp recording and intrathecal injection were purchased from Sigma, except that the LPA 1 inhibitor VPC32183 was from Avanti Polar Lipids and PKCϵ inhibitor ϵV 1-2 was from Biomol (Plymouth Meeting, PA).

    Techniques:

    LPA 1 receptor antagonist VPC32183 attenuates mechanical allodynia and thermal hyperalgesia in bone cancer rats . Injections of VPC32183 (i.t., 0.6 mM, 30 μl) or saline (30 μl) were made before cancer cell injection (D 0 ), and D 2 , D 4 , D 7 , D 9 after cancer cells injection. A: Alleviation of bone cancer-induced mechanical allodynia by LPA 1 antagonist. Ipsilateral PWTs to stimuli of von Frey filaments were standardized with baseline. PWTs of Saline + Cancer rats decreased gradually 5 days after operation, significantly lower than that of Saline + Saline rats at D 5 ( p < 0.01), D 7 ( p < 0.01), D 9 ( p < 0.001), D 11 ( p < 0.001), D 13 ( p < 0.001) and D 16 ( p < 0.05). Compared with saline injection, administration of LPA 1 antagonist VPC32183 increased PWTs at D 7 ( p < 0.05), D 9 ( p < 0.01) and D 11 ( p < 0.05) after cancer cell injection. B: Ipsilateral PWLs to radiant heating were increased by VPC32183 at D 9 ( p < 0.01) and D 11 ( p < 0.01) after cancer cell injection. #: (Saline + Cancer) vs. (Saline + Saline); *: (VPC32183 + Cancer) vs. (Saline + Cancer).

    Journal: Molecular Pain

    Article Title: Involvement of lysophosphatidic acid in bone cancer pain by potentiation of TRPV1 via PKCϵ pathway in dorsal root ganglion neurons

    doi: 10.1186/1744-8069-6-85

    Figure Lengend Snippet: LPA 1 receptor antagonist VPC32183 attenuates mechanical allodynia and thermal hyperalgesia in bone cancer rats . Injections of VPC32183 (i.t., 0.6 mM, 30 μl) or saline (30 μl) were made before cancer cell injection (D 0 ), and D 2 , D 4 , D 7 , D 9 after cancer cells injection. A: Alleviation of bone cancer-induced mechanical allodynia by LPA 1 antagonist. Ipsilateral PWTs to stimuli of von Frey filaments were standardized with baseline. PWTs of Saline + Cancer rats decreased gradually 5 days after operation, significantly lower than that of Saline + Saline rats at D 5 ( p < 0.01), D 7 ( p < 0.01), D 9 ( p < 0.001), D 11 ( p < 0.001), D 13 ( p < 0.001) and D 16 ( p < 0.05). Compared with saline injection, administration of LPA 1 antagonist VPC32183 increased PWTs at D 7 ( p < 0.05), D 9 ( p < 0.01) and D 11 ( p < 0.05) after cancer cell injection. B: Ipsilateral PWLs to radiant heating were increased by VPC32183 at D 9 ( p < 0.01) and D 11 ( p < 0.01) after cancer cell injection. #: (Saline + Cancer) vs. (Saline + Saline); *: (VPC32183 + Cancer) vs. (Saline + Cancer).

    Article Snippet: All the drugs for patch-clamp recording and intrathecal injection were purchased from Sigma, except that the LPA 1 inhibitor VPC32183 was from Avanti Polar Lipids and PKCϵ inhibitor ϵV 1-2 was from Biomol (Plymouth Meeting, PA).

    Techniques: Injection