Review

rabbit derived ab (Bio-Rad)

Bio-Rad is a verified supplier

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Bio-Rad rabbit derived ab
Rabbit Derived Ab, supplied by Bio-Rad, used in various techniques. Bioz Stars score: 95/100, based on 347 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/rabbit derived ab/product/Bio-Rad
Average 95 stars, based on 347 article reviews

rabbit derived ab - by Bioz Stars, 2026-04

95/100 stars

Images

Image Search Results

Figure 3 ｜ Gene and protein verification in sciatic nerve injury in rats treated with AKBA. (A) mRNA expression levels (relative to GAPDH) of NGFR (A1), NGF (A2), BDNF (A3), and MPO (A4) in the rat sciatic nerve using qPCR. (B) Protein expression levels (relative to GAPDH) of NGFR (B2), NGF (B3), BDNF (B4), and MPO (B5) in the rat sciatic nerve by western blot assay. Data are expressed as the mean ± SD (n = 3 rats/group) and were analyzed using a one-way analysis of variance followed by the least significant difference test. BDNF: Brain derived neurotrophic factor; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; MPO: myeloperoxidase; NGF: nerve growth factor; NGFR: nerve growth factor receptor; qPCR: real-time polymerase chain reaction.

Journal: Neural regeneration research

Article Title: Acetyl-11-keto-beta-boswellic acid promotes sciatic nerve repair after injury: molecular mechanism.

doi: 10.4103/1673-5374.339494

Figure Lengend Snippet: Figure 3 ｜ Gene and protein verification in sciatic nerve injury in rats treated with AKBA. (A) mRNA expression levels (relative to GAPDH) of NGFR (A1), NGF (A2), BDNF (A3), and MPO (A4) in the rat sciatic nerve using qPCR. (B) Protein expression levels (relative to GAPDH) of NGFR (B2), NGF (B3), BDNF (B4), and MPO (B5) in the rat sciatic nerve by western blot assay. Data are expressed as the mean ± SD (n = 3 rats/group) and were analyzed using a one-way analysis of variance followed by the least significant difference test. BDNF: Brain derived neurotrophic factor; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; MPO: myeloperoxidase; NGF: nerve growth factor; NGFR: nerve growth factor receptor; qPCR: real-time polymerase chain reaction.

Article Snippet: Supplier BDNF 1:500 Rabbit DF6387 AB_2838350 Affinity Biosciences (Beijing, China) NGFR 1:500 Rabbit DF6821 AB_2838781 Affinity Biosciences MPO 1:500 Rabbit A1374 AB_2760599 ABclonal Technology (Wuhan, China) NGF 1:500 Rabbit A14216 AB_2761076 ABclonal Technology GAPDH 1:1000 Rabbit Bs-2188R AB_11065664 Bioss Biotechnology (Beijing, China) IL-1β 1:400 Rabbit WLH3903 AB_2894981 Wanleibio (Shenyang, China) Pro-IL-1β 1:500 Rabbit WL02257 AB_2894987 Wanleibio TNF-α 1:500 Rabbit WL01581 AB_2894992 Wanleibio β-Actin 1:1000 Rabbit bs-0061R AB_10855480 Bioss Biotechnology BDNF: Brain derived neurotrophic factor; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IL-1β: interleukin 1 beta; MPO: myeloperoxidase; NGF: nerve growth factor; NGFR: nerve growth factor receptor; Pro-IL-1β: pro interleukin 1 beta; TNF-α: tumor necrosis factor-alpha.

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

Figure 2 ｜ Genomics analysis after sciatic nerve injury treated with AKBA in rats. (A) Differential gene expression volcano map. (A1) AKBA group vs. Model group. (A2) AKBA group vs. Sham group. (A3) Model group vs. Sham group. (B) KEGG analysis of differential gene expression in the sciatic nerve. (B1) AKBA group vs. Model group. (B2) Heat map of KEGG enrichment analysis of differentially expressed mRNA between the AKBA and Model groups. Each row represents an enriched KEGG pathway, and each column represents differential mRNA expression. The red color indicates that the mRNA was detected in the corresponding KEGG pathway, and vice versa, and the gray color indicates that no enrichment was detected. (B3) The most significantly different gene expression was in the phagosome pathway. A redder color indicates more up-regulation of gene expression in the AKBA group than in the Model group, and a greener color indicates more down-regulation in the AKBA group than in the Model group. (B4) Expression of different genes after normalization (FRKM values). (B5) AKBA group vs. Sham group. (B6) Model group vs. Sham group. Data are expressed as the mean ± SD (n = 5 rats/group). BDNF: Brain derived neurotrophic factor; Cybb: cytochrome B-245 beta chain; C3: complement C3; NGF: nerve growth factor; NGFR: nerve growth factor receptor: MPO: myeloperoxidase; RT1-M2: RT1 class Ib: locus M2; Stx7: syntaxin 7; Tcirg1: T cell immune regulator 1; Thbs2: thrombospondin 2.

Journal: Neural regeneration research

Article Title: Acetyl-11-keto-beta-boswellic acid promotes sciatic nerve repair after injury: molecular mechanism.

doi: 10.4103/1673-5374.339494

Figure Lengend Snippet: Figure 2 ｜ Genomics analysis after sciatic nerve injury treated with AKBA in rats. (A) Differential gene expression volcano map. (A1) AKBA group vs. Model group. (A2) AKBA group vs. Sham group. (A3) Model group vs. Sham group. (B) KEGG analysis of differential gene expression in the sciatic nerve. (B1) AKBA group vs. Model group. (B2) Heat map of KEGG enrichment analysis of differentially expressed mRNA between the AKBA and Model groups. Each row represents an enriched KEGG pathway, and each column represents differential mRNA expression. The red color indicates that the mRNA was detected in the corresponding KEGG pathway, and vice versa, and the gray color indicates that no enrichment was detected. (B3) The most significantly different gene expression was in the phagosome pathway. A redder color indicates more up-regulation of gene expression in the AKBA group than in the Model group, and a greener color indicates more down-regulation in the AKBA group than in the Model group. (B4) Expression of different genes after normalization (FRKM values). (B5) AKBA group vs. Sham group. (B6) Model group vs. Sham group. Data are expressed as the mean ± SD (n = 5 rats/group). BDNF: Brain derived neurotrophic factor; Cybb: cytochrome B-245 beta chain; C3: complement C3; NGF: nerve growth factor; NGFR: nerve growth factor receptor: MPO: myeloperoxidase; RT1-M2: RT1 class Ib: locus M2; Stx7: syntaxin 7; Tcirg1: T cell immune regulator 1; Thbs2: thrombospondin 2.

Techniques: Gene Expression, Expressing, Derivative Assay

Platelet-derived growth factor-BB activates nociceptor-like cultured DRG neurons and induces nocifensive behavior and pain hypersensitivity. (A) Representative trace (12 of 18 neurons) of current-clamp perforated patch recordings from nociceptor-like cultured DRG neurons showing membrane voltage response to continuous focal application (marked by horizontal bar) of 125 ng/mL of PDGF-BB. Dashed lines indicate resting potentials before drug application (−57 mV). (B) Mean ± SEM of changes in resting membrane potential ΔV (V t − V 0 ) after focal application of PDGF-BB alone (red) or vehicle (5 μM HCl, light gray ). Time point “Before 1” indicates the time where V 0 values were measured (3 minutes before application of either PDGF-BB or vehicle). Time point “Before 2” indicates the time just before application of either PDGF-BB or vehicle. ns, not significant, * P < 0.05, ** P < 0.01; *** P < 0.001; Repeated-measures (RM) 2-way ANOVA with post hoc Bonferroni. In the “PDGF-BB,” only neurons that showed depolarization without firing (n = 6 neurons) were used for the analysis; n = 5 cells for the “Vehicle” group. (C) Graph comparing box plots and individual values of the total time (in seconds) spent by rats licking, biting, flinching, and guarding the hind paw (nocifensive behavior) during 45 minutes after intraplantar injection of 50 μg/mL of PDGF-BB or its vehicle (2 mM of HCl). ** P < 0.01; Student t -test; n = 6 rats per group. Box plots depict mean, 25th, 75th percentile, and SD. (D) The decrease in thermal (radiant heat) paw withdrawal latency (PWL, left ) and mechanical threshold (electronic von Frey, right ) after intraplantar injection of 12 μg/mL of PDGF-BB as compared to injection of vehicle (500 μM HCl, n = 6 rats per group, *** P < 0.001; ** P < 0.01; RM 2-way ANOVA with post hoc Bonferroni). ANOVA, analysis of variance; DRG, dorsal root ganglion; PDGF, platelet-derived growth factor.

Journal: Pain

Article Title: Platelet-derived growth factor activates nociceptive neurons by inhibiting M-current and contributes to inflammatory pain

doi: 10.1097/j.pain.0000000000001523

Figure Lengend Snippet: Platelet-derived growth factor-BB activates nociceptor-like cultured DRG neurons and induces nocifensive behavior and pain hypersensitivity. (A) Representative trace (12 of 18 neurons) of current-clamp perforated patch recordings from nociceptor-like cultured DRG neurons showing membrane voltage response to continuous focal application (marked by horizontal bar) of 125 ng/mL of PDGF-BB. Dashed lines indicate resting potentials before drug application (−57 mV). (B) Mean ± SEM of changes in resting membrane potential ΔV (V t − V 0 ) after focal application of PDGF-BB alone (red) or vehicle (5 μM HCl, light gray ). Time point “Before 1” indicates the time where V 0 values were measured (3 minutes before application of either PDGF-BB or vehicle). Time point “Before 2” indicates the time just before application of either PDGF-BB or vehicle. ns, not significant, * P < 0.05, ** P < 0.01; *** P < 0.001; Repeated-measures (RM) 2-way ANOVA with post hoc Bonferroni. In the “PDGF-BB,” only neurons that showed depolarization without firing (n = 6 neurons) were used for the analysis; n = 5 cells for the “Vehicle” group. (C) Graph comparing box plots and individual values of the total time (in seconds) spent by rats licking, biting, flinching, and guarding the hind paw (nocifensive behavior) during 45 minutes after intraplantar injection of 50 μg/mL of PDGF-BB or its vehicle (2 mM of HCl). ** P < 0.01; Student t -test; n = 6 rats per group. Box plots depict mean, 25th, 75th percentile, and SD. (D) The decrease in thermal (radiant heat) paw withdrawal latency (PWL, left ) and mechanical threshold (electronic von Frey, right ) after intraplantar injection of 12 μg/mL of PDGF-BB as compared to injection of vehicle (500 μM HCl, n = 6 rats per group, *** P < 0.001; ** P < 0.01; RM 2-way ANOVA with post hoc Bonferroni). ANOVA, analysis of variance; DRG, dorsal root ganglion; PDGF, platelet-derived growth factor.

Article Snippet: The following antibodies were used: rabbit polyclonal Ab against platelet-derived growth factor (PDGF)-B (#ab178409; Abcam, Cambridge, United Kingdom) at a dilution of 1:500, rabbit polyclonal Ab against GAPDH (#ab37168; Abcam) at a dilution of 1:500, and a horseradish peroxidase–conjugated goat anti-rabbit antibody IgG (#ab97080; Abcam) at a dilution of 1:10,000.

Techniques: Derivative Assay, Cell Culture, Membrane, Injection

Platelet-derived growth factor-BB increases the excitability of nociceptor-like DRG neurons and increases the R in . (A) Representative traces of typical voltage responses to 500 ms current steps (shown in middle ) recorded from the same neuron before ( left ) and after ∼15 minutes of focal continuous application of 125 ng/mL of PDGF-BB ( right , representative of n = 7). (B) Mean frequency–intensity (f-I) curves of DRG neurons recorded before ( gray diamonds ) and ∼15 minutes after ( red inverted triangles ) application of PDGF-BB. Note that PDGF-BB induced a significant increase in gain (m, dotted lines; * P < 0.05, paired t test; n = 7, see also Table ). (C) Superimposed representative traces of a single action potential recorded from the same neuron before ( gray ) and after ( red ) the application of PDGF-BB. Arrows indicate the AP threshold, derived from the phase plots shown in (D). (D) Representative phase plots of rate of change of the membrane potential (dV/dt) vs membrane potential (V m ) during an action potential recorded from the same neuron before ( gray ) and 10 to 20 minutes after the application of PDGF-BB ( red ). Arrows and dashed lines indicate shift in threshold voltage and quantified in (E). (E) Thresholds for generation of action potentials calculated from the same neurons before and ∼15 minutes after application of PDGF-BB (mean ± SEM, * P < 0.05, paired t test, n = 7). (F) Bar graph depicting R in before ( gray ) and after ∼15 minutes exposure to PDGF-BB ( red ); * P < 0.05, paired t test, n = 8. Inset : representative typical voltage responses to 500 ms, −100 pA current before ( gray ) and after ( red ) the treatment with PDGF-BB. All measurements described in this figure were performed at the native resting potential of each cell, adjusted after PDGF-BB application by injecting the appropriate repolarizing DC currents. AP, action potential; DRG, dorsal root ganglion; PDGF, platelet-derived growth factor.

Journal: Pain

Article Title: Platelet-derived growth factor activates nociceptive neurons by inhibiting M-current and contributes to inflammatory pain

doi: 10.1097/j.pain.0000000000001523

Figure Lengend Snippet: Platelet-derived growth factor-BB increases the excitability of nociceptor-like DRG neurons and increases the R in . (A) Representative traces of typical voltage responses to 500 ms current steps (shown in middle ) recorded from the same neuron before ( left ) and after ∼15 minutes of focal continuous application of 125 ng/mL of PDGF-BB ( right , representative of n = 7). (B) Mean frequency–intensity (f-I) curves of DRG neurons recorded before ( gray diamonds ) and ∼15 minutes after ( red inverted triangles ) application of PDGF-BB. Note that PDGF-BB induced a significant increase in gain (m, dotted lines; * P < 0.05, paired t test; n = 7, see also Table ). (C) Superimposed representative traces of a single action potential recorded from the same neuron before ( gray ) and after ( red ) the application of PDGF-BB. Arrows indicate the AP threshold, derived from the phase plots shown in (D). (D) Representative phase plots of rate of change of the membrane potential (dV/dt) vs membrane potential (V m ) during an action potential recorded from the same neuron before ( gray ) and 10 to 20 minutes after the application of PDGF-BB ( red ). Arrows and dashed lines indicate shift in threshold voltage and quantified in (E). (E) Thresholds for generation of action potentials calculated from the same neurons before and ∼15 minutes after application of PDGF-BB (mean ± SEM, * P < 0.05, paired t test, n = 7). (F) Bar graph depicting R in before ( gray ) and after ∼15 minutes exposure to PDGF-BB ( red ); * P < 0.05, paired t test, n = 8. Inset : representative typical voltage responses to 500 ms, −100 pA current before ( gray ) and after ( red ) the treatment with PDGF-BB. All measurements described in this figure were performed at the native resting potential of each cell, adjusted after PDGF-BB application by injecting the appropriate repolarizing DC currents. AP, action potential; DRG, dorsal root ganglion; PDGF, platelet-derived growth factor.

Techniques: Derivative Assay, Membrane

Journal: Pain

Article Title: Platelet-derived growth factor activates nociceptive neurons by inhibiting M-current and contributes to inflammatory pain

doi: 10.1097/j.pain.0000000000001523

Figure Lengend Snippet: Parameters of excitability of nociceptor-like DRG neurons before and after the application of PDGF (125 ng/mL).

Techniques:

Application of PDGF-BB leads to inhibition of I M in DRG neurons. (A) Voltage-clamp perforated patch recordings from DRG neurons showing families of I M evoked by a series of 1-second, 5-mV hyperpolarizing voltage steps from a holding potential of −20 mV (shown in inset ). The 3 subpanels show the current responses before ( left ), after focal application of 125 ng/mL of PDGF-BB ( middle ), and after bath application of 10 μM of XE991 on top of focal application of PDGF-BB ( right ). The dotted line indicates zero current level. The current response obtained by stepping to −45 mV is shown at the bottom of each subpanel. The I M relaxation was fitted with a biexponential line (red), which was extrapolated to the beginning of the voltage step. (B) Subtracted trace of I M evoked by stepping to −45 mV before the application of PDGF-BB minus I M trace evoked by stepping to −45 mV after PDGF. (C) Left , bar graph depicting mean ± SEM of peak I M amplitude (measured by stepping to −45 mV), before ( gray ), 10 minutes after the application of PDGF-BB ( red ), and 10 minutes after the treatment with XE991 on top of PDGF-BB ( orange ). ** P < 0.01, ns, not significant, RM one-way ANOVA with post hoc Bonferroni test, n = 7 neurons. Right , same as left but showing that a 10-minute application of vehicle ( light gray ) has no effect on I M amplitude, ns, not significant, * P < 0.05, RM one-way ANOVA with post hoc Bonferroni test n = 5 neurons. (D) Peak I M amplitude (measured by stepping to −45 mV, mean ± SEM), plotted vs time of application of PDGF-BB. Platelet-derived growth factor-BB application is indicated by the arrow (time “0”). One-way ANOVA with post hoc Bonferroni test, n = 13 neurons for 6 minutes, n = 11 neurons for 9 minutes. In 7 out of 9 neurons, ∼15 minutes washout of PDGF-BB led to full recovery of I M . ns, not significant; ** P < 0.01. ANOVA, analysis of variance; DRG, dorsal root ganglion; PDGF, platelet-derived growth factor; RM, repeated-measures.

Journal: Pain

Article Title: Platelet-derived growth factor activates nociceptive neurons by inhibiting M-current and contributes to inflammatory pain

doi: 10.1097/j.pain.0000000000001523

Figure Lengend Snippet: Application of PDGF-BB leads to inhibition of I M in DRG neurons. (A) Voltage-clamp perforated patch recordings from DRG neurons showing families of I M evoked by a series of 1-second, 5-mV hyperpolarizing voltage steps from a holding potential of −20 mV (shown in inset ). The 3 subpanels show the current responses before ( left ), after focal application of 125 ng/mL of PDGF-BB ( middle ), and after bath application of 10 μM of XE991 on top of focal application of PDGF-BB ( right ). The dotted line indicates zero current level. The current response obtained by stepping to −45 mV is shown at the bottom of each subpanel. The I M relaxation was fitted with a biexponential line (red), which was extrapolated to the beginning of the voltage step. (B) Subtracted trace of I M evoked by stepping to −45 mV before the application of PDGF-BB minus I M trace evoked by stepping to −45 mV after PDGF. (C) Left , bar graph depicting mean ± SEM of peak I M amplitude (measured by stepping to −45 mV), before ( gray ), 10 minutes after the application of PDGF-BB ( red ), and 10 minutes after the treatment with XE991 on top of PDGF-BB ( orange ). ** P < 0.01, ns, not significant, RM one-way ANOVA with post hoc Bonferroni test, n = 7 neurons. Right , same as left but showing that a 10-minute application of vehicle ( light gray ) has no effect on I M amplitude, ns, not significant, * P < 0.05, RM one-way ANOVA with post hoc Bonferroni test n = 5 neurons. (D) Peak I M amplitude (measured by stepping to −45 mV, mean ± SEM), plotted vs time of application of PDGF-BB. Platelet-derived growth factor-BB application is indicated by the arrow (time “0”). One-way ANOVA with post hoc Bonferroni test, n = 13 neurons for 6 minutes, n = 11 neurons for 9 minutes. In 7 out of 9 neurons, ∼15 minutes washout of PDGF-BB led to full recovery of I M . ns, not significant; ** P < 0.01. ANOVA, analysis of variance; DRG, dorsal root ganglion; PDGF, platelet-derived growth factor; RM, repeated-measures.

Techniques: Inhibition, Derivative Assay

Inhibition of PI3K pathway prevents PDGF-induced inhibition of I M . (A) Voltage-clamp perforated patch recordings from DRG neurons pretreated before the experiment and perfused during the experiment with extracellular solution containing 20 nM of wortmannin. Families of I M evoked by a series of 1-second, 5-mV hyperpolarizing voltage steps from a holding potential of −20 mV (shown in inset ). The 3 subpanels show the current responses in cells treated with wortmannin, before ( left ), after the focal application of 125 ng/mL of PDGF-BB ( middle ), and after the bath application of 10 μM of XE991 on top of focal application of PDGF-BB ( right ). The dotted line indicates zero current level. The current response obtained by stepping to −45 mV is shown at the bottom of each subpanel. (B) Subtracted trace of I M trace evoked by stepping to −45 mV before application of PDGF-BB minus I M trace evoked by stepping to −45 mV after PDGF-BB. (C) Bar graph depicting mean ± SEM of peak I M amplitude in cells pretreated with 20 nM of wortmannin and measured by stepping to −45 mV, before ( gray ), 10 minutes after the application of PDGF-BB (yellow) , and 10 minutes after the bath application of XE991 on top of PDGF-BB (orange) . ns, not significant, * P < 0.05, RM one-way ANOVA with post hoc Bonferroni test, n = 7. (D) Comparison of changes in peak I M amplitude (measured by stepping to −45 mV, mean ± SEM) with time, after focal application of PDGF-BB ( red circles ), vehicle ( light gray diamonds ), PDGF-BB onto cells treated with imatinib ( blue inverted triangles ), and PDGF-BB onto cells treated with wortmannin ( yellow triangles ). Black letters “ns”, comparison by the time points between the “Vehicle,” “Imatinib + PDGF-BB,” and “Wortmannin + PDGF-BB” groups; light gray letters and asterisks— comparison by the time points between the “PDGF-BB” and the “Vehicle” groups; blue letters and asterisks— comparison by the time points between the “PDGF-BB” and the “Imatinib + PDGF-BB” groups; orange letters and asterisks— comparison by the time points between the “PDGF-BB” and the “Wortmannin + PDGF-BB” groups. RM 2-way ANOVA with post hoc Bonferroni test, n = 9 for the “PDGF-BB” group; n = 7 neurons for the “Imatinib + PDGF-BB” and the “Wortmannin + PDGF-BB” groups, n = 4 for the “Vehicle” group. ns, not significant; * P < 0.05; *** P < 0.001. In each experiment, 10 minutes after the application of either PDGF-BB or vehicle, XE991 was added for 7 minutes (light gray shading). At time point “XE991,” the statistical comparison shown is between the peak I M amplitude values at the “9 minute” time point and the values after ∼7 minutes of XE991. ns, not significant; * P < 0.05; *** P < 0.001. ANOVA, analysis of variance; DRG, dorsal root ganglion; PDGF, platelet-derived growth factor; RM, repeated-measures.

Journal: Pain

Article Title: Platelet-derived growth factor activates nociceptive neurons by inhibiting M-current and contributes to inflammatory pain

doi: 10.1097/j.pain.0000000000001523

Figure Lengend Snippet: Inhibition of PI3K pathway prevents PDGF-induced inhibition of I M . (A) Voltage-clamp perforated patch recordings from DRG neurons pretreated before the experiment and perfused during the experiment with extracellular solution containing 20 nM of wortmannin. Families of I M evoked by a series of 1-second, 5-mV hyperpolarizing voltage steps from a holding potential of −20 mV (shown in inset ). The 3 subpanels show the current responses in cells treated with wortmannin, before ( left ), after the focal application of 125 ng/mL of PDGF-BB ( middle ), and after the bath application of 10 μM of XE991 on top of focal application of PDGF-BB ( right ). The dotted line indicates zero current level. The current response obtained by stepping to −45 mV is shown at the bottom of each subpanel. (B) Subtracted trace of I M trace evoked by stepping to −45 mV before application of PDGF-BB minus I M trace evoked by stepping to −45 mV after PDGF-BB. (C) Bar graph depicting mean ± SEM of peak I M amplitude in cells pretreated with 20 nM of wortmannin and measured by stepping to −45 mV, before ( gray ), 10 minutes after the application of PDGF-BB (yellow) , and 10 minutes after the bath application of XE991 on top of PDGF-BB (orange) . ns, not significant, * P < 0.05, RM one-way ANOVA with post hoc Bonferroni test, n = 7. (D) Comparison of changes in peak I M amplitude (measured by stepping to −45 mV, mean ± SEM) with time, after focal application of PDGF-BB ( red circles ), vehicle ( light gray diamonds ), PDGF-BB onto cells treated with imatinib ( blue inverted triangles ), and PDGF-BB onto cells treated with wortmannin ( yellow triangles ). Black letters “ns”, comparison by the time points between the “Vehicle,” “Imatinib + PDGF-BB,” and “Wortmannin + PDGF-BB” groups; light gray letters and asterisks— comparison by the time points between the “PDGF-BB” and the “Vehicle” groups; blue letters and asterisks— comparison by the time points between the “PDGF-BB” and the “Imatinib + PDGF-BB” groups; orange letters and asterisks— comparison by the time points between the “PDGF-BB” and the “Wortmannin + PDGF-BB” groups. RM 2-way ANOVA with post hoc Bonferroni test, n = 9 for the “PDGF-BB” group; n = 7 neurons for the “Imatinib + PDGF-BB” and the “Wortmannin + PDGF-BB” groups, n = 4 for the “Vehicle” group. ns, not significant; * P < 0.05; *** P < 0.001. In each experiment, 10 minutes after the application of either PDGF-BB or vehicle, XE991 was added for 7 minutes (light gray shading). At time point “XE991,” the statistical comparison shown is between the peak I M amplitude values at the “9 minute” time point and the values after ∼7 minutes of XE991. ns, not significant; * P < 0.05; *** P < 0.001. ANOVA, analysis of variance; DRG, dorsal root ganglion; PDGF, platelet-derived growth factor; RM, repeated-measures.

Techniques: Inhibition, Comparison, Derivative Assay

Inhibition of PDGFR prevents PDGF-BB–mediated I M attenuation. (A) Voltage-clamp perforated patch recordings from DRG neurons treated before and during the experiment with extracellular solution containing 10 µM of imatinib. Families of I M evoked by a series of 1-second, 5-mV hyperpolarizing voltage steps from a holding potential of −20 mV (shown in inset ). The 3 subpanels show the current responses in cells treated with imatinib, before ( left ), after focal application of 125 ng/mL of PDGF-BB ( middle ), and after bath application of 10 μM of XE991 on top of focal application of PDGF-BB ( right ). The dotted line indicates zero current level. The current response obtained by stepping to −45 mV is shown at the bottom of each subpanel. (B) Subtracted I M trace, evoked by a −45-mV step before application of PDGF-BB from an I M trace evoked by the same step after PDGF-BB. (C) Bar graph depicting mean ± SEM of peak I M amplitude (measured by stepping to −45 mV) in cells treated with 10 µM of imatinib before ( gray ), 10 minutes after the application of PDGF-BB (blue) , and 10 minutes after the bath application of XE991 on top of PDGF-BB (orange) . n = 7, ns, not significant, ** P < 0.01, RM one-way ANOVA with post hoc Bonferroni test. ANOVA, analysis of variance; DRG, dorsal root ganglion; PDGF, platelet-derived growth factor; RM, repeated-measures.

Journal: Pain

Article Title: Platelet-derived growth factor activates nociceptive neurons by inhibiting M-current and contributes to inflammatory pain

doi: 10.1097/j.pain.0000000000001523

Figure Lengend Snippet: Inhibition of PDGFR prevents PDGF-BB–mediated I M attenuation. (A) Voltage-clamp perforated patch recordings from DRG neurons treated before and during the experiment with extracellular solution containing 10 µM of imatinib. Families of I M evoked by a series of 1-second, 5-mV hyperpolarizing voltage steps from a holding potential of −20 mV (shown in inset ). The 3 subpanels show the current responses in cells treated with imatinib, before ( left ), after focal application of 125 ng/mL of PDGF-BB ( middle ), and after bath application of 10 μM of XE991 on top of focal application of PDGF-BB ( right ). The dotted line indicates zero current level. The current response obtained by stepping to −45 mV is shown at the bottom of each subpanel. (B) Subtracted I M trace, evoked by a −45-mV step before application of PDGF-BB from an I M trace evoked by the same step after PDGF-BB. (C) Bar graph depicting mean ± SEM of peak I M amplitude (measured by stepping to −45 mV) in cells treated with 10 µM of imatinib before ( gray ), 10 minutes after the application of PDGF-BB (blue) , and 10 minutes after the bath application of XE991 on top of PDGF-BB (orange) . n = 7, ns, not significant, ** P < 0.01, RM one-way ANOVA with post hoc Bonferroni test. ANOVA, analysis of variance; DRG, dorsal root ganglion; PDGF, platelet-derived growth factor; RM, repeated-measures.

Techniques: Inhibition, Derivative Assay

PDGFR is required for PDGF-BB–induced spontaneous firing and hypersensitivity to pain. (A) Representative trace (7 of 7 neurons) of membrane voltage changes in nociceptor-like cultured DRG neurons treated with 10 µM of imatinib. In these conditions, focal application (marked by the horizontal bar) of 125 ng/mL of PDGF-BB did not lead to membrane depolarization. Free-run recording was interrupted (marked by boxes) to examine the excitable properties of the neuron. Dashed lines indicate resting potentials before drug application (−57 mV). All recorded neurons (n = 7) showed no PDGF-BB–induced hyperexcitability, but fired normally in response to a depolarizing current step ( inset ). (B) Mean ± SEM of changes in resting membrane potential ΔV (V t − V 0 ) after focal application of PDGF-BB alone ( red ), vehicle (5 μM of HCl, light gray ), or PDGF-BB on cells pretreated with imatinib ( blue ). Time point “Before 1” indicates the time where V 0 values were measured (3 minutes before application of either PDGF-BB or vehicle). Time point “Before 2” indicates the time just before application of either PDGF-BB or vehicle. ns, not significant, * P < 0.05, ** P < 0.01; *** P < 0.001; blue asterisks —comparison between “PDGF-BB” and “Vehicle” groups; light gray asterisks —comparison between “PDGF-BB” and “Imatinib + PDGF-BB” groups; black —comparison between “Imatinib + PDGF-BB” and “Vehicle” groups. RM 2-way ANOVA with post hoc Bonferroni, n = 5 cells in each group. The data of “PDGF-BB” and “Vehicle” is presented in Figure B and used here for the convenient comparison between these groups and the “Imatinib + PDGF-BB” group. Note that there is no significant difference between the “Imatinib + PDGF-BB” and the vehicle group. (C) Paw withdrawal latency (PWL, radiant heat, left ) and mechanical threshold (von Frey, right ) after intraplantar injection of 12 µg/mL of PDGF-BB together with 12 ng/g of imatinib as compared to injection of imatinib alone (12 ng/g). n = 6 rats per group, ns, not significant, RM 2-way ANOVA with post hoc Bonferroni. ANOVA, analysis of variance; DRG, dorsal root ganglion; PDGF, platelet-derived growth factor; RM, repeated-measures.

Journal: Pain

Article Title: Platelet-derived growth factor activates nociceptive neurons by inhibiting M-current and contributes to inflammatory pain

doi: 10.1097/j.pain.0000000000001523

Figure Lengend Snippet: PDGFR is required for PDGF-BB–induced spontaneous firing and hypersensitivity to pain. (A) Representative trace (7 of 7 neurons) of membrane voltage changes in nociceptor-like cultured DRG neurons treated with 10 µM of imatinib. In these conditions, focal application (marked by the horizontal bar) of 125 ng/mL of PDGF-BB did not lead to membrane depolarization. Free-run recording was interrupted (marked by boxes) to examine the excitable properties of the neuron. Dashed lines indicate resting potentials before drug application (−57 mV). All recorded neurons (n = 7) showed no PDGF-BB–induced hyperexcitability, but fired normally in response to a depolarizing current step ( inset ). (B) Mean ± SEM of changes in resting membrane potential ΔV (V t − V 0 ) after focal application of PDGF-BB alone ( red ), vehicle (5 μM of HCl, light gray ), or PDGF-BB on cells pretreated with imatinib ( blue ). Time point “Before 1” indicates the time where V 0 values were measured (3 minutes before application of either PDGF-BB or vehicle). Time point “Before 2” indicates the time just before application of either PDGF-BB or vehicle. ns, not significant, * P < 0.05, ** P < 0.01; *** P < 0.001; blue asterisks —comparison between “PDGF-BB” and “Vehicle” groups; light gray asterisks —comparison between “PDGF-BB” and “Imatinib + PDGF-BB” groups; black —comparison between “Imatinib + PDGF-BB” and “Vehicle” groups. RM 2-way ANOVA with post hoc Bonferroni, n = 5 cells in each group. The data of “PDGF-BB” and “Vehicle” is presented in Figure B and used here for the convenient comparison between these groups and the “Imatinib + PDGF-BB” group. Note that there is no significant difference between the “Imatinib + PDGF-BB” and the vehicle group. (C) Paw withdrawal latency (PWL, radiant heat, left ) and mechanical threshold (von Frey, right ) after intraplantar injection of 12 µg/mL of PDGF-BB together with 12 ng/g of imatinib as compared to injection of imatinib alone (12 ng/g). n = 6 rats per group, ns, not significant, RM 2-way ANOVA with post hoc Bonferroni. ANOVA, analysis of variance; DRG, dorsal root ganglion; PDGF, platelet-derived growth factor; RM, repeated-measures.

Techniques: Membrane, Cell Culture, Comparison, Injection, Derivative Assay

Platelet-derived growth factor scavenging and inhibition of PDGFR reduces formalin-induced inflammatory pain. (A) Mean ± SEM of duration of paw licking and biting per 5 minutes plotted vs time after injection of 2% formalin with vehicle (PBS, gray squares ); 2% formalin with 500 ng/40 μL of PDGFR-β-Fc ( orange circles ) and 500 ng/40 μL of PDGFR-β-Fc alone ( light orange triangles ). RM two-way ANOVA with post hoc Bonferroni, n = 6 rats per group; black bar and asterisks —comparison between the “Formalin + vehicle” and the “Formalin + PDGFR-β-Fc” groups; light orange bar and asterisks —comparison between the “PDGFR-β-Fc alone” and the “Formalin + PDGFR-β-Fc” groups. (B) Mean ± SEM of duration of paw licking and biting per 5 minutes plotted vs time after injection (at time “0”) of 2% formalin ( dark gray ); 2% formalin together with 60 ng/g of imatinib ( blue ) and 60 ng/g of imatinib alone ( light blue ). RM 2-way ANOVA with post hoc Bonferroni; n = 6 rats per group, ns, not significant; * P < 0.05; ** P < 0.01, *** P < 0.001 black bar and asterisks —comparison between the “Formalin + vehicle” and the “Formalin + imatinib” groups; light blue bar and asterisks —comparison between the “Imatinib alone” and the “Formalin + imatinib” groups. (C) Summary of mean ± SEM of total duration of time spent in licking and biting in phase I (0-10 minutes) and phase II (10-60 minutes) after injection of 2% formalin with vehicle ( dark gray ); 2% formalin together with 500 ng/40 μL of PDGFR-β-Fc ( orange ); 2% formalin together with 60 ng/g of imatinib ( blue ); 2% formalin together with 1.5 mg/kg (green) and 5 mg/kg of morphine ( dark green ) Student t -test; ns, not significant; * P < 0.05, ** P < 0.01; *** P < 0.001; n = 6 animals in all groups apart from the “Formalin + vehicle” group containing n = 12 animals. ANOVA, analysis of variance; PDGF, platelet-derived growth factor; RM, repeated-measures.

Journal: Pain

Article Title: Platelet-derived growth factor activates nociceptive neurons by inhibiting M-current and contributes to inflammatory pain

doi: 10.1097/j.pain.0000000000001523

Figure Lengend Snippet: Platelet-derived growth factor scavenging and inhibition of PDGFR reduces formalin-induced inflammatory pain. (A) Mean ± SEM of duration of paw licking and biting per 5 minutes plotted vs time after injection of 2% formalin with vehicle (PBS, gray squares ); 2% formalin with 500 ng/40 μL of PDGFR-β-Fc ( orange circles ) and 500 ng/40 μL of PDGFR-β-Fc alone ( light orange triangles ). RM two-way ANOVA with post hoc Bonferroni, n = 6 rats per group; black bar and asterisks —comparison between the “Formalin + vehicle” and the “Formalin + PDGFR-β-Fc” groups; light orange bar and asterisks —comparison between the “PDGFR-β-Fc alone” and the “Formalin + PDGFR-β-Fc” groups. (B) Mean ± SEM of duration of paw licking and biting per 5 minutes plotted vs time after injection (at time “0”) of 2% formalin ( dark gray ); 2% formalin together with 60 ng/g of imatinib ( blue ) and 60 ng/g of imatinib alone ( light blue ). RM 2-way ANOVA with post hoc Bonferroni; n = 6 rats per group, ns, not significant; * P < 0.05; ** P < 0.01, *** P < 0.001 black bar and asterisks —comparison between the “Formalin + vehicle” and the “Formalin + imatinib” groups; light blue bar and asterisks —comparison between the “Imatinib alone” and the “Formalin + imatinib” groups. (C) Summary of mean ± SEM of total duration of time spent in licking and biting in phase I (0-10 minutes) and phase II (10-60 minutes) after injection of 2% formalin with vehicle ( dark gray ); 2% formalin together with 500 ng/40 μL of PDGFR-β-Fc ( orange ); 2% formalin together with 60 ng/g of imatinib ( blue ); 2% formalin together with 1.5 mg/kg (green) and 5 mg/kg of morphine ( dark green ) Student t -test; ns, not significant; * P < 0.05, ** P < 0.01; *** P < 0.001; n = 6 animals in all groups apart from the “Formalin + vehicle” group containing n = 12 animals. ANOVA, analysis of variance; PDGF, platelet-derived growth factor; RM, repeated-measures.

Techniques: Derivative Assay, Inhibition, Injection, Comparison

(A) Horizontal section of the medulla of NP6520 -Gal4/UAS-mCD8-GFP flies immunolabeled with anti-PER antibody. The nuclei of GFP-expressing EnGl (frames 1–3) are PER-positive, which is well visible in higher magnification (panels 1–3). The processes of EnGl (arrowheads in panels 1–3) span the medula neuropil (Mn). R, retina; Lc, Lamina cortex; Ln, lamina neuropil; oCh, outer chiasm; Mc, medulla cortex; iCh, inner chiasm. Scale bars: 20 μm for (A) and 10 μm for panel 1, 2, and 3. (B) The nuclei of GFP-positive EnGl show high level of REPO-specific immunofluorescence (arrow). Arrowhead-the EnGl processes. Scale bar: 10 μm. (C) The distal part of the medulla in horizontal section of NP6520 -Gal4/UAS-mCD8-GFP flies immunolabeled with anti-DmMANF antibody. The processes of EnGl are marked with arrows. R, retina; Lc, lamina cortex; Ln, lamina neuropil; Mc, medulla cortex; Mn, medulla neuropil. Scale bar: 20 μm. (D-D”) Higher magnification of EnGl marked in (C) . The GFP-positive processes of EnGl ( D , arrows) are marked with DmMANF (D',D”) . DmMANF is also visible in the perinuclear space of cell bodies in the medulla cortex (D', arrowheads). Scale bar: 10 μm.

Journal: Frontiers in Physiology

Article Title: Different Levels of Expression of the Clock Protein PER and the Glial Marker REPO in Ensheathing and Astrocyte-Like Glia of the Distal Medulla of Drosophila Optic Lobe

doi: 10.3389/fphys.2018.00361

Figure Lengend Snippet: (A) Horizontal section of the medulla of NP6520 -Gal4/UAS-mCD8-GFP flies immunolabeled with anti-PER antibody. The nuclei of GFP-expressing EnGl (frames 1–3) are PER-positive, which is well visible in higher magnification (panels 1–3). The processes of EnGl (arrowheads in panels 1–3) span the medula neuropil (Mn). R, retina; Lc, Lamina cortex; Ln, lamina neuropil; oCh, outer chiasm; Mc, medulla cortex; iCh, inner chiasm. Scale bars: 20 μm for (A) and 10 μm for panel 1, 2, and 3. (B) The nuclei of GFP-positive EnGl show high level of REPO-specific immunofluorescence (arrow). Arrowhead-the EnGl processes. Scale bar: 10 μm. (C) The distal part of the medulla in horizontal section of NP6520 -Gal4/UAS-mCD8-GFP flies immunolabeled with anti-DmMANF antibody. The processes of EnGl are marked with arrows. R, retina; Lc, lamina cortex; Ln, lamina neuropil; Mc, medulla cortex; Mn, medulla neuropil. Scale bar: 20 μm. (D-D”) Higher magnification of EnGl marked in (C) . The GFP-positive processes of EnGl ( D , arrows) are marked with DmMANF (D',D”) . DmMANF is also visible in the perinuclear space of cell bodies in the medulla cortex (D', arrowheads). Scale bar: 10 μm.

Article Snippet: Cryosections of 20 μm thickness were cut and immunolabeled with primary antibodies as follows: mouse anti-REPO Ab (1:40, Developmental Studies Hybridoma Bank), mouse anti-PDF Ab (1:500, Developmental Studies Hybridoma Bank) rabbit anti-GFP Ab (1:1000, Novus Biologicals), mouse anti-GFP Ab (1:1000, Novus Biologicals), rabbit anti-PER Ab (1:1000, a kind gift of R. Stanewsky), and rabbit anti- Drosophila melanogaster MESENCEPHALIC ASTROCYTE-DERIVED NEUROTROPHIC FACTOR or DmMANF Ab (1:500, GenScript, prepared using PolyExpress Premium Antigen-Specific Affinity Purified pAb and tested for specificity on homogenates of DmMANF -deficient flies).

Techniques: Immunolabeling, Expressing, Immunofluorescence

Review

Structured Review

Images

Similar Products

Image Search Results