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Liggett Group Inc b2-adrenergic receptor
B2 Adrenergic Receptor, supplied by Liggett Group Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Autoradiography:

Article Title: A peptide of the RGS domain of GRK2 binds and inhibits Gα(q) to suppress pathological cardiac hypertrophy and dysfunction.
Article Snippet: G. W. Dorn II, N. M. Tepe, J. N. Lorenz, W. J. Koch, S. B. Liggett, Low- and high-level transgenic expression of b2-adrenergic receptors differentially affect cardiac hypertrophy and function in Gaq-overexpressing mice.

Article Title: Spontaneous activation of beta(2)- but not beta(1)-adrenoceptors expressed in cardiac myocytes from beta(1)beta(2) double knockout mice.
Article Snippet: Although ligand-free, constitutive b2-adrenergic receptor (AR) signaling has been demonstrated in naive cell lines and in transgenic mice overexpressing cardiac b2-AR, it is unclear whether the dominant cardiac b-AR subtype, b1-AR, shares the ability of spontaneous activation.. In the present study, we expressed human b1or b2-AR via recombinant adenoviral infection in ventricular myocytes isolated from b1b2-AR double knockout mice, creating pure b1-AR and b2-AR systems with variable receptor densities.. A contractile response to a nonselective b-AR agonist, isoproterenol, was absent in double knockout mouse myocytes but was fully restored after adenoviral b1-AR or adenoviral b2-AR infection.

Article Title: Ozone-induced alteration in beta-adrenergic pharmacological modulation of pulmonary macrophages.
Article Snippet: of b-adrenergic receptors on pulmonary macrophages results Ozone-Induced Alteration in b-Adrenergic Pharmacological in a down-regulation of immune function and changes in the Modulation of Pulmonary Macrophages.. MCGOVERN, T. J., ELstate of cell activation (Nijkamp and Henricks, 1990).. FAWAL, H. A. N., CHEN, L. C., AND SCHLESINGER, R. B. (1996).

Article Title: Developing Genetically Encoded Optical Tools for Imaging Brain Circuits and Pharmacology
Article Snippet: 13, eaaw3122 (2020). doi:10.1126/scisignal.aaw3122 Medline J. E. Saffitz, S. B. Liggett, Subcellular distribution of B2-adrenergic receptors delineated with quantitative ultrastructural autoradiography of radioligand binding sites.

Binding Assay:

Article Title: A peptide of the RGS domain of GRK2 binds and inhibits Gα(q) to suppress pathological cardiac hypertrophy and dysfunction.
Article Snippet: G. W. Dorn II, N. M. Tepe, J. N. Lorenz, W. J. Koch, S. B. Liggett, Low- and high-level transgenic expression of b2-adrenergic receptors differentially affect cardiac hypertrophy and function in Gaq-overexpressing mice.

Article Title: Spontaneous activation of beta(2)- but not beta(1)-adrenoceptors expressed in cardiac myocytes from beta(1)beta(2) double knockout mice.
Article Snippet: Although ligand-free, constitutive b2-adrenergic receptor (AR) signaling has been demonstrated in naive cell lines and in transgenic mice overexpressing cardiac b2-AR, it is unclear whether the dominant cardiac b-AR subtype, b1-AR, shares the ability of spontaneous activation.. In the present study, we expressed human b1or b2-AR via recombinant adenoviral infection in ventricular myocytes isolated from b1b2-AR double knockout mice, creating pure b1-AR and b2-AR systems with variable receptor densities.. A contractile response to a nonselective b-AR agonist, isoproterenol, was absent in double knockout mouse myocytes but was fully restored after adenoviral b1-AR or adenoviral b2-AR infection.

Article Title: Ozone-induced alteration in beta-adrenergic pharmacological modulation of pulmonary macrophages.
Article Snippet: of b-adrenergic receptors on pulmonary macrophages results Ozone-Induced Alteration in b-Adrenergic Pharmacological in a down-regulation of immune function and changes in the Modulation of Pulmonary Macrophages.. MCGOVERN, T. J., ELstate of cell activation (Nijkamp and Henricks, 1990).. FAWAL, H. A. N., CHEN, L. C., AND SCHLESINGER, R. B. (1996).

Article Title: Developing Genetically Encoded Optical Tools for Imaging Brain Circuits and Pharmacology
Article Snippet: 13, eaaw3122 (2020). doi:10.1126/scisignal.aaw3122 Medline J. E. Saffitz, S. B. Liggett, Subcellular distribution of B2-adrenergic receptors delineated with quantitative ultrastructural autoradiography of radioligand binding sites.

Transgenic Assay:

Article Title: A peptide of the RGS domain of GRK2 binds and inhibits Gα(q) to suppress pathological cardiac hypertrophy and dysfunction.
Article Snippet: G. W. Dorn II, N. M. Tepe, J. N. Lorenz, W. J. Koch, S. B. Liggett, Low- and high-level transgenic expression of b2-adrenergic receptors differentially affect cardiac hypertrophy and function in Gaq-overexpressing mice.

Article Title: Spontaneous activation of beta(2)- but not beta(1)-adrenoceptors expressed in cardiac myocytes from beta(1)beta(2) double knockout mice.
Article Snippet: Although ligand-free, constitutive b2-adrenergic receptor (AR) signaling has been demonstrated in naive cell lines and in transgenic mice overexpressing cardiac b2-AR, it is unclear whether the dominant cardiac b-AR subtype, b1-AR, shares the ability of spontaneous activation.. In the present study, we expressed human b1or b2-AR via recombinant adenoviral infection in ventricular myocytes isolated from b1b2-AR double knockout mice, creating pure b1-AR and b2-AR systems with variable receptor densities.. A contractile response to a nonselective b-AR agonist, isoproterenol, was absent in double knockout mouse myocytes but was fully restored after adenoviral b1-AR or adenoviral b2-AR infection.

Article Title: Ozone-induced alteration in beta-adrenergic pharmacological modulation of pulmonary macrophages.
Article Snippet: of b-adrenergic receptors on pulmonary macrophages results Ozone-Induced Alteration in b-Adrenergic Pharmacological in a down-regulation of immune function and changes in the Modulation of Pulmonary Macrophages.. MCGOVERN, T. J., ELstate of cell activation (Nijkamp and Henricks, 1990).. FAWAL, H. A. N., CHEN, L. C., AND SCHLESINGER, R. B. (1996).

Article Title: Developing Genetically Encoded Optical Tools for Imaging Brain Circuits and Pharmacology
Article Snippet: 13, eaaw3122 (2020). doi:10.1126/scisignal.aaw3122 Medline J. E. Saffitz, S. B. Liggett, Subcellular distribution of B2-adrenergic receptors delineated with quantitative ultrastructural autoradiography of radioligand binding sites.

Expressing:

Article Title: A peptide of the RGS domain of GRK2 binds and inhibits Gα(q) to suppress pathological cardiac hypertrophy and dysfunction.
Article Snippet: G. W. Dorn II, N. M. Tepe, J. N. Lorenz, W. J. Koch, S. B. Liggett, Low- and high-level transgenic expression of b2-adrenergic receptors differentially affect cardiac hypertrophy and function in Gaq-overexpressing mice.

Article Title: Spontaneous activation of beta(2)- but not beta(1)-adrenoceptors expressed in cardiac myocytes from beta(1)beta(2) double knockout mice.
Article Snippet: Although ligand-free, constitutive b2-adrenergic receptor (AR) signaling has been demonstrated in naive cell lines and in transgenic mice overexpressing cardiac b2-AR, it is unclear whether the dominant cardiac b-AR subtype, b1-AR, shares the ability of spontaneous activation.. In the present study, we expressed human b1or b2-AR via recombinant adenoviral infection in ventricular myocytes isolated from b1b2-AR double knockout mice, creating pure b1-AR and b2-AR systems with variable receptor densities.. A contractile response to a nonselective b-AR agonist, isoproterenol, was absent in double knockout mouse myocytes but was fully restored after adenoviral b1-AR or adenoviral b2-AR infection.

Article Title: Ozone-induced alteration in beta-adrenergic pharmacological modulation of pulmonary macrophages.
Article Snippet: of b-adrenergic receptors on pulmonary macrophages results Ozone-Induced Alteration in b-Adrenergic Pharmacological in a down-regulation of immune function and changes in the Modulation of Pulmonary Macrophages.. MCGOVERN, T. J., ELstate of cell activation (Nijkamp and Henricks, 1990).. FAWAL, H. A. N., CHEN, L. C., AND SCHLESINGER, R. B. (1996).

Article Title: Developing Genetically Encoded Optical Tools for Imaging Brain Circuits and Pharmacology
Article Snippet: 13, eaaw3122 (2020). doi:10.1126/scisignal.aaw3122 Medline J. E. Saffitz, S. B. Liggett, Subcellular distribution of B2-adrenergic receptors delineated with quantitative ultrastructural autoradiography of radioligand binding sites.



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Figure 2. Effects of <t>b2</t> <t>adrenergic</t> receptor (AR) agonist on enhanced spinal microglia activation in a rat model of persistent postop- erative pain. Sections of spinal cord were collected from rats 8 days following plantar incision and following treatment with DbH-saporin to deplete spinal noradrenergic terminals or control IgG-saporin. Rats were chronically administered clenbuterol (0.5 mg/kg, 2/day, i.p.) or saline vehicle 6 days prior to and for 8 days after plantar incision. Depletion of spinal noradrenergic fibers was verified immunohisto- chemically with an antibody against dopamine b hydroxylase (DbH, (a)–(c)). Representative confocal images of IBA1-IR (blue, (d)–(f)) and phospho-p38 MAPK-IR (purple, (g)–(i)) in the ipsilateral spinal cord of incision rats. Localization of p38 MAPK in microglia was confirmed by colocalization with an antibody against the cell surface antigen CD11b (green, inset in (h)). Quantification of IBA1-IR in ipsilateral and contralateral spinal cord of rats with incision (j). Data represent mean SEM, n ¼ 3 rats per group. Two way ANOVA indicated effect of group: p < 0.001 but not side p ¼ 0.184 or interaction: p ¼ 0.59 with SNK pairwise comparisons *p < 0.001 versus Incisionþ DbH- saporinþ vehicle. Quantification of phospho-p38 MAPK microglial in the ipsilateral and contralateral spinal cord of rats with incision (k). Data represent mean SEM, n ¼ 3 rats per group. Two way ANOVA indicate effect of group: p ¼ 0.002 but not side p ¼ 0.398 or interaction: p ¼ 0.67 with SNK pairwise comparisons * p < 0.005 versus Incisionþ DbH-saporinþ vehicle.
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Figure 2. Effects of <t>b2</t> <t>adrenergic</t> receptor (AR) agonist on enhanced spinal microglia activation in a rat model of persistent postop- erative pain. Sections of spinal cord were collected from rats 8 days following plantar incision and following treatment with DbH-saporin to deplete spinal noradrenergic terminals or control IgG-saporin. Rats were chronically administered clenbuterol (0.5 mg/kg, 2/day, i.p.) or saline vehicle 6 days prior to and for 8 days after plantar incision. Depletion of spinal noradrenergic fibers was verified immunohisto- chemically with an antibody against dopamine b hydroxylase (DbH, (a)–(c)). Representative confocal images of IBA1-IR (blue, (d)–(f)) and phospho-p38 MAPK-IR (purple, (g)–(i)) in the ipsilateral spinal cord of incision rats. Localization of p38 MAPK in microglia was confirmed by colocalization with an antibody against the cell surface antigen CD11b (green, inset in (h)). Quantification of IBA1-IR in ipsilateral and contralateral spinal cord of rats with incision (j). Data represent mean SEM, n ¼ 3 rats per group. Two way ANOVA indicated effect of group: p < 0.001 but not side p ¼ 0.184 or interaction: p ¼ 0.59 with SNK pairwise comparisons *p < 0.001 versus Incisionþ DbH- saporinþ vehicle. Quantification of phospho-p38 MAPK microglial in the ipsilateral and contralateral spinal cord of rats with incision (k). Data represent mean SEM, n ¼ 3 rats per group. Two way ANOVA indicate effect of group: p ¼ 0.002 but not side p ¼ 0.398 or interaction: p ¼ 0.67 with SNK pairwise comparisons * p < 0.005 versus Incisionþ DbH-saporinþ vehicle.
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Figure 2. Effects of <t>b2</t> <t>adrenergic</t> receptor (AR) agonist on enhanced spinal microglia activation in a rat model of persistent postop- erative pain. Sections of spinal cord were collected from rats 8 days following plantar incision and following treatment with DbH-saporin to deplete spinal noradrenergic terminals or control IgG-saporin. Rats were chronically administered clenbuterol (0.5 mg/kg, 2/day, i.p.) or saline vehicle 6 days prior to and for 8 days after plantar incision. Depletion of spinal noradrenergic fibers was verified immunohisto- chemically with an antibody against dopamine b hydroxylase (DbH, (a)–(c)). Representative confocal images of IBA1-IR (blue, (d)–(f)) and phospho-p38 MAPK-IR (purple, (g)–(i)) in the ipsilateral spinal cord of incision rats. Localization of p38 MAPK in microglia was confirmed by colocalization with an antibody against the cell surface antigen CD11b (green, inset in (h)). Quantification of IBA1-IR in ipsilateral and contralateral spinal cord of rats with incision (j). Data represent mean SEM, n ¼ 3 rats per group. Two way ANOVA indicated effect of group: p < 0.001 but not side p ¼ 0.184 or interaction: p ¼ 0.59 with SNK pairwise comparisons *p < 0.001 versus Incisionþ DbH- saporinþ vehicle. Quantification of phospho-p38 MAPK microglial in the ipsilateral and contralateral spinal cord of rats with incision (k). Data represent mean SEM, n ¼ 3 rats per group. Two way ANOVA indicate effect of group: p ¼ 0.002 but not side p ¼ 0.398 or interaction: p ¼ 0.67 with SNK pairwise comparisons * p < 0.005 versus Incisionþ DbH-saporinþ vehicle.
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Figure 2. Effects of <t>b2</t> <t>adrenergic</t> receptor (AR) agonist on enhanced spinal microglia activation in a rat model of persistent postop- erative pain. Sections of spinal cord were collected from rats 8 days following plantar incision and following treatment with DbH-saporin to deplete spinal noradrenergic terminals or control IgG-saporin. Rats were chronically administered clenbuterol (0.5 mg/kg, 2/day, i.p.) or saline vehicle 6 days prior to and for 8 days after plantar incision. Depletion of spinal noradrenergic fibers was verified immunohisto- chemically with an antibody against dopamine b hydroxylase (DbH, (a)–(c)). Representative confocal images of IBA1-IR (blue, (d)–(f)) and phospho-p38 MAPK-IR (purple, (g)–(i)) in the ipsilateral spinal cord of incision rats. Localization of p38 MAPK in microglia was confirmed by colocalization with an antibody against the cell surface antigen CD11b (green, inset in (h)). Quantification of IBA1-IR in ipsilateral and contralateral spinal cord of rats with incision (j). Data represent mean SEM, n ¼ 3 rats per group. Two way ANOVA indicated effect of group: p < 0.001 but not side p ¼ 0.184 or interaction: p ¼ 0.59 with SNK pairwise comparisons *p < 0.001 versus Incisionþ DbH- saporinþ vehicle. Quantification of phospho-p38 MAPK microglial in the ipsilateral and contralateral spinal cord of rats with incision (k). Data represent mean SEM, n ¼ 3 rats per group. Two way ANOVA indicate effect of group: p ¼ 0.002 but not side p ¼ 0.398 or interaction: p ¼ 0.67 with SNK pairwise comparisons * p < 0.005 versus Incisionþ DbH-saporinþ vehicle.
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Figure 2. Effects of <t>b2</t> <t>adrenergic</t> receptor (AR) agonist on enhanced spinal microglia activation in a rat model of persistent postop- erative pain. Sections of spinal cord were collected from rats 8 days following plantar incision and following treatment with DbH-saporin to deplete spinal noradrenergic terminals or control IgG-saporin. Rats were chronically administered clenbuterol (0.5 mg/kg, 2/day, i.p.) or saline vehicle 6 days prior to and for 8 days after plantar incision. Depletion of spinal noradrenergic fibers was verified immunohisto- chemically with an antibody against dopamine b hydroxylase (DbH, (a)–(c)). Representative confocal images of IBA1-IR (blue, (d)–(f)) and phospho-p38 MAPK-IR (purple, (g)–(i)) in the ipsilateral spinal cord of incision rats. Localization of p38 MAPK in microglia was confirmed by colocalization with an antibody against the cell surface antigen CD11b (green, inset in (h)). Quantification of IBA1-IR in ipsilateral and contralateral spinal cord of rats with incision (j). Data represent mean SEM, n ¼ 3 rats per group. Two way ANOVA indicated effect of group: p < 0.001 but not side p ¼ 0.184 or interaction: p ¼ 0.59 with SNK pairwise comparisons *p < 0.001 versus Incisionþ DbH- saporinþ vehicle. Quantification of phospho-p38 MAPK microglial in the ipsilateral and contralateral spinal cord of rats with incision (k). Data represent mean SEM, n ¼ 3 rats per group. Two way ANOVA indicate effect of group: p ¼ 0.002 but not side p ¼ 0.398 or interaction: p ¼ 0.67 with SNK pairwise comparisons * p < 0.005 versus Incisionþ DbH-saporinþ vehicle.
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Image Search Results


Figure 2. Effects of b2 adrenergic receptor (AR) agonist on enhanced spinal microglia activation in a rat model of persistent postop- erative pain. Sections of spinal cord were collected from rats 8 days following plantar incision and following treatment with DbH-saporin to deplete spinal noradrenergic terminals or control IgG-saporin. Rats were chronically administered clenbuterol (0.5 mg/kg, 2/day, i.p.) or saline vehicle 6 days prior to and for 8 days after plantar incision. Depletion of spinal noradrenergic fibers was verified immunohisto- chemically with an antibody against dopamine b hydroxylase (DbH, (a)–(c)). Representative confocal images of IBA1-IR (blue, (d)–(f)) and phospho-p38 MAPK-IR (purple, (g)–(i)) in the ipsilateral spinal cord of incision rats. Localization of p38 MAPK in microglia was confirmed by colocalization with an antibody against the cell surface antigen CD11b (green, inset in (h)). Quantification of IBA1-IR in ipsilateral and contralateral spinal cord of rats with incision (j). Data represent mean SEM, n ¼ 3 rats per group. Two way ANOVA indicated effect of group: p < 0.001 but not side p ¼ 0.184 or interaction: p ¼ 0.59 with SNK pairwise comparisons *p < 0.001 versus Incisionþ DbH- saporinþ vehicle. Quantification of phospho-p38 MAPK microglial in the ipsilateral and contralateral spinal cord of rats with incision (k). Data represent mean SEM, n ¼ 3 rats per group. Two way ANOVA indicate effect of group: p ¼ 0.002 but not side p ¼ 0.398 or interaction: p ¼ 0.67 with SNK pairwise comparisons * p < 0.005 versus Incisionþ DbH-saporinþ vehicle.

Journal: Molecular pain

Article Title: Systemic administration of a β2-adrenergic receptor agonist reduces mechanical allodynia and suppresses the immune response to surgery in a rat model of persistent post-incisional hypersensitivity.

doi: 10.1177/1744806921997206

Figure Lengend Snippet: Figure 2. Effects of b2 adrenergic receptor (AR) agonist on enhanced spinal microglia activation in a rat model of persistent postop- erative pain. Sections of spinal cord were collected from rats 8 days following plantar incision and following treatment with DbH-saporin to deplete spinal noradrenergic terminals or control IgG-saporin. Rats were chronically administered clenbuterol (0.5 mg/kg, 2/day, i.p.) or saline vehicle 6 days prior to and for 8 days after plantar incision. Depletion of spinal noradrenergic fibers was verified immunohisto- chemically with an antibody against dopamine b hydroxylase (DbH, (a)–(c)). Representative confocal images of IBA1-IR (blue, (d)–(f)) and phospho-p38 MAPK-IR (purple, (g)–(i)) in the ipsilateral spinal cord of incision rats. Localization of p38 MAPK in microglia was confirmed by colocalization with an antibody against the cell surface antigen CD11b (green, inset in (h)). Quantification of IBA1-IR in ipsilateral and contralateral spinal cord of rats with incision (j). Data represent mean SEM, n ¼ 3 rats per group. Two way ANOVA indicated effect of group: p < 0.001 but not side p ¼ 0.184 or interaction: p ¼ 0.59 with SNK pairwise comparisons *p < 0.001 versus Incisionþ DbH- saporinþ vehicle. Quantification of phospho-p38 MAPK microglial in the ipsilateral and contralateral spinal cord of rats with incision (k). Data represent mean SEM, n ¼ 3 rats per group. Two way ANOVA indicate effect of group: p ¼ 0.002 but not side p ¼ 0.398 or interaction: p ¼ 0.67 with SNK pairwise comparisons * p < 0.005 versus Incisionþ DbH-saporinþ vehicle.

Article Snippet: We used a previously characterized antibody against b2 adrenergic receptors (AAR-016, b2-AR, 1:1000, rabbit anti-mouse, Alomone Labs; Jerusalem, Israel).

Techniques: Activation Assay, Control, Saline

Figure 5. Beta 2-adrenergic receptor immunoreactivity in the spinal cord of rats under naı¨ve conditions and two days following plantar incision. Transverse section of L4 spinal cord of rat reacted with antibody against b2 adrenergic receptor ((a), b2-AR, green). There is a high density of immunoreactivity in cellular profiles throughout dorsal and ventral horn. There is also dense immunoreactivity in axon terminals within the lateral portion of the superficial laminae (arrow) and ependymal cells in the vicinity of the central canal (Arrowhead). Note lack of staining for b2-AR in motor neurons within the ventral horn (asterisk). Higher magnification confocal images show b2-AR-IR ((c), green) is present in a subpopulation of neurons ((d), NeuN, purple) in the dorsal spinal cord. Most b2-AR-IR cellular profiles colocalized with NeuN with the exception of a few non-neuronal profiles with morphology typical of microglia (arrows, (c)–(f)). b2-AR-IR non-neuronal cellular profiles in the spinal cord colocalized with the microglial marker IBA1 (red, (e) and (f)). Arrows in F indicate IBA1 negative neuronal cellular profiles. Representative images of b2 mRNA and DAPI in the dorsal spinal cord (g) with high power image showing colocalization with a subset of nuclei (h).

Journal: Molecular pain

Article Title: Systemic administration of a β2-adrenergic receptor agonist reduces mechanical allodynia and suppresses the immune response to surgery in a rat model of persistent post-incisional hypersensitivity.

doi: 10.1177/1744806921997206

Figure Lengend Snippet: Figure 5. Beta 2-adrenergic receptor immunoreactivity in the spinal cord of rats under naı¨ve conditions and two days following plantar incision. Transverse section of L4 spinal cord of rat reacted with antibody against b2 adrenergic receptor ((a), b2-AR, green). There is a high density of immunoreactivity in cellular profiles throughout dorsal and ventral horn. There is also dense immunoreactivity in axon terminals within the lateral portion of the superficial laminae (arrow) and ependymal cells in the vicinity of the central canal (Arrowhead). Note lack of staining for b2-AR in motor neurons within the ventral horn (asterisk). Higher magnification confocal images show b2-AR-IR ((c), green) is present in a subpopulation of neurons ((d), NeuN, purple) in the dorsal spinal cord. Most b2-AR-IR cellular profiles colocalized with NeuN with the exception of a few non-neuronal profiles with morphology typical of microglia (arrows, (c)–(f)). b2-AR-IR non-neuronal cellular profiles in the spinal cord colocalized with the microglial marker IBA1 (red, (e) and (f)). Arrows in F indicate IBA1 negative neuronal cellular profiles. Representative images of b2 mRNA and DAPI in the dorsal spinal cord (g) with high power image showing colocalization with a subset of nuclei (h).

Article Snippet: We used a previously characterized antibody against b2 adrenergic receptors (AAR-016, b2-AR, 1:1000, rabbit anti-mouse, Alomone Labs; Jerusalem, Israel).

Techniques: Staining, Marker

Figure 6. b2-adrenergic receptor immunoreactivity (b2AR-IR) in hindpaw of rats under naı¨ve conditions and following plantar incision. Skin sections were obtained from the hind paw of naı¨ve rats and incision rats two days following surgery. Sixteen-lm-thick sections were stained with antibodies against b2AR-IR (green, (a)–(c)), IBA1 (red, (d)–(f)) to label all monocytes/and macrophage, CD68 (blue, (g)–(i)) for activated M1 macrophage) and DAPI ((j) and (k)) to label all nuclei. b2-AR IR was present in keratinocytes of both naı¨ve and incision rats. Two days following plantar incision there were increased b2-AR IR cellular profiles in predominantly the dermal layers of the skin. Higher magnification confocal images ((c), (f), (i), and (l)) indicate colocalization of b2-AR in IBA1þ cells and a subset of which express CD68-IR. Note in naı¨ve skin IBA1-IR was primarily present at the epidermal/dermal interface and had reduced dermal cellularity (DAPIþ cells) compared to skin adjacent to the wound in incision rats.

Journal: Molecular pain

Article Title: Systemic administration of a β2-adrenergic receptor agonist reduces mechanical allodynia and suppresses the immune response to surgery in a rat model of persistent post-incisional hypersensitivity.

doi: 10.1177/1744806921997206

Figure Lengend Snippet: Figure 6. b2-adrenergic receptor immunoreactivity (b2AR-IR) in hindpaw of rats under naı¨ve conditions and following plantar incision. Skin sections were obtained from the hind paw of naı¨ve rats and incision rats two days following surgery. Sixteen-lm-thick sections were stained with antibodies against b2AR-IR (green, (a)–(c)), IBA1 (red, (d)–(f)) to label all monocytes/and macrophage, CD68 (blue, (g)–(i)) for activated M1 macrophage) and DAPI ((j) and (k)) to label all nuclei. b2-AR IR was present in keratinocytes of both naı¨ve and incision rats. Two days following plantar incision there were increased b2-AR IR cellular profiles in predominantly the dermal layers of the skin. Higher magnification confocal images ((c), (f), (i), and (l)) indicate colocalization of b2-AR in IBA1þ cells and a subset of which express CD68-IR. Note in naı¨ve skin IBA1-IR was primarily present at the epidermal/dermal interface and had reduced dermal cellularity (DAPIþ cells) compared to skin adjacent to the wound in incision rats.

Article Snippet: We used a previously characterized antibody against b2 adrenergic receptors (AAR-016, b2-AR, 1:1000, rabbit anti-mouse, Alomone Labs; Jerusalem, Israel).

Techniques: Staining