α2c adrenergic receptor  (Bio-Techne corporation)

Journal: International journal of molecular sciences

Article Title: α1D Adrenergic Receptor Antagonism Protects Against High Glucose-Induced Mitochondrial Dysfunction and Blood Retinal Barrier Breakdown in ARPE-19 Cells.

doi: 10.3390/ijms26030967

Figure Lengend Snippet: Figure 2. Effect of α1D and α2C receptors agonists/antagonists on ARPE-19 cell viability in NG (MTT assay). Treatment with the α1DR antagonist (BMY 7378 0.001–1 µM) (A) and agonist (phenylephrine 0.1–10 µM) (B) did not reduce cell viability. Only the higher tested concentrations of BMY 7378 (10 µM) and phenylephrine (50–100 µM) significantly (p < 0.05) affected ARPE-19 viability compared to untreated cells (Ctrl). α2CR antagonist, JP 1302 (0.01–1 µM) (C), and agonist, dexmedetomidine (0.001–1 µM) (D), were tolerated by ARPE-19 cells. Dexmedetomidine at 10 µM led to a significant (p < 0.05) reduction in cell viability as compared to control cells (D). Values are reported as mean ± SD; n = 4. Data were analyzed by one-way ANOVA and the Tukey post hoc test for multiple comparisons. * p < 0.05 vs. control.

Article Snippet: The α2C adrenergic receptors ligands JP 1302 dihydrochloride (Tocris Bioscience, Cat.No.

Techniques: MTT Assay, Control

Journal: International journal of molecular sciences

Article Title: α1D Adrenergic Receptor Antagonism Protects Against High Glucose-Induced Mitochondrial Dysfunction and Blood Retinal Barrier Breakdown in ARPE-19 Cells.

doi: 10.3390/ijms26030967

Figure Lengend Snippet: Figure 3. Effect of α1D and α2C receptors agonists/antagonists on ARPE-19 cell viability in NG (LDH Release Assay). Exposure to α1DR antagonist (BMY 7378 0.001–1 µM) (A) and agonist (phenylephrine 0.1–10 µM) (B) did not increase LDH release compared to control cells. However, treatment with BMY 7378 (10 µM) and phenylephrine (50 and 100 µM) led to a significant (p < 0.05) increase in the LDH release as compared to control cells. No significant change in LDH release was detected in ARPE-19 treated with the α2CR antagonist (JP 1302, 0.01–1 µM) (C) and agonist (dexmedetomidine, 0.001–1 µM) (D). Treatment with the higher tested concentration of dexmedetomidine (10 µM) led to a significant (p < 0.05) increase in cell permeability (LDH release) as compared to untreated cells. Values are reported as mean ± SD; n = 4. Data were analyzed by one-way ANOVA and the Tukey post hoc test for multiple comparisons. * p < 0.05 vs. control.

Article Snippet: The α2C adrenergic receptors ligands JP 1302 dihydrochloride (Tocris Bioscience, Cat.No.

Techniques: Lactate Dehydrogenase Assay, Control, Concentration Assay, Permeability

Journal: International journal of molecular sciences

Article Title: α1D Adrenergic Receptor Antagonism Protects Against High Glucose-Induced Mitochondrial Dysfunction and Blood Retinal Barrier Breakdown in ARPE-19 Cells.

doi: 10.3390/ijms26030967

Figure Lengend Snippet: Figure 4. Effect of α2C and α1D receptor agonists/antagonists on OCR and ECAR in ARPE-19 cells exposed to HG. Dexmedetomidine and JP 1302 did not modify the negative effect of HG on mitochondrial respiration, as measured by the oxygen consumption rate (OCR) (A). Treatment with α2C receptor agonist (dexmedetomidine 0.01 and 1 µM) did not significantly restore the decrease in ECAR mediated by HG, while exposure to the antagonist JP 1302 (0.01–1 µM) showed a different effect based on the tested concentration (B). The α1D receptor antagonist BMY 7378 (0.1 and 1 µM) significantly (p < 0.05) restored impairment in cellular OCR induced by HG (C) and ECAR (D). Phenylephrine exposure (1 and 10 µM) exacerbated the depression of ARPE-19 respiration caused by HG and did not modify ARPE-19 glycolysis compared to HG treatment alone, as indicated by OCR (C) and ECAR (D), respectively. Values are reported as mean ± SD; n = 4. Data were analyzed by two-way ANOVA and the Tukey post hoc test for multiple comparisons.

Article Snippet: The α2C adrenergic receptors ligands JP 1302 dihydrochloride (Tocris Bioscience, Cat.No.

Techniques: Concentration Assay

Journal: Neurobiology of disease

Article Title: Inhibitory designer receptors aggravate memory loss in a mouse model of down syndrome

doi: 10.1016/j.nbd.2019.104616

Figure Lengend Snippet: α-ARs immunostaining in response to DREADD hM4Di inhibition of the LC. For all α-ARs, the main effects were attributable to treatment since compensatory receptor expressions were seen in (A) Regions examined by α-AR IF. Representative immunofluorescence for α1a-AR comparing all cohorts (parietal region) (B). Normalized fluorescent intensities for (C) α1a-AR (F1,56 = 9.45, p = .003), (D) α2a-AR (F1,56 = 17.2, p = .0001), (E) α2b-AR (F1,44 = 43.91, p < .0001) and (F) α2c-AR (F1,44 = 26.40, p < .0001). A significant effect could also be attributed to karyotype in α1a-AR (F1,56 = 8.40, p = .005), and α2c-AR (F1,44 = 17.73, p = .0001). Scale bar = 100 μm. (G) Expression levels of α2a-, α2b- and α2c-ARs negatively correlated with 24-h NORT DI performance. Error bars represent the mean ± SEM. Dotted lines represented the 95% confidence interval.

Article Snippet: For ARs, sections were incubated overnight at room temperature with anti-β1 (#AAR-023, dil. 1:400), anti-β2 (#AAR-016, dil. 1:200), anti-β3 (#AAR-017, dil. 1:100), anti-α1a (#AAR-015, dil. 1:100), anti-α2a (#AAR-020, dil. 1:200), anti-α2b (#AAR-021, dil. 1:100), or anti-α2c (#AAR-021, dil. 1:100) AR antibodies with or without blocking peptides at the recommended concentrations (Alomone Labs, Jerusalem, Israel).

Techniques: Immunostaining, Inhibition, Immunofluorescence, Expressing