Fig. 3
From: A novel role for protein tyrosine phosphatase 1B as a positive regulator of neuroinflammation
PTP1B potentiates LPS-induced NO production. a PTP1B expression in BV-2 cells overexpressing HA-PTP1B. Western blot analysis showed a 2.59-fold increase in PTP1B expression in cells stably expressing HA-PTP1B. β-actin was used as a loading control. b LPS-induced NO production in BV-2 cells with or without PTP1B overexpression. BV-2 cells were treated with LPS at the indicated concentration (0–1000 ng/ml) for 24 h. Nitrite accumulation was measured using the Griess reaction. Real-time RT-PCR was performed to determine mRNA expression of TNF-α (c), iNOS (d), and IL-6 (e) in either control or HA-PTP1B-transfected BV-2 cells after LPS (100 ng/ml) treatment for 6 h. *p < 0.05 versus control BV-2 with LPS; analyzed by one-way ANOVA with Tukey’s multiple comparison test. f PTP1B expression in BV-2 cells transfected with PTP1B siRNA (siPTP1B). Real-time RT-PCR was performed to determine mRNA expression of PTP1B. g LPS-induced NO production in BV-2 cells after knockdown of PTP1B expression. The data were expressed as the mean ± SEM (n = 3). *p < 0.05 versus control BV-2 cells transfected with control siRNA (siCont)