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. Author manuscript; available in PMC: 2020 Dec 28.
Published in final edited form as: J Neuroimmune Pharmacol. 2008 Jun 26;3(3):154–164. doi: 10.1007/s11481-008-9105-7

Fig. 1.

Fig. 1

Upregulation of CD38 expression and function in activated astrocytes. Primary human astrocytes were activated with different doses of HIV-1gp120MN (5, 50, and 500 and 5 μM) with or without IL-1β (20 ng/ml). CD38 mRNA levels were measured by real-time PCR (A). HIV-1gp120MN showed a dose-dependent increase in CD38 mRNA expression when co-administered with IL-1β in primary astrocytes. Co-treatment with 50 nM (P<0.05), 500 nM (P<0.01), and 5 μM (P<0.001) of HIV-1gp120MN with 20 ng/ml IL-1β showed a significant increase in CD38 mRNA expression as compared to astrocytes treated with IL-1β alone (A). Total cell lysates from control, IL-1β-, and HIV-1gp120MN-activated astrocytes were analyzed for CD38 ADP-ribosyl cyclase activity as a functional read-out system (B). HIV-1gp120MN (5 μM) led to a 1.58-fold increase in CD38 enzyme activity over control (P<0.05). IL-1β-activation significantly increased CD38 ADP-ribosyl cyclase activity over control astrocytes (P<0.01). Five 5 micromolars HIV-1gp120MN-and IL-1β co-activation led to a 2.46-fold increase in CD38 ADP-ribosyl cyclase activity (P<0.001) over cells activated with IL-1β alone. One-way analysis of variance (ANOVA) analyses were performed using GraphPad Prism 4.0 software. The data is representative of the mean ± SEM of two independent astrocyte donors analyzed in multiple replicates