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. Author manuscript; available in PMC: 2019 Sep 1.
Published in final edited form as: J Neuroimmune Pharmacol. 2018 May 11;13(3):355–370. doi: 10.1007/s11481-018-9788-3

Fig. 2.

Fig. 2

Beclin1 facilitates Tat-induced inflammatory molecule secretion and autophagy dysregulation. Indicated cytokines and chemokines secreted from C57BL/6J and Becn1+/− mixed glia supernatants were measured by ELISA at 8 (a) and 24 hours (b) following increasing concentrations of HIV Tat (10 nM, 50 nM, 100 nM). Arrows indicate decreased Tat-induced secretion of RANTES (red), MCP-1 (blue), and IL-6 (green) from Becn1+/− derived glia. Values were determined from standard curves and are presented as the mean ± SEM of 5 independent experiments. Whole cell lysates from C57BL/6J and Becn1+/− glia after 24-hours of treatment were subjected to immunoblotting with antibodies to Beclin1 (a), LC3 (b), and p62/SQSTM1 (c). Densitometry was performed for quantification, and the ratios of each protein to β-actin are presented graphically. Error bars show the SEM of 3 independent experiments. P < 0.05 * vs. Control; # vs. C57BL/6J