Skip to main content
. Author manuscript; available in PMC: 2017 Nov 1.
Published in final edited form as: Mol Neurobiol. 2015 Nov 17;53(9):6377–6387. doi: 10.1007/s12035-015-9536-0

Figure 6. CREB is essential for PDGF-BB mediated protective effect from HIV Tat& cocaine caused loss of neuronal differentiation.

Figure 6

(a)Representative blot of PDGF-mediated nucleus translocation of CREB in NPCs under HIV Tat & cocaine exposure with or without PDGF-BB treatment in the presence or absence of CREB pathway inhibitor protein kinase A (PKA) inhibitor H89(10μM). (b) Representative blot of PDGF-mediated neuronal differentiation in NPCs under HIV Tat & cocaine exposure with or without PDGF-BB treatment in the presence or absence of CREB pathway inhibitor H89. (c-d) Quantification analysis of CREB/ Lamin B, β-III-Tubulin/ β-actin from three individual experiments. *P<0.05; **P<0.01 versus control group; ##P<0.01 both PDGF and HIV Tat & cocaine-treated group. (e) Cultured NPCs were transfected with siRNA targeting CREB (siCREB) or a control nontargeting siRNA (siCtl). At 36 h post-transfection, the knocking down efficiency was checked by immunoblotting. (f) Representative blot of PDGF-BB-mediated neuronal differentiation in siRNA transfected NPCs followed by cocaine&Tat exposure. (g) Representative immunofluorescence images showing the β-III-Tubulin expression in differentiated NPCs under HIV Tat & cocaine exposure with or without PDGF-BB treatment in the presence or absence of CREB pathway inhibitor H89. Scale bar: 20 μm.