Secreted CNTF induces GFAP expression in GSNO-treated astrocytes. Cortical astrocytes were plated in 6-well cell culture plates as detailed in the Fig. 1 legend. A, the composite mean ± S.E. of four experiments depicts the ratio of GFAP to β-actin mRNA transcripts in treated astrocytes for 24 h. Abs, antibodies. B, a representative autoradiograph (n = 4) depicts GFAP levels in treated astrocytes for 48 h. C, the Composite mean ± S.E. of three experiments depicts the ratio of GFAP to β-actin mRNA transcripts in treated astrocytes transiently transfected with control (scramble) or CNTF siRNAs. D, the composite mean ± S.E. of three experiments depicts the ratio of GFAP to β-actin mRNA transcripts in treated astrocytes with GSNO (0.2 mm) or CNTF (30 ng/ml) in the presence or absence of JAK2 inhibitor II (50 μm) or STAT3 inhibitor peptide (5 μg/ml) for 24 h. E, the composite mean ± S.E. of three experiments depicts the ratio of GFAP to β-actin mRNA transcripts in treated astrocytes after transient transfection with JAK2 or STAT3 siRNAs. F, a representative autoradiograph (n = 3) depicts % change in the protein level of JAK2 and STAT3 compared with controls in transiently transfected astrocytes (E). Statistical significance is as indicated. **, p < 0.01; ***, p < 0.001; NS, not significant.