Skip to main content
. 2015 Jan 12;21(1):134–142. doi: 10.2119/molmed.2014.00189

Figure 1.

Figure 1

JAK3 activation by H5N1 HA results in the inhibition of cAMP-dependent CFTR Cl−channels. Tracheal tissues isolated from wild-type and JAK3 gene-deficient heterozygous (JAK3+/−) mice were pretreated with exposure of apical membranes to H5N1 HA (40 μg/mL) for 10 min or 20 min and then mounted into a perfused micro-Ussing chamber to perform short-circuit current assay. (A) Basal short-circuit current (Isc) and changes in the short-circuit current (ΔIsc) in response to forskolin (FSK, 10 μmol/L) addition (n = 5 per group, *p < 0.05 versus JAK3+/+ mice with saline). (B) Isc and ΔIsc measurement in wild-type mice treated with JAK3 inhibitor VI (JAK3inh, 0.15 mg/kg) or saline prior to exposure to HA (n = 5 per group, *p < 0.05 versus mice treated with saline; #p < 0.05 versus mice treated with HA).