Skip to main content
Figure 6 | Cell Communication and Signaling

Figure 6

From: β-adrenergic receptor activation in immortalized human urothelial cells stimulates inflammatory responses by PKA-independent mechanisms

Figure 6

β-AR stimulated expression of pro-inflammatory mediators occurs through PKA-independent mechanisms. After a 30 min pre-incubation with 100 nM of H-89 (panel A) or 10 μM of Rp-cAMPS (panel B), UROtsa cells were stimulated with 100 nM isoproterenol in serum-free DMEM for the indicated times and immunoblotted with anti-COX-2 or anti-iNOS antibody to determine β-AR mediated changes in protein expression. Peak UROtsa cell expression of the pro-inflammatory mediators COX-2 and iNOS was observed 2 hrs after addition of isoproterenol even after pre-incubation with selective PKA inhibitors (panels C and D). Levels of COX-2 generated in the presence of H-89 or Rp-cAMPS were significantly increased 3.0 ± 0.4 and 2.5 ± 0.7 fold over basal, respectively. However these isoproterenol induced levels of COX-2 were not significantly different from cells pretreated in the absence of inhibitor (1.9 ± 0.5 fold over basal). Likewise, levels (fold over basal) of iNOS production generated by isoproterenol after H-89 (1.8 ± 0.3) or Rp-cAMPS pretreatment (2.2 ± 0.6) were significantly greater than basal. However these responses were not significantly different from levels observed for isoproterenol induced iNOS production in the absence of PKA inhibitors (2.0 ± 0.7). Values are presented as the mean ± S.E. and the autoradiographs are representative immunoblots of n = 3–5 independent UROtsa cell treatments.

Back to article page