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. 2015 Mar;352(3):509–518. doi: 10.1124/jpet.114.221929

Fig. 7.

Fig. 7.

Increase in PDE1A activity by inflammation. (A) Longitudinal muscle cells isolated from colons of control and TNBS-treated mice or from muscle strips cultured in the presence of IL-1β (10 ng/ml) or TNF-α (1 nM) for 48 hours were used to measure PDE1A activity as described in Materials and Methods. In some experiments, muscle strips were cultured with IL-1β (10 ng/ml) or TNF-α (1 nM) in the presence of NF-κB inhibitor MG132 (10 µM) for 48 hours. Values are the means ± S.E.M. of five experiments. **P < 0.01, significant increase in PDE1A activity compared with control. (B) Longitudinal muscle cells isolated from colons of control and TNBS-treated mice or from muscle strips cultured in the presence of IL-1β (10 ng/ml) or TNF-α (1 nM) for 48 hours were used to measure cGMP-hydrolyzing activity in the presence or absence of PDE1 inhibitor vinpocetine (50 µM). Total cGMP-hydrolyzing activity reflects the activity in the absence of vinpocetine. PDE1A activity was calculated as the percentage of total cGMP-hydrolyzing activity that was inhibited by vinpocetine. Values are the means ± S.E.M. of five experiments. **P < 0.01, significant increase in PDE1A activity compared with control.