Background RhoA/Rho kinase and PKC/CPI17mediated signaling can inhibit myosin phosphatase to induce contraction in smooth muscles. However it is still unclear how the signaling plays an important role to regulate gastrointestinal motility in vivo.
Aim Intestinal and colonic contractile and transit abilities were tested using CPI17 deficient (KO),phospho-inactive mutant CPI17knock in (TA) and wild type mice (WT).
Methods Isometric force and phosphorylation of Myosin light chain (MLC) and CPI17 stimulatedwith Carbochol(Cch)were measured. Transit abilities were observed by FITC dextran and dextran　beads method, respectively.
Results High concentration of KCl induced contractions were no difference among WT, KO and TA of ileal and colonic circular muscles. However the sustained contraction by Cch of ileum and colon in KO and TA were decreased compared with WT. The MLC phosphorylation level was also lower in KO and TA than WT. Ileal transit ability did not change in KO and TA compared with WT.In contrast,colonic transit in KO and TA were significantly delayed compared with WT.
Conclusion CPI17 is important to maintain the sustained contraction of gastrointestinal tract due to receptor stimulation in vitro. In addition, the PKC/CPI17 pathway is more important for maintenance in colon transit ability than ileal part in vivo.