Relationship between uterine smooth muscular CPI-17-signal pathway-mediated Ca2+ sensitivity changes and uterine atony-induced postpartum haemorrhage.

This study aimed to investigate the changes of protein kinase C (PKC)-potentiated phosphatase inhibitor of 17 ku (CPI-17) expression, PKC activity and Rho kinase activity in the maternal uterine smooth muscle (USM), and their roles in the occurrence of uterine atony-induced postpartum haemorrhage (UAI-PPH). Sixty primiparaes who had a caesarean section performed were divided into the case group (with UAI-PPH) and the control group (the uterine contraction was good, without the PPH). The USM-p-CPI-17 (Thr38) protein levels, the activities of PKC and Rho kinase in the case group and the control group were 0.43 ± 0.20, 4.30 ± 0.91, 10.85 ± 1.70 and 0.67 ± 0.32, 0.099 ± 0.028, 0.20 ± 0.071, respectively (p < .05). The down-regulated expression of CPI-17 phosphorylated proteins might be one of the important factors of UAI-PPH, while the activity reduction of PKC and Rho kinase might be the reason that led to the phosphorylation level reduction of USM-CPI-17 in UAI-PPH. Impact Statement What is already known on this subject? The studies have shown that in the late pregnancy period, the total protein and phosphorylated protein of myometrial CPI-17 are significantly higher than in the non-pregnancy state, and they were all involved in regulating and enhancing the Ca2+ sensitivity of USMC during the pregnancy. The data regarding the CPI-17-signal pathway-mediated Ca2+ sensitivity in UAI-PPH is sparse. What do the results of this study add? We have shown that the down-regulated expression of CPI-17 phosphorylated proteins might be one of the important factors of UAI-PPH, while the activity reduction of PKC and Rho kinase might be the reason that led to the phosphorylation level reduction of USM-CPI-17 in UAI-PPH. What are the implications of these findings for clinical practice and/or further research? Further studies are needed to confirm the pathogenesis of CPI-17-signal pathway-mediated Ca2+ sensitivity in UAI-PPH.