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Original Article

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

, , , , , & show all
Pages 302-307 | Published online: 14 Nov 2018
 

Abstract

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.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This work was supported by the Key Clinical Specialty Discipline Construction of Fujian, P.R.C ([2015] no. 593), Fujian Science and Technology Leading Project (2016Y0060), Fujian Medical Innovation Subject (2017-CX-11) and Fujian Science and Technology Leading Project (2018Y0005).

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