[Corrigendum] Roles and mechanisms of TRPC3 and the PLCγ/PKC/CPI-17 signaling pathway in regulating parturition

• Authors:
  • Jing Chen
  • Dongming Zheng
  • Hong Cui
  • Sishi Liu
  • Lijuan Zhang
  • Caixia Liu

• View Affiliations

  
  Affiliations: Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110016, P.R. China
• Published online on: February 7, 2018     https://doi.org/10.3892/mmr.2018.8572
• Pages: 6201-6201

• Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Article

Mol Med Rep 17: [Related article:] 898-910, 2018; DOI: 10.3892/mmr.2017.7998

Subsequent to the publication of the above paper, the authors have realized that there were errors in Fig. 1 on page 902; essentially, the experimental data described as being ‘Preterm’ and ‘Infected preterm’ should have been labelled as ‘Full-term without labor’ and ‘Preterm’, respectively. Note that these errors in Fig. 1 were not reflected in the published figure legend.

Figure 1. Expression levels of TRPC3, Cav1.2, Cav.3.1 and Cav3.2 in human myometrial smooth muscle cells derived from the non-pregnant, full-term without labor onset, preterm, and full-term with labor onset patient groups (n=20/group). (A) Western blot analysis of protein expression levels in the different groups. GAPDH was used as the loading control. Quantified western blot analyses of relative expression levels of (B) TRPC3, (C) Cav1.2, (D) Cav.3.1 and (E) Cav3.2. Data are presented as the mean ±≈standard error. *P<0.05 vs. non-pregnant group. TRPC3, canonical transient receptor potential 3.

The corrected version of Fig. 1 is shown below. The authors sincerely apologize for this mistake, and regret any inconvenience this mistake has caused.