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Increased apoptosis rate of human decidual cells and cytotrophoblasts in patients with recurrent spontaneous abortion as a result of abnormal expression of CDKN1A and Bax

  • Authors:
    • Xiaomei Lv
    • Zhenhong Cai
    • Su Li
  • View Affiliations / Copyright

    Affiliations: Department of Obstetrics and Gynecology, Jinan Central Hospital Affiliated to Shandong University, Jinan, Shangdong 250014, P.R. China
    Copyright: © Lv et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 2865-2868
    |
    Published online on: September 9, 2016
       https://doi.org/10.3892/etm.2016.3692
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Abstract

In the present study, we analyzed the proliferation and apoptosis of trophoblasts and human decidual cells in patients with recurrent spontaneous abortion and the related cellular pathway mechanism. Thirty-four patients with recurrent abortion and 30 healthy pregnant women undergoing planned artificial abortion were selected. The trophoblast and decidual cells were collected by negative pressure aspiration technique. TUNEL method was used to detect the apoptosis rate. Immunohistochemical method was used for detection of TP53 protein. Quantitative real-time PCR was used for detection of the relative expression level of CDKN1A and Bax mRNA. It was found that the cell apoptosis rate in the recurrent miscarriage group was significantly increased and the expression levels of TP53 protein, CDKN1A and Bax mRNA were also significantly increased (p<0.05). In conclusion, the trophoblast and decidual cells of patients with recurrent abortion were obviously apoptotic, which was probably related to abnormal expression of the CDKN1A and Bax genes mediated by TP53 protein through cellular pathways.
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Copy and paste a formatted citation
Spandidos Publications style
Lv X, Cai Z and Li S: Increased apoptosis rate of human decidual cells and cytotrophoblasts in patients with recurrent spontaneous abortion as a result of abnormal expression of CDKN1A and Bax. Exp Ther Med 12: 2865-2868, 2016.
APA
Lv, X., Cai, Z., & Li, S. (2016). Increased apoptosis rate of human decidual cells and cytotrophoblasts in patients with recurrent spontaneous abortion as a result of abnormal expression of CDKN1A and Bax. Experimental and Therapeutic Medicine, 12, 2865-2868. https://doi.org/10.3892/etm.2016.3692
MLA
Lv, X., Cai, Z., Li, S."Increased apoptosis rate of human decidual cells and cytotrophoblasts in patients with recurrent spontaneous abortion as a result of abnormal expression of CDKN1A and Bax". Experimental and Therapeutic Medicine 12.5 (2016): 2865-2868.
Chicago
Lv, X., Cai, Z., Li, S."Increased apoptosis rate of human decidual cells and cytotrophoblasts in patients with recurrent spontaneous abortion as a result of abnormal expression of CDKN1A and Bax". Experimental and Therapeutic Medicine 12, no. 5 (2016): 2865-2868. https://doi.org/10.3892/etm.2016.3692
Copy and paste a formatted citation
x
Spandidos Publications style
Lv X, Cai Z and Li S: Increased apoptosis rate of human decidual cells and cytotrophoblasts in patients with recurrent spontaneous abortion as a result of abnormal expression of CDKN1A and Bax. Exp Ther Med 12: 2865-2868, 2016.
APA
Lv, X., Cai, Z., & Li, S. (2016). Increased apoptosis rate of human decidual cells and cytotrophoblasts in patients with recurrent spontaneous abortion as a result of abnormal expression of CDKN1A and Bax. Experimental and Therapeutic Medicine, 12, 2865-2868. https://doi.org/10.3892/etm.2016.3692
MLA
Lv, X., Cai, Z., Li, S."Increased apoptosis rate of human decidual cells and cytotrophoblasts in patients with recurrent spontaneous abortion as a result of abnormal expression of CDKN1A and Bax". Experimental and Therapeutic Medicine 12.5 (2016): 2865-2868.
Chicago
Lv, X., Cai, Z., Li, S."Increased apoptosis rate of human decidual cells and cytotrophoblasts in patients with recurrent spontaneous abortion as a result of abnormal expression of CDKN1A and Bax". Experimental and Therapeutic Medicine 12, no. 5 (2016): 2865-2868. https://doi.org/10.3892/etm.2016.3692
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