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The Cyclin Dependent Kinase Inhibitor Protein 21 Cytoplasmic Expression Depressing the Apoptosis of Human Bronchial Epithelial Cell

Received: 15 June 2019    Accepted: 10 December 2019    Published: 8 January 2020
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Abstract

AIMS: To investigate the cytoplasmic P21 expression regulating the apoptosis of human bronchial epithelial cell. MOTHEDS: The relationship of the cytoplasmic P21 expression with the apoptosis of 16HBE cells was studied after the plasmid pEGFP-N1-P21 was transfected into the 16HBE cells. After the 16HBE cells was the stimulated by the TGF-β1, the cytoplasmic and nucleic P21 expression and the apoptosis of 16HBE cell was detected, then the relationship of the P21 expression with the apoptosis of 16HBE cells was studied. RESULTS: The 16HBE cell had the basic low cytoplasmic and mainly high nucleic P21 protein expression, the plasmid PEGFP-N1-P21 could express P21 protein only in the cytoplasm of 16HBE cell and did not affect the nucleic P21 protein level. The apoptosis of 16HBE cells after transfection of the PEGFP-N1-P21 decreased. The apoptosis of 16HBE cells decreased as the time of the PEGFP-N1-P21 transfection increased, but the apoptosis of 16HBE cells increased without the PEGFP-N1-P21 transfection. The stimulation by TGF-β1 led to the expression of the cytoplasmic and nucleic P21 proteins, but mainly the cytoplasmic P21 protein expression, as the stimulation concentration of TGF-β1 increased, the cytoplasmic P21 expression decreased, but the nucleic P21 did not change. The apoptosis of 16HBE cells increased as the cytoplasmic P21 expression decreased after the concentration of TGF-β1 stimulation increased. CONCLUSIONS: The apoptosis of 16HBE cell was inhibited by the high cytoplasmic P21 expression through the transfection of PEGFP-N1-P21. TGF-β1 stimulation promoted the apoptosis of 16HBE cell by inhibiting the cytoplasmic P21 expression. The cytoplasmic P21 expression depresses the apoptosis of 16HBE cells.

Published in International Journal of Clinical and Developmental Anatomy (Volume 6, Issue 1)
DOI 10.11648/j.ijcda.20200601.12
Page(s) 1-7
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This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Cyclin Dependent Kinase Inhibitor P21, Transforming Growth Factor-β1, Apoptosis

References
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[2] Daisuke Arai, Norihiro Nomura, Kunihiko Fukuchi et al. Cytoplasmic localization of cyclin kinase inhibitor p21 delays the progression of apoptosis [J]. Cancer Genomics & Proteomics, 2006, 3, 29-38.
[3] Katsuyuki Tomita, Gaetano Caramori, Sam Lim, et al. Increased p21cip1/waf1 and b cell lymphoma leukemia-x1 expression and reduced apoptosis in alveolar macrophages from smokers [J]. American Journal of Respiratory and Critical Care Medicine, 2002, 166, 724-731.
[4] AraiD., Nomura N., Fukuchi K., et al. Cytoplasmic localization of cyclin kinase inhibitor p21 delays the progression of apoptosis [J]. Cancer Genomics & Proteomics, 2006, 3, 29-38.
[5] Puddicombe S. M., Carlos T. L., Richter A. Increased expression of p21waf cyclin-dependent kinase inhibitor in asthmatic bronchial epithelium [J]. American Journal of Respiratory Cell and Molecular Biology. 2003, 28, 61-68.
[6] Blobe GC, Schiemann WP, Lodish HF. Role of transforming growth factor beta in human disease. N Engl J Med 2000, 342, 1350–1358.
[7] Yamasaki M., Kang HR, Homer R. J., et al. p21 regulates TGF-β1–induced pulmonary responses via a TNF–αsignaling pathway [J]. American Journal of Respiratory Cell and Molecular Biology, 2008, 38, 346-353.
[8] Gartel, A. L.; Tyner, A. L. The role of the cyclin-dependent kinase inhibitor P21 in apoptosis. Mol. Cancer Ther [J]. 2002, 1, 639–649.
[9] Gartel, A. L. The conflicting roles of the cdk inhibitor p21 (CIP1/WAF1) in apoptosis [J]. Leuk. Res. 2005, 29, 1237–1238.
[10] Asada M, Yamada T, Ichijol H, et al. The role of P21 in apoptosis, proliferation, cell arrest and antioxidant activity in URB-irradiated human HacaT keratinocytes [J]. Med SCI Monit Basic Rec, 2015, 21, 86-95.
[11] Karimian A, Ahmadi Y, Yousefi B. Multiple functions of p21 in cell cycle, apoptosis and transcriptional regulation after DNA damage [J]. DNA Repair, 2016, 42, 63-71.
[12] Huang YF, Wang WM, Chen YS, et al. The opposite prognostic significance of nuclear and cytoplasmic p21 expression in resectable gastric cancer patients. J Gastroenterol [J], 2014, 49, 1441-52.
[13] Dai M, Al-Odaini AA, Arakelian, A, et al. A novel function for p21Cip1 and acetyltransferase p/CAF as critical transcriptional regulators of TGFbeta-mediated breast cancer cell migration and invasion. Breast Cancer Res [J], 2012, 14, R127.
[14] Dai M, Al-Odaini AA, Fils-Aime N, et al. Cyclin D1 cooperates with p21 to regulate TGFbeta-mediated breast cancer cell migration and tumor local invasion. Breast Cancer Res [J]. 2013, 15, R49.
[15] Qian X, Hulit J, Suyama K, et al. p21CIP1 mediates reciprocal switching between proliferation and invasion during metastasis [J]. Oncogene 2013, 32, 2292–2303.
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  • APA Style

    Zou Guoming, Xiao Zuke. (2020). The Cyclin Dependent Kinase Inhibitor Protein 21 Cytoplasmic Expression Depressing the Apoptosis of Human Bronchial Epithelial Cell. International Journal of Clinical and Developmental Anatomy, 6(1), 1-7. https://doi.org/10.11648/j.ijcda.20200601.12

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    ACS Style

    Zou Guoming; Xiao Zuke. The Cyclin Dependent Kinase Inhibitor Protein 21 Cytoplasmic Expression Depressing the Apoptosis of Human Bronchial Epithelial Cell. Int. J. Clin. Dev. Anat. 2020, 6(1), 1-7. doi: 10.11648/j.ijcda.20200601.12

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    AMA Style

    Zou Guoming, Xiao Zuke. The Cyclin Dependent Kinase Inhibitor Protein 21 Cytoplasmic Expression Depressing the Apoptosis of Human Bronchial Epithelial Cell. Int J Clin Dev Anat. 2020;6(1):1-7. doi: 10.11648/j.ijcda.20200601.12

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  • @article{10.11648/j.ijcda.20200601.12,
      author = {Zou Guoming and Xiao Zuke},
      title = {The Cyclin Dependent Kinase Inhibitor Protein 21 Cytoplasmic Expression Depressing the Apoptosis of Human Bronchial Epithelial Cell},
      journal = {International Journal of Clinical and Developmental Anatomy},
      volume = {6},
      number = {1},
      pages = {1-7},
      doi = {10.11648/j.ijcda.20200601.12},
      url = {https://doi.org/10.11648/j.ijcda.20200601.12},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ijcda.20200601.12},
      abstract = {AIMS: To investigate the cytoplasmic P21 expression regulating the apoptosis of human bronchial epithelial cell. MOTHEDS: The relationship of the cytoplasmic P21 expression with the apoptosis of 16HBE cells was studied after the plasmid pEGFP-N1-P21 was transfected into the 16HBE cells. After the 16HBE cells was the stimulated by the TGF-β1, the cytoplasmic and nucleic P21 expression and the apoptosis of 16HBE cell was detected, then the relationship of the P21 expression with the apoptosis of 16HBE cells was studied. RESULTS: The 16HBE cell had the basic low cytoplasmic and mainly high nucleic P21 protein expression, the plasmid PEGFP-N1-P21 could express P21 protein only in the cytoplasm of 16HBE cell and did not affect the nucleic P21 protein level. The apoptosis of 16HBE cells after transfection of the PEGFP-N1-P21 decreased. The apoptosis of 16HBE cells decreased as the time of the PEGFP-N1-P21 transfection increased, but the apoptosis of 16HBE cells increased without the PEGFP-N1-P21 transfection. The stimulation by TGF-β1 led to the expression of the cytoplasmic and nucleic P21 proteins, but mainly the cytoplasmic P21 protein expression, as the stimulation concentration of TGF-β1 increased, the cytoplasmic P21 expression decreased, but the nucleic P21 did not change. The apoptosis of 16HBE cells increased as the cytoplasmic P21 expression decreased after the concentration of TGF-β1 stimulation increased. CONCLUSIONS: The apoptosis of 16HBE cell was inhibited by the high cytoplasmic P21 expression through the transfection of PEGFP-N1-P21. TGF-β1 stimulation promoted the apoptosis of 16HBE cell by inhibiting the cytoplasmic P21 expression. The cytoplasmic P21 expression depresses the apoptosis of 16HBE cells.},
     year = {2020}
    }
    

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  • TY  - JOUR
    T1  - The Cyclin Dependent Kinase Inhibitor Protein 21 Cytoplasmic Expression Depressing the Apoptosis of Human Bronchial Epithelial Cell
    AU  - Zou Guoming
    AU  - Xiao Zuke
    Y1  - 2020/01/08
    PY  - 2020
    N1  - https://doi.org/10.11648/j.ijcda.20200601.12
    DO  - 10.11648/j.ijcda.20200601.12
    T2  - International Journal of Clinical and Developmental Anatomy
    JF  - International Journal of Clinical and Developmental Anatomy
    JO  - International Journal of Clinical and Developmental Anatomy
    SP  - 1
    EP  - 7
    PB  - Science Publishing Group
    SN  - 2469-8008
    UR  - https://doi.org/10.11648/j.ijcda.20200601.12
    AB  - AIMS: To investigate the cytoplasmic P21 expression regulating the apoptosis of human bronchial epithelial cell. MOTHEDS: The relationship of the cytoplasmic P21 expression with the apoptosis of 16HBE cells was studied after the plasmid pEGFP-N1-P21 was transfected into the 16HBE cells. After the 16HBE cells was the stimulated by the TGF-β1, the cytoplasmic and nucleic P21 expression and the apoptosis of 16HBE cell was detected, then the relationship of the P21 expression with the apoptosis of 16HBE cells was studied. RESULTS: The 16HBE cell had the basic low cytoplasmic and mainly high nucleic P21 protein expression, the plasmid PEGFP-N1-P21 could express P21 protein only in the cytoplasm of 16HBE cell and did not affect the nucleic P21 protein level. The apoptosis of 16HBE cells after transfection of the PEGFP-N1-P21 decreased. The apoptosis of 16HBE cells decreased as the time of the PEGFP-N1-P21 transfection increased, but the apoptosis of 16HBE cells increased without the PEGFP-N1-P21 transfection. The stimulation by TGF-β1 led to the expression of the cytoplasmic and nucleic P21 proteins, but mainly the cytoplasmic P21 protein expression, as the stimulation concentration of TGF-β1 increased, the cytoplasmic P21 expression decreased, but the nucleic P21 did not change. The apoptosis of 16HBE cells increased as the cytoplasmic P21 expression decreased after the concentration of TGF-β1 stimulation increased. CONCLUSIONS: The apoptosis of 16HBE cell was inhibited by the high cytoplasmic P21 expression through the transfection of PEGFP-N1-P21. TGF-β1 stimulation promoted the apoptosis of 16HBE cell by inhibiting the cytoplasmic P21 expression. The cytoplasmic P21 expression depresses the apoptosis of 16HBE cells.
    VL  - 6
    IS  - 1
    ER  - 

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Author Information
  • Respiratory and Critical Medical Department, Jiangxi Provincial People's Hospital, Nanchang, China

  • Respiratory and Critical Medical Department, Jiangxi Provincial People's Hospital, Nanchang, China

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