Deregulation of the cyclin-dependent kinase inhibitor p27 as a putative candidate for transformation in <i>Chlamydia trachomatis</i> infected mesenchymal stem cells

Mohammad A. Abu-Lubad; Wael Al-Zereini; Munir A. Al-Zeer; Mohammad A. Abu-Lubad; Wael Al-Zereini; Munir A. Al-Zeer

doi:10.3934/microbiol.2023009

AIMS Microbiology

2023, Volume 9, Issue 1: 131-150. doi: 10.3934/microbiol.2023009

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Research article

Deregulation of the cyclin-dependent kinase inhibitor p27 as a putative candidate for transformation in Chlamydia trachomatis infected mesenchymal stem cells

1.
Department of Medical Microbiology and Pathology, Faculty of Medicine, Mutah University, Al-Karak, Jordan
2.
Biological Sciences Department, Faculty of Science, Mutah University, Al-Karak, Jordan
3.
Department of Applied Biochemistry, Institute of Biotechnology, Technical University of Berlin, Berlin, Germany
4.
Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany

Received: 30 August 2022 Revised: 05 February 2023 Accepted: 19 February 2023 Published: 28 February 2023

Purpose
Several pathological conditions might cause the degradation of the cyclin-dependent kinase inhibitor (CKI) p27 and cell cycle arrest at the G1 phase, including cancers and infections. Chlamydia trachomatis (Ctr), as an obligatory intracellular pathogen, has been found to alter the fate of the cell from different aspects. In this study, we aimed to investigate the effect of Ctr infection on the expression of the important cell cycle regularity protein p27 in mesenchymal stem cells (MSCs).
Methods
Isolation of MSCs from healthy human fallopian tube was confirmed by detection of the stemness markers Sox2, Nanog and Oct4 and the surface markers CD44, CD73 and CD90 by Western blotting and fluorescence-activated cell sorting analysis. The expression of p27 was downregulated at the protein level upon Ctr D infection measured by Real-Time Quantitative Reverse Transcription PCR (qRT-PCR), IF and Western blotting. Recovery of p27 in Ctr D-infected MSCs was achieved by treatment with difluoromethylornithine (DFMO). Ctr D infected MSCs were able to produce colonies in anchorage-independent soft agar assay.
Conclusion
Ctr D infection was able to downregulate the expression of the important cell cycle regulator protein p27, which will be considered a putative candidate for transformation in Ctr D infected MSCs.
- p27,
- cell cycle arrest,
- cellular transformation,
- Chlamydia trachomatis,
- mesenchymal stem cells
Citation: Mohammad A. Abu-Lubad, Wael Al-Zereini, Munir A. Al-Zeer. Deregulation of the cyclin-dependent kinase inhibitor p27 as a putative candidate for transformation in Chlamydia trachomatis infected mesenchymal stem cells[J]. AIMS Microbiology, 2023, 9(1): 131-150. doi: 10.3934/microbiol.2023009

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Abstract

Purpose

Several pathological conditions might cause the degradation of the cyclin-dependent kinase inhibitor (CKI) p27 and cell cycle arrest at the G1 phase, including cancers and infections. Chlamydia trachomatis (Ctr), as an obligatory intracellular pathogen, has been found to alter the fate of the cell from different aspects. In this study, we aimed to investigate the effect of Ctr infection on the expression of the important cell cycle regularity protein p27 in mesenchymal stem cells (MSCs).

Methods

Isolation of MSCs from healthy human fallopian tube was confirmed by detection of the stemness markers Sox2, Nanog and Oct4 and the surface markers CD44, CD73 and CD90 by Western blotting and fluorescence-activated cell sorting analysis. The expression of p27 was downregulated at the protein level upon Ctr D infection measured by Real-Time Quantitative Reverse Transcription PCR (qRT-PCR), IF and Western blotting. Recovery of p27 in Ctr D-infected MSCs was achieved by treatment with difluoromethylornithine (DFMO). Ctr D infected MSCs were able to produce colonies in anchorage-independent soft agar assay.

Conclusion

Ctr D infection was able to downregulate the expression of the important cell cycle regulator protein p27, which will be considered a putative candidate for transformation in Ctr D infected MSCs.

Acknowledgments

The authors would like to thank Prof. Thomas F. Meyer, Max Planck Institute for Infection Biology, for his support to carry out the analysis in his lab.

Funding

The authors have no relevant financial or non-financial interests to disclose.

Conflict of interest

The authors declare that there are no conflicts of interest.

Data availability

The datasets generated during and/or analyzed during the current study are not publicly available but are available from the corresponding author on reasonable request.

Ethics approval

This project was conducted with approval from the Ethics Committee according to the Max Planck local institutional ethical considerations and guidelines that are in agreement with the Declaration of Helsinki.

Author contributions

All authors contributed to the study conception and design. Material preparation, data collection and analysis were performed by Mohammad A. Abu-Lubad and Munir A. Al-Zeer. The first draft of the manuscript was written by Mohammad A. Abu-Lubad, and all authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.

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