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Doxycycline Protects Thymic Epithelial Cells from Mitomycin C-Mediated Apoptosis in Vitro Via Trx2-Nf-Κb-Bcl-2/Bax Axis
SUNLONG BIOTECH / 2024-01-09
  • Author:Wang, J., Zhuo, Y., Yin, L., Wang, H., Jiang, Y., Liu, X., Zhang, M., Du, F., Xia, S. & Shao, Q.

  • Periodical:Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 38, 449-460 (2016)

  • Article source

BACKGROUND/AIMS: Age-associated and stress-induced involution of the thymus is accompanied by reduced numbers of thymic epithelial cells (TECs) and severe reduction in peripheral T cell repertoire specificities. These events seriously affect immune function, but the mechanisms involved are unclear. Our preliminary findings showed that doxycycline (Dox) could drive the proliferation of a TEC line (MTEC1 cells) partially via the MAPK signaling pathway. Dox can also up-regulate IL-6 and GM-CSF expression via the NF-κB and MAPK/ERK pathways. Herein, we investigate the effects and mechanisms used by Dox that protect against mitomycin C (MMC)-induced MTEC1 cell apoptosis. METHODS: MTEC1 cells were treated with Dox, MMC, and Dox plus MMC for different amounts of time. The expression of Trx2, NF-κB, Bcl-2, and Bax proteins were then detected by western blotting. RESULTS: Our findings show that Dox protects MTEC1 cells from MMC-induced apoptosis. Dox up-regulated the expression of Trx2 and promoted NF-κB phosphorylation. Meanwhile, Dox also increased the expression of Bcl-2, partially reduced the expression of Bax, and normalized the ratio of Bcl-2 to Bax. CONCLUSION: Dox exerts an anti-apoptosis function via the NF-κB-Bcl-2/Bax and Trx2-ASK1/JNK pathways in vitro. Therefore, Dox may represent a drug that could be used to attenuate thymic senescence, rescue thymic function, and promote T cell reconstitution.

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