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Intracellular alkalinization in dexamethasone-induced thymocyte apoptosis
1Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan, Republic of China. hylei@mail.nuku.edu.tw
Apoptosis : an International Journal on Programmed Cell Death
|January 1, 1997
Summary
Glucocorticoids like dexamethasone trigger thymocyte apoptosis, a process linked to increased intracellular pH. Inhibiting this pH rise can slow down programmed cell death in these immune cells.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Glucocorticoids are known to induce thymocyte apoptosis.
- The precise molecular mechanisms underlying this process remain incompletely understood.
Purpose of the Study:
- To investigate the role of intracellular pH in dexamethasone-induced thymocyte apoptosis.
- To elucidate the signaling pathways involved in glucocorticoid-mediated cell death.
Main Methods:
- Assessing apoptosis rates under varying NaCl concentrations and pH levels.
- Measuring intracellular pH (pHi) in thymocytes.
- Utilizing inhibitors of the Na+/H+ antiporter, glucocorticoid receptor, and protein/RNA synthesis.
Main Results:
- Dexamethasone-induced apoptosis correlated with intracellular alkalinization (increased pHi).
- Apoptosis was modulated by extracellular NaCl concentration and medium pH.
- Inhibitors of the Na+/H+ antiporter (5-(N,N'-dimethyl)-amiloride), glucocorticoid receptor (RU486), and protein/RNA synthesis (cycloheximide, actinomycin D) all attenuated dexamethasone's effects.
- Pre-apoptotic thymocytes exhibited higher pHi compared to non-apoptotic cells.
Conclusions:
- Intracellular pH elevation is a key event in dexamethasone-induced thymocyte apoptosis.
- Modulating intracellular pH offers a potential strategy to control glucocorticoid-induced cell death.