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Updated: Aug 6, 2026
13:42
Multi-parameter Measurement of the Permeability Transition Pore Opening in Isolated Mouse Heart Mitochondria
Published on: September 7, 2012
Modulation of mitochondrial transition pore components by thyroid hormone
Einav Yehuda-Shnaidman1, Bella Kalderon, Jacob Bar-Tana
1Department of Human Nutrition and Metabolism, Hebrew University Medical School, Jerusalem 91120, Israel.
Endocrinology
|February 5, 2005
Summary
Thyroid hormone (T3) uncouples mitochondria via low-conductance pore opening. This process involves changes in Bax-Bcl2 family proteins, affecting metabolic efficiency.
Area of Science:
- Biochemistry
- Cell Biology
- Endocrinology
Background:
- Thyroid hormone (TH) regulates metabolic efficiency by influencing mitochondrial oxidative phosphorylation.
- The precise mechanism of TH-induced mitochondrial uncoupling remains unclear.
Purpose of the Study:
- To elucidate the role of the mitochondrial transition pore (MTP) in TH-induced mitochondrial uncoupling.
- To investigate the involvement of MTP protein components, particularly the Bax-Bcl2 family, in T3's effects.
Main Methods:
- Treatment of Jurkat and GH3 cells with T3.
- Assessment of mitochondrial depolarization and MTP component expression.
- Analysis of protein levels (Bax, Bak, Bcl2) in mitochondria.
- Functional studies involving Bcl2 overexpression.
Main Results:
- T3 treatment induced Cyclosporin A-sensitive mitochondrial depolarization in cells.
- T3 increased mitochondrial Bax and Bak while decreasing Bcl2.
- Overexpression of Bcl2 inhibited T3-induced mitochondrial depolarization.
- Certain MTP components (e.g., VDAC, CypD) were not involved in T3-mediated MTP gating.
Conclusions:
- TH-induced mitochondrial uncoupling is mediated by low-conductance MTP gating.
- This gating is regulated by T3-induced alterations in the balance of mitochondrial proapoptotic (Bax, Bak) and antiapoptotic (Bcl2) proteins.
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