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Transcriptional Co-Activator With PDZ Binding Motif (TAZ) Inhibits Dexamethasone-Induced Muscle Atrophy via mTOR

Kyung Min Kim¹, Ho Taek Oh¹, Youjin Do¹

¹Division of Life Sciences, Korea University, Seoul, South Korea.

Journal of Cachexia, Sarcopenia and Muscle

|March 31, 2025

Abstract

Background:

Glucocorticoid therapy has a beneficial effect in several diseases, but chronic treatment has adverse effects, including muscle atrophy, which refers to the gradual decrease in muscle mass, size and strength. It is important to know how the muscle atrophy occurs, but the underlying mechanism is not yet fully understood. This study shows that dexamethasone decreases levels of the transcriptional co-activator with PDZ binding motif (TAZ), which facilitates dexamethasone-induced muscle atrophy.

Methods:

To induce muscle atrophy, C2C12 myotubes were treated with dexamethasone, and mice were fed with water containing dexamethasone. Muscle atrophy was analysed for the expression of myosin heavy chain, MuRF1 and Atrogin-1 using immunofluorescence staining, immunoblot analysis and qRT-PCR. Muscle tissue was analysed by haematoxylin and eosin staining. Adeno-associated virus was used for overexpression of wild-type and mutant TAZ.

Results:

TAZ levels decrease in dexamethasone-treated mice (0.36-fold, p < 0.001) and C2C12 myotubes (0.44-fold, p = 0.024). Overexpression of the TAZ mutant, which resists its proteolytic degradation, inhibits dexamethasone-induced muscle atrophy. Atrogin-1 and MuRF1 interact with TAZ and facilitate its degradation in dexamethasone-treated C2C12 myotubes. TAZ mutant stimulates protein synthesis through activation of mTOR signalling via induction of RhebL1 (DEX; Con vs, TAZ4SA: 5.1-fold, p < 0.001) in dexamethasone-treated mice. Ginsenoside Rb3 increases TAZ levels in dexamethasone-treated mice (1.49-fold, p = 0.007) and C2C12 myotubes (1.63-fold, p = 0.01), which stimulates mTOR signalling and inhibits dexamethasone-induced muscle atrophy.

Conclusions:

Our results demonstrate a novel regulatory mechanism of dexamethasone-induced muscle atrophy by TAZ, suggesting that stabilisation of TAZ in muscle cells ameliorates the muscle atrophy. These results suggest that TAZ may be a drug target for the dexamethasone-induced muscle atrophy.

Insights

Dexamethasone causes muscle atrophy by decreasing TAZ levels. Stabilizing TAZ or using Ginsenoside Rb3 can prevent this, suggesting TAZ as a drug target for muscle wasting.

Area of Science:

Biochemistry
Molecular Biology
Physiology

Background:

Glucocorticoid therapy, while beneficial, can cause muscle atrophy (loss of muscle mass, size, and strength).
The precise mechanisms underlying dexamethasone-induced muscle atrophy are not fully understood.
This study investigates the role of the transcriptional co-activator with PDZ binding motif (TAZ) in this process.

Purpose of the Study:

To elucidate the mechanism of dexamethasone-induced muscle atrophy.
To determine the role of TAZ in dexamethasone-induced muscle atrophy.
To explore potential therapeutic strategies targeting TAZ.

Main Methods:

Muscle atrophy was induced in C2C12 myotubes and mice using dexamethasone.
TAZ levels were analyzed using immunofluorescence, immunoblotting, and qRT-PCR.
Adeno-associated virus was used for TAZ overexpression, and protein-protein interactions were studied.

Main Results:

Dexamethasone treatment significantly decreased TAZ levels in both cell cultures and mice.
Overexpression of a TAZ mutant resistant to degradation inhibited dexamethasone-induced muscle atrophy.
Atrogin-1 and MuRF1 were found to interact with and degrade TAZ.
Ginsenoside Rb3 treatment increased TAZ levels, stimulated mTOR signaling, and inhibited muscle atrophy.

Conclusions:

TAZ plays a critical role in regulating dexamethasone-induced muscle atrophy.
Stabilizing TAZ in muscle cells can ameliorate muscle atrophy.
TAZ represents a potential therapeutic target for treating dexamethasone-induced muscle atrophy.

Read full analysis

Keywords:

dexamethasone ginsenoside mTOR muscle atrophy

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