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Are Aminoglycoside Antibiotics TRPing Your Metabolic Switches?
Alfredo Franco-Obregón1,2,3,4,5,6, Yee Kit Tai1,2,3,4
1Department of Surgery, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119228, Singapore.
Abstract:
Transient receptor potential (TRP) channels are broadly implicated in the developmental programs of most tissues. Amongst these tissues, skeletal muscle and adipose are noteworthy for being essential in establishing systemic metabolic balance. TRP channels respond to environmental stimuli by supplying intracellular calcium that instigates enzymatic cascades of developmental consequence and often impinge on mitochondrial function and biogenesis. Critically, aminoglycoside antibiotics (AGAs) have been shown to block the capacity of TRP channels to conduct calcium entry into the cell in response to a wide range of developmental stimuli of a biophysical nature, including mechanical, electromagnetic, thermal, and chemical. Paradoxically, in vitro paradigms commonly used to understand organismal muscle and adipose development may have been led astray by the conventional use of streptomycin, an AGA, to help prevent bacterial contamination. Accordingly, streptomycin has been shown to disrupt both in vitro and in vivo myogenesis, as well as the phenotypic switch of white adipose into beige thermogenic status. In vivo, streptomycin has been shown to disrupt TRP-mediated calcium-dependent exercise adaptations of importance to systemic metabolism. Alternatively, streptomycin has also been used to curb detrimental levels of calcium leakage into dystrophic skeletal muscle through aberrantly gated TRPC1 channels that have been shown to be involved in the etiology of X-linked muscular dystrophies. TRP channels susceptible to AGA antagonism are critically involved in modulating the development of muscle and adipose tissues that, if administered to behaving animals, may translate to systemwide metabolic disruption. Regenerative medicine and clinical communities need to be made aware of this caveat of AGA usage and seek viable alternatives, to prevent contamination or infection in in vitro and in vivo paradigms, respectively.
Insights
Aminoglycoside antibiotics disrupt calcium signaling in Transient Receptor Potential (TRP) channels, affecting muscle and adipose tissue development. Researchers must consider this when using these antibiotics in studies.
Area of Science:
- Cellular Biology
- Metabolic Research
- Pharmacology
Background:
- Transient Receptor Potential (TRP) channels regulate calcium influx crucial for skeletal muscle and adipose tissue development and systemic metabolic balance.
- Aminoglycoside antibiotics (AGAs) are known to block calcium conduction through TRP channels in response to various stimuli.
- The common use of streptomycin, an AGA, for bacterial contamination in cell cultures may confound research findings.
Purpose of the Study:
- To investigate the impact of aminoglycoside antibiotics (AGAs) on TRP channel function and its consequences for muscle and adipose tissue development.
- To highlight the paradoxical effects of streptomycin, an AGA, on myogenesis and adipose tissue thermogenesis.
- To alert the scientific community about the potential for AGAs to disrupt TRP-mediated calcium signaling and systemic metabolism.
Main Methods:
- Review of existing literature on TRP channel function, AGA mechanisms, and their effects on cellular development.
- Analysis of studies investigating streptomycin's impact on myogenesis, adipogenesis, and in vivo metabolic adaptations.
- Examination of streptomycin's role in managing calcium leakage in dystrophic muscle models.
Main Results:
- AGAs, specifically streptomycin, disrupt TRP channel-mediated calcium entry, interfering with myogenesis and the white-to-beige adipose tissue switch.
- In vivo, streptomycin impairs TRP-dependent, calcium-mediated exercise adaptations vital for metabolism.
- Streptomycin has been used to mitigate detrimental calcium leakage in dystrophic skeletal muscle via TRPC1 channels.
Conclusions:
- TRP channels antagonized by AGAs are critical for muscle and adipose tissue development and systemic metabolism.
- The administration of AGAs in experimental models can lead to widespread metabolic disruption.
- The regenerative medicine and clinical communities should be aware of this significant caveat and seek alternative methods for contamination prevention.
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