Effects of Salmeterol on Skeletal Muscle Cells

Duranti, Guglielmo; Rosa, Piergiorgio La; Dimauro, Ivan; Wannenes, Francesca; Бонини, С.; Sabatini, Stefania; Parisi, Paolo; Caporossi, Daniela

doi:10.1249/mss.0b013e3182223094

Cited by 12 publications

(8 citation statements)

References 39 publications

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“…For example, in Duranti's study, rat L6C5 and mouse C2C12 skeletal muscle cells were treated with up to 20 μM of the β 2 -adrenergic receptor agonist salmeterol at a concentration of 1 × 10 4 cells per square centimeter, conditions comparable to our AAS experiments (Duranti et al, 2011). Indeed, the initial concentration of cells per square centimeter used in our studies is the minimum required to allow neuron-like cells to create a neurite network.…”

Section: Discussionmentioning

confidence: 54%

“…During this time, cells attached to the substratum and produced a network of neurites. Differentiated PC12 cultures were treated with vehicle (dimethyl ether, DME) or the steroid hormones androsterone, nandrolone, methandienone and 17-α-methyltestosterone (Cerilliant Corporation, Round Rock, Texas) at a concentration of 50–75 μM for times defined as short term (24 h), and long term (48 h) (Duranti et al, 2011), and pre-incubated for 2 h with vehicle control or 10 μM hydroxyflutamide (Sigma-Aldrich, St. Louis, MO) (Nguyen et al, 2007) where indicated. Preliminary experiments verified that DME did not have any effects compared to an evaluation of untreated cells (data not shown).…”

Section: Methodsmentioning

confidence: 99%

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Supraphysiological doses of performance enhancing anabolic-androgenic steroids exert direct toxic effects on neuron-like cells

Basile¹,

Binmadi²,

Zhou³

et al. 2013

Front. Cell. Neurosci.

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Anabolic-androgenic steroids (AAS) are lipophilic hormones often taken in excessive quantities by athletes and bodybuilders to enhance performance and increase muscle mass. AAS exert well known toxic effects on specific cell and tissue types and organ systems. The attention that androgen abuse has received lately should be used as an opportunity to educate both athletes and the general population regarding their adverse effects. Among numerous commercially available steroid hormones, very few have been specifically tested for direct neurotoxicity. We evaluated the effects of supraphysiological doses of methandienone and 17-α-methyltestosterone on sympathetic-like neuron cells. Vitality and apoptotic effects were analyzed, and immunofluorescence staining and western blot performed. In this study, we demonstrate that exposure of supraphysiological doses of methandienone and 17-α-methyltestosterone are toxic to the neuron-like differentiated pheochromocytoma cell line PC12, as confirmed by toxicity on neurite networks responding to nerve growth factor and the modulation of the survival and apoptosis-related proteins ERK, caspase-3, poly (ADP-ribose) polymerase and heat-shock protein 90. We observe, in contrast to some previous reports but in accordance with others, expression of the androgen receptor (AR) in neuron-like cells, which when inhibited mitigated the toxic effects of AAS tested, suggesting that the AR could be binding these steroid hormones to induce genomic effects. We also note elevated transcription of neuritin in treated cells, a neurotropic factor likely expressed in an attempt to resist neurotoxicity. Taken together, these results demonstrate that supraphysiological exposure to the AAS methandienone and 17-α-methyltestosterone exert neurotoxic effects by an increase in the activity of the intrinsic apoptotic pathway and alterations in neurite networks.

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Section: Discussionmentioning

confidence: 54%

Section: Methodsmentioning

confidence: 99%

Supraphysiological doses of performance enhancing anabolic-androgenic steroids exert direct toxic effects on neuron-like cells

Basile¹,

Binmadi²,

Zhou³

et al. 2013

Front. Cell. Neurosci.

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“…β 2 -adrenergic receptors are certainly found in abundance in extrafusal muscle where they mediate diverse functions including: metabolic regulation [46]; myocyte hypertrophy [47]; and repair [48]. These actions occur over a protracted time course and are therefore unlikely to be responsible for salbutamol's rapid effects on tremor.…”

Section: Discussionmentioning

confidence: 99%

Beta-Adrenergic Modulation of Tremor and Corticomuscular Coherence in Humans

Baker

2012

PLoS ONE

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Coherence between the bioelectric activity of sensorimotor cortex and contralateral muscles can be observed around 20 Hz. By contrast, physiological tremor has a dominant frequency around 10 Hz. Although tremor has multiple sources, it is partly central in origin, reflecting a component of motoneuron discharge at this frequency. The motoneuron response to ∼20 Hz descending input could be altered by non-linear interactions with ∼10 Hz motoneuron firing. We investigated this further in eight healthy human subjects by testing the effects of the beta-adrenergic agents propranolol (non-selective β-antagonist) and salbutamol (β2-agonist), which are known to alter the size of physiological tremor. Corticomuscular coherence was assessed during an auxotonic precision grip task; tremor was quantified using accelerometry during index finger extension. Experiments with propranolol used a double-blind, placebo-controlled crossover design. A single oral dose of propranolol (40 mg) significantly increased beta band (15.3–32.2 Hz) corticomuscular coherence compared with placebo, but reduced tremor in the 6.2–11.9 Hz range. Salbutamol (2.5 mg) was administered by inhalation. Whilst salbutamol significantly increased tremor amplitude as expected, it did not change corticomuscular coherence. The opposite direction of the effects of propranolol on corticomuscular coherence and tremor, and the fact that salbutamol enhances tremor but does not affect coherence, implies that the magnitude of corticomuscular coherence is little influenced by non-linear interactions with 10 Hz oscillations in motoneurons or the periphery. Instead, we suggest that propranolol and salbutamol may affect both tremor and corticomuscular coherence partly via a central site of action.

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“…In high serum, myoblasts proliferate, while after serum removal, they go into an early differentiation stage. Later, cells begin to fuse, forming multinucleated myotubes positive for the characteristic muscle-specific protein MHC [ 20 , 21 , 22 ].…”

Section: Skeletal Muscle Differentiationmentioning

confidence: 99%

Skeletal Muscle Pathophysiology: The Emerging Role of Spermine Oxidase and Spermidine

et al. 2018

Self Cite

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Skeletal muscle comprises approximately 40% of the total body mass. Preserving muscle health and function is essential for the entire body in order to counteract chronic diseases such as type II diabetes, cardiovascular diseases, and cancer. Prolonged physical inactivity, particularly among the elderly, causes muscle atrophy, a pathological state with adverse outcomes such as poor quality of life, physical disability, and high mortality. In murine skeletal muscle C2C12 cells, increased expression of the spermine oxidase (SMOX) enzyme has been found during cell differentiation. Notably, SMOX overexpression increases muscle fiber size, while SMOX reduction was enough to induce muscle atrophy in multiple murine models. Of note, the SMOX reaction product spermidine appears to be involved in skeletal muscle atrophy/hypertrophy. It is effective in reactivating autophagy, ameliorating the myopathic defects of collagen VI-null mice. Moreover, spermidine treatment, if combined with exercise, can affect D-gal-induced aging-related skeletal muscle atrophy. This review hypothesizes a role for SMOX during skeletal muscle differentiation and outlines its role and that of spermidine in muscle atrophy. The identification of new molecular pathways involved in the maintenance of skeletal muscle health could be beneficial in developing novel therapeutic lead compounds to treat muscle atrophy.

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Effects of Salmeterol on Skeletal Muscle Cells

Cited by 12 publications

References 39 publications

Supraphysiological doses of performance enhancing anabolic-androgenic steroids exert direct toxic effects on neuron-like cells

Supraphysiological doses of performance enhancing anabolic-androgenic steroids exert direct toxic effects on neuron-like cells

Beta-Adrenergic Modulation of Tremor and Corticomuscular Coherence in Humans

Skeletal Muscle Pathophysiology: The Emerging Role of Spermine Oxidase and Spermidine

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