Protection against dexamethasone-induced muscle atrophy is related to modulation by testosterone of FOXO1 and PGC-1α

Qin, Weiping; Pan, Jiangping; Wu, Yong; Bauman, William A.; Cardozo, Christopher P.

doi:10.1016/j.bbrc.2010.11.061

Cited by 66 publications

(63 citation statements)

References 34 publications

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“…The action of androgens on the skeletal muscle involves several pathways of cellular and molecular interaction. Laboratory studies have shown that androgens clearly affect muscular hypertrophy through increasing insulin-like growth factor-1 (IGF-1) expression, controlling forkhead box O (FOXO1), peroxisome proliferator-activated receptorgamma coactivator 1 alpha (PGC-1), and p38 mitogenactivated protein kinases (MAPK), and stimulates hypertrophy via intracellular androgen receptor signaling cascade dependent upon Erk and mammalian target of rapamycin (mTOR) (Sculthorpe et al 2012;Qin et al 2010;Wu et al 2010).…”

Section: Discussionmentioning

confidence: 99%

Effects of testosterone on lean mass gain in elderly men: systematic review with meta-analysis of controlled and randomized studies

Neto

Gama

Rocha

et al. 2015

AGE

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The objective of this study was to evaluate the effects of steroid anabolic androgenic hormones use on lean mass gain in elderly men through a systematic review with a meta-analysis of randomized controlled studies. We systematically searched PubMed database until 4th October 2013. We included randomized placebo-controlled trials (RCT) that studied testosterone replacement therapy in men over 60 years of age, with total testosterone levels ≤550 ng/dl, observing gains in weight, lean mass tissue and fat mass as outcome. We excluded duplicated studies, studies which mixed men and women, and studies using weak androgens such as dehydroepiandrosterone or androstenedione. The initial search yielded 2681 articles, of which 26 were selected for full text analysis. In the end, 11 studies were included. However, 3 studies were not included in the metaanalysis. Meta-analysis showed that mean weight increased (lean mass), ranging from 1.65 (95 % CI, AGE (2015) ) kg, although it was heterogeneous (I 2 =98 %). Effect estimate was 3.59 [2.38-4.81]. Androgen therapy decreased fat mass; effect estimate was −1.78 [−2.57, −0.99] that analysis had also a high level of heterogeneity (I 2 =81 %). The results suggest that testosterone replacement therapy is able to increase muscle mass in elderly men and that is affected by the time that the treatment is carried out and the method of administration of the drug.

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Section: Discussionmentioning

confidence: 99%

Effects of testosterone on lean mass gain in elderly men: systematic review with meta-analysis of controlled and randomized studies

Neto

Gama

Rocha

et al. 2015

AGE

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“…Total RNA was extracted from ex vivo cultured osteoblasts and osteoclasts using phenol-chloroform (23)(24)(25) and then further enriched using RNeasy minicolumns (Qiagen, Valencia, CA). Microarray analysis was performed by the Microarray Core Facility at the Children's National Medical Center using rat Illumina mRNA bead profiling arrays.…”

Section: Methodsmentioning

confidence: 99%

“…Quantitative PCR-Total RNA from ex vivo cultured osteoblasts and osteoclasts was used for real time PCR determination of mRNA levels as described previously (23)(24)(25), using Assay on Demand probe sets obtained from Applied Biosystems (Forster City, CA). The quantitative PCR reactions were performed in triplicate, and the average of the crossing points for three replicates was used in subsequent calculations.…”

Section: Methodsmentioning

confidence: 99%

The Central Nervous System (CNS)-independent Anti-bone-resorptive Activity of Muscle Contraction and the Underlying Molecular and Cellular Signatures

Qin

Sun

Cao

et al. 2013

Journal of Biological Chemistry

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Background: Mechanisms by which muscle regulates bone are poorly understood. Results: Electrically stimulated muscle contraction reversed elevations in bone resorption and increased Wnt signaling in bone-derived cells after spinal cord transection. Conclusion: Muscle contraction reduced resorption of unloaded bone independently of the CNS, through mechanical effects and, potentially, nonmechanical signals (e.g. myokines). Significance: The study provides new insights regarding muscle-bone interactions.

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“…In contrast to glucocorticoids, androgens moderately increase muscle mass and strength in hypogonadal men [35] by decreasing the expression of atrogin-1 and MuRF1 and by increasing the expression of IGF-1 in muscle [36] . Furthermore, androgens repress muscle atrophy induced by glucocorticoids [9,[37][38][39][40] . Androgens abolish the glucocorticoid-induced increase of atrogin-1, MuRF1, and FOXO1 and the glucocorticoid-induced decrease of IGF-1 in muscle [37,38,40] .…”

Section: Regulation Of Muscle Massmentioning

confidence: 99%

“…Furthermore, androgens repress muscle atrophy induced by glucocorticoids [9,[37][38][39][40] . Androgens abolish the glucocorticoid-induced increase of atrogin-1, MuRF1, and FOXO1 and the glucocorticoid-induced decrease of IGF-1 in muscle [37,38,40] . Interestingly, androgens and glucocorticoids decrease the expression of GR and AR, respectively [10,36] .…”

Section: Regulation Of Muscle Massmentioning

confidence: 99%

Competitive and compensatory effects of androgen signaling and glucocorticoid signaling

Harada

Inui

Yamaji

2015

Receptor Clin Invest

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Androgens and glucocorticoids have competitive and compensatory effects in several physiological and pathophysiological processes. Although blood androgen levels affect blood glucocorticoid levels and vice versa, it does not fully explain the relationship between the effects of androgens and glucocorticoids. Androgens and glucocorticoids exert their functions through binding to androgen receptor (AR) and glucocorticoid receptor (GR), respectively. AR homodimer and GR homodimer bind to the androgen response element (ARE) and glucocorticoid response element (GRE), respectively, where they positively or negatively regulate transcription. AR/GR heterodimer can also form but whether it has a physiological role is unclear. Notably, some ARE/GRE sites are recognized by both AR and GR. This review focuses on the functional interventions between androgen signaling and glucocorticoid signaling in target cells that are involved in muscle atrophy, lipid metabolism in adipocytes and hepatocytes, and pancreatic β-cell death. Androgens and glucocorticoids exert opposite effects by differentially regulating key genes (e.g., insulin-like growth factor-1, atrogin-1, and thioredoxin-interacting protein) involved in these physiological processes. We also review functional compensation between these steroids in the development of castration-resistant prostate cancer in which glucocorticoids compensate for the castration-induced loss of AR function by activating key genes (e.g., serum/glucocorticoid-regulated kinase 1). The gene expressions regulated by androgens and glucocorticoids are regulated through at least three different mechanisms in target cells: (i) regulation of applicable ligand levels by modulation of steroid metabolite enzyme levels, (ii) regulation of each other's receptor levels, and (iii) competitive binding between AR and GR on ARE/GRE sites. Recent findings shed light on the complicated relationship between androgen signaling and glucocorticoid signaling in various cellular processes.

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Protection against dexamethasone-induced muscle atrophy is related to modulation by testosterone of FOXO1 and PGC-1α

Cited by 66 publications

References 34 publications

Effects of testosterone on lean mass gain in elderly men: systematic review with meta-analysis of controlled and randomized studies

Effects of testosterone on lean mass gain in elderly men: systematic review with meta-analysis of controlled and randomized studies

The Central Nervous System (CNS)-independent Anti-bone-resorptive Activity of Muscle Contraction and the Underlying Molecular and Cellular Signatures

Competitive and compensatory effects of androgen signaling and glucocorticoid signaling

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