TGF-β1and TNF-α are involved in the transcription of type I collagen α2gene in soleus muscle atrophied by mechanical unloading

Hirose, Tatsuro; Nakazato, Koichi; Song, Hyun Ju; Ishii, Naokata

doi:10.1152/japplphysiol.00463.2006

Cited by 43 publications

(44 citation statements)

References 31 publications

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“…The changes in IL-6 mRNA expression followed a similar pattern to those of TNF-α mRNA, but did not reach significance until 21 days of immobilization. Although a previous study denied a major role for TNF-α in muscle disuse atrophy, except under cachexic conditions (15), our observation in the soleus muscle was consistent with other recently reported studies using hindlimb suspension (1,14), hindlimb immobilization (7,18), and denervation (27), as experimental models. However, in our previous study, MAFbx/ atrogin-1 and MuRF1 mRNA levels in the soleus muscle peaked after 3 days (6.3-fold), declined at 7 days (4.7-fold) and 14 days (2.0-fold), and then reterior muscles after 21 days of immobilization when no change in active phosphorylated Akt was observed in the immobilized muscles (24).…”

Section: Discussionsupporting

confidence: 93%

“…Muscle-specific overexpression of FOXO1 or FOXO3a is sufficient to cause skeletal muscle atrophy in vivo (17,36). Studies using inactivity-induced atrophy models also report that 14), hindlimb immobilization (7,18), and denervation (27). Kim et al (19) reported that mRNA levels of inflammatory cytokines increased in the mixed fiber-type gastrocnemius muscle after 14 days of cast immobilization.…”

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confidence: 99%

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Changes in FOXO and proinflammatory cytokines in the late stage of immobilized fast and slow muscle atrophy

Okamoto

Machida

2017

Biomed. Res.

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The present study aimed to examine the changes in the expression of Forkhead box protein O (FOXO) and proinflammatory cytokines in both slow-twitch soleus and fast-twitch plantaris muscles following cast immobilization. Male C57BL/6 mice were subjected to cast immobilization for 7 and 21 days. Cast immobilization increased FOXO3a mRNA and total protein expression in both the soleus and plantaris muscles. Although FOXO3a phosphorylation tended to increase in response to cast immobilization in both muscles, a significant increase was evident after 21 days of immobilization only in the soleus muscle. The degree of the response of FOXO3a was very different between the soleus and plantaris muscles; however, the kinetics of FOXO3a in both muscles were similar. Thus, the regulation of muscle atrophy by FOXO might act via a common mechanism in both slow-twitch soleus and fast-twitch plantaris muscles. Gene expression of proinflammatory cytokines tended to increase in response to cast immobilization, and a significant increase was evident after 21 days of immobilization in the soleus muscle. However, in the plantaris muscle, proinflammatory cytokine gene expression remained unchanged throughout the immobilization period; nevertheless, immobilization induced greater reduction in muscle fiber cross-sectional area in the plantaris than in the soleus muscle. Thus, these observations indicate that regulation of muscle atrophy by proinflammatory cytokines might contribute to muscle fiber type-specific mechanisms.Skeletal muscle inactivity resulting from bed rest, microgravity, and immobilization leads to significant muscle atrophy, which not only reduces mobility and quality of life, but also elicits disease and affects overall health (44,45). Muscle atrophy in these conditions is a result of both reduced protein synthesis and increased protein degradation; however, it appears that the latter plays the larger role (21). Protein degradation is mediated primarily through the ubiquitin proteasome pathway (16, 42), and two commonly used markers of this pathway are the muscle-specific E3 ligases, namely muscle atrophy F-box (MAFbx)/atrogin-1, and muscle-specific RING finger 1 (MuRF1) (5, 11). The expressions of both MAFbx/atrogin-1 and MuRF1 are regulated by the Forkhead box protein O (FOXO) family of transcription factors (36,39). FOXO transcription factors play key roles in cell proliferation, cell cycle, and cellular survival, and are expressed in all cells of the human body (2, 13, 32). In skeletal muscle, FOXO proteins contribute to determine muscle size by regulating the transcription of atrogene products, such as the muscle-specific E3 ligases (5,26,36). Muscle-specific overexpression of FOXO1 or FOXO3a is sufficient to cause skeletal muscle atrophy in vivo (17,36). Studies using inactivity-induced atrophy models also report that

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Section: Discussionsupporting

confidence: 93%

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confidence: 99%

Changes in FOXO and proinflammatory cytokines in the late stage of immobilized fast and slow muscle atrophy

Okamoto

Machida

2017

Biomed. Res.

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“…Overall, body weight during HU was smaller than that of C (aged-matched at 14 days). Indeed, a significant body weight decrease is generally observed during the first week of HU, but thereafter the growing showed the same time course of C rats (13,16).…”

Section: Resultsmentioning

confidence: 87%

Electrostimulation during hindlimb unloading modulates PI3K-AKT downstream targets without preventing soleus atrophy and restores slow phenotype through ERK

Dupont¹,

Cieniewski-Bernard²,

Bastide³

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Our aim was to analyze the role of phosphatidylinositol 3-kinase (PI3K)-AKT and MAPK signaling pathways in the regulation of muscle mass and slow-to-fast phenotype transition during hindlimb unloading (HU). For that purpose, we studied, in rat slow soleus and fast extensor digitorum longus muscles, the time course of anabolic PI3K-AKT-mammalian target of rapamycin, catabolic PI3K-AKT-forkhead box O (FOXO), and MAPK signaling pathway activation after 7, 14, and 28 days of HU. Moreover, we performed chronic low-frequency soleus electrostimulation during HU to maintain exclusively contractile phenotype and so to determine more precisely the role of these signaling pathways in the modulation of muscle mass. HU induced a downregulation of the anabolic AKT, mammalian target of rapamycin, 70-kDa ribosomal protein S6 kinase, 4E-binding protein 1, and glycogen synthase kinase-3β targets, and an upregulation of the catabolic FOXO1 and muscle-specific RING finger protein-1 targets correlated with soleus muscle atrophy. Unexpectedly, soleus electrostimulation maintained 70-kDa ribosomal protein S6 kinase, 4E-binding protein 1, FOXO1, and muscle-specific RING finger protein-1 to control levels, but failed to reduce muscle atrophy. HU decreased ERK phosphorylation, while electrostimulation enabled the maintenance of ERK phosphorylation similar to control level. Moreover, slow-to-fast myosin heavy chain phenotype transition and upregulated glycolytic metabolism were prevented by soleus electrostimulation during HU. Taken together, our data demonstrated that the processes responsible for gradual disuse muscle plasticity in HU conditions involved both PI3-AKT and MAPK pathways. Moreover, electrostimulation during HU restored PI3K-AKT activation without counteracting soleus atrophy, suggesting the involvement of other signaling pathways. Finally, electrostimulation maintained initial contractile and metabolism properties in parallel to ERK activation, reinforcing the idea of a predominant role of ERK in the regulation of muscle slow phenotype.

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“…Furthermore, immobilization using different techniques is associated with transient alterations of the canonical (15) and noncanonical TGF-β signaling pathways (19, 38). We therefore evaluated whether losartan would have beneficial effects on skeletal muscle of 21-month-old mice subjected to immobilization of the TA muscle for 21 days using a surgical staple procedure (39).…”

Section: Resultsmentioning

confidence: 99%

Losartan Restores Skeletal Muscle Remodeling and Protects Against Disuse Atrophy in Sarcopenia

et al. 2011

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Sarcopenia, a critical loss of muscle mass and function because of the physiological process of aging, contributes to disability and mortality in older adults. It increases the incidence of pathologic fractures, causing prolonged periods of hospitalization and rehabilitation. The molecular mechanisms underlying sarcopenia are poorly understood, but recent evidence suggests that increased transforming growth factor–β (TGF-β) signaling contributes to impaired satellite cell function and muscle repair in aged skeletal muscle. We therefore evaluated whether antagonism of TGF-β signaling via losartan, an angiotensin II receptor antagonist commonly used to treat high blood pressure, had a beneficial impact on the muscle remodeling process of sarcopenic mice. We demonstrated that mice treated with losartan developed significantly less fibrosis and exhibited improved in vivo muscle function after cardiotoxin-induced injury. We found that losartan not only blunted the canonical TGF-β signaling cascade but also modulated the noncanonical TGF-β mitogen-activated protein kinase pathway. We next assessed whether losartan was able to combat disuse atrophy in aged mice that were subjected to hindlimb immobilization. We showed that immobilized mice treated with losartan were protected against loss of muscle mass. Unexpectedly, this protective mechanism was not mediated by TGF-β signaling but was due to an increased activation of the insulin-like growth factor 1 (IGF-1)/Akt/mammalian target of rapamycin (mTOR) pathway. Thus, blockade of the AT1 (angiotensin II type I) receptor improved muscle remodeling and protected against disuse atrophy by differentially regulating the TGF-β and IGF-1/Akt/mTOR signaling cascades, two pathways critical for skeletal muscle homeostasis. Thus, losartan, a Food and Drug Administration–approved drug, may prove to have clinical benefits to combat injury-related muscle remodeling and provide protection against disuse atrophy in humans with sarcopenia.

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TGF-β₁and TNF-α are involved in the transcription of type I collagen α₂gene in soleus muscle atrophied by mechanical unloading

Cited by 43 publications

References 31 publications

<b>Changes in FOXO and proinflammatory cytokines in the late stage of immobilized fast and slow muscle atr</b><b>ophy </b>

<b>Changes in FOXO and proinflammatory cytokines in the late stage of immobilized fast and slow muscle atr</b><b>ophy </b>

Electrostimulation during hindlimb unloading modulates PI3K-AKT downstream targets without preventing soleus atrophy and restores slow phenotype through ERK

Losartan Restores Skeletal Muscle Remodeling and Protects Against Disuse Atrophy in Sarcopenia

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