Pharmacological inhibition of GSK-3 in a guinea pig model of LPS-induced pulmonary inflammation: II. Effects on skeletal muscle atrophy

Verhees, Koen J P; Pansters, N.A.M.; Baarsma, Hoeke A.; Remels, Alexander; Haegens, Astrid; Theije, Chiel C. de; Schols, A.M.W.J.; Gosens, Reinoud; Langen, Ramon

doi:10.1186/1465-9921-14-117

Cited by 19 publications

(16 citation statements)

References 84 publications

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“…Pharmacological inhibition of GSK3β attenuates TNF-α and glucocorticoid induced suppression of MyoD expression and myotube formation in C2C12 and primary satellite cells (Ma et al, 2014, Verhees et al, 2013). TDZD-8 also improved muscle strength and Pax7 expression (a marker for satellite cells) in HSA LR mice, a mouse model of myotonic dystrophy (Jones et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Angiotensin-II-induced Muscle Wasting is Mediated by 25-Hydroxycholesterol via GSK3β Signaling Pathway

et al. 2017

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While angiotensin II (ang II) has been implicated in the pathogenesis of cardiac cachexia (CC), the molecules that mediate ang II's wasting effect have not been identified. It is known TNF-α level is increased in patients with CC, and TNF-α release is triggered by ang II. We therefore hypothesized that ang II induced muscle wasting is mediated by TNF-α. Ang II infusion led to skeletal muscle wasting in wild type (WT) but not in TNF alpha type 1 receptor knockout (TNFR1KO) mice, suggesting that ang II induced muscle loss is mediated by TNF-α through its type 1 receptor. Microarray analysis identified cholesterol 25-hydroxylase (Ch25h) as the down stream target of TNF-α. Intraperitoneal injection of 25-hydroxycholesterol (25-OHC), the product of Ch25h, resulted in muscle loss in C57BL/6 mice, accompanied by increased expression of atrogin-1, MuRF1 and suppression of IGF-1/Akt signaling pathway. The identification of 25-OHC as an inducer of muscle wasting has implications for the development of specific treatment strategies in preventing muscle loss.

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Section: Discussionmentioning

confidence: 99%

Angiotensin-II-induced Muscle Wasting is Mediated by 25-Hydroxycholesterol via GSK3β Signaling Pathway

et al. 2017

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“…In summary, IGF-1/Akt controls two protein synthetic pathways via mTORC1 and GSK3β. Although these pathways are decreased in various muscle atrophy conditions [ 16 , 17 , 18 , 19 ], the exact relationship and interaction between these pathways in skeletal muscle atrophy and hypertrophy conditions remain to be determined. IGF-1 also affects protein synthesis via myostatin signaling, and the mechanism is discussed below.…”

Section: Muscle Protein Synthesis and Igf-1 Signalingmentioning

confidence: 99%

Mechanisms of IGF-1-Mediated Regulation of Skeletal Muscle Hypertrophy and Atrophy

Yoshida

Delafontaine

2020

Cells

341

209

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Insulin-like growth factor-1 (IGF-1) is a key growth factor that regulates both anabolic and catabolic pathways in skeletal muscle. IGF-1 increases skeletal muscle protein synthesis via PI3K/Akt/mTOR and PI3K/Akt/GSK3β pathways. PI3K/Akt can also inhibit FoxOs and suppress transcription of E3 ubiquitin ligases that regulate ubiquitin proteasome system (UPS)-mediated protein degradation. Autophagy is likely inhibited by IGF-1 via mTOR and FoxO signaling, although the contribution of autophagy regulation in IGF-1-mediated inhibition of skeletal muscle atrophy remains to be determined. Evidence has suggested that IGF-1/Akt can inhibit muscle atrophy-inducing cytokine and myostatin signaling via inhibition of the NF-κΒ and Smad pathways, respectively. Several miRNAs have been found to regulate IGF-1 signaling in skeletal muscle, and these miRs are likely regulated in different pathological conditions and contribute to the development of muscle atrophy. IGF-1 also potentiates skeletal muscle regeneration via activation of skeletal muscle stem (satellite) cells, which may contribute to muscle hypertrophy and/or inhibit atrophy. Importantly, IGF-1 levels and IGF-1R downstream signaling are suppressed in many chronic disease conditions and likely result in muscle atrophy via the combined effects of altered protein synthesis, UPS activity, autophagy, and muscle regeneration.

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“…Moreover, it has been presented that activation of the GSK3β signal pathway leads to elevated expression of proteolysis markers, myogenesis disruption, and to muscle loss (Shen et al 2017 ). However, inhibition of GSK3β prevents muscle atrophy in mice (Shen et al 2017 ) and guinea pigs (Verhees et al 2013 ), and it further prevents development of myotonic dystrophy type 1 (DM1), eventually leading to skeletal muscle being characterized by higher fiber density, and normal fiber size (Wei et al 2018 ). Other researchers also observed that GSK3β is a negative regulator of skeletal muscle growth, and its insufficiency stimulates myogenic differentiation and myotube formation (van der Velden et al 2008 ; Ma et al 2014 ).…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic profile of semitendinosus muscle of bulls of different breed and performance

2020

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The aim of the study was to compare the transcriptomic profiles of fully differentiated skeletal muscle derived from bulls belonging to different breeds of varying performance. Microarray analyses were performed to determine the differences in the expression profiles of genes between semitendinosus muscles of 15-month-old beef-breed bulls (Limousin-LIM and Hereford-HER) and dairy-breed bulls (Holstein Friesian-HF). These analyses allowed for the identification of those genes the expression of which is similar and characteristic of fully differentiated muscle in beef breeds, but differs in skeletal muscle of a typical dairy breed. The analysis revealed 463 transcripts showing similar expression in the semitendinosus muscle of beef breeds (LIM/HER), in comparison with the dairy breed (HF). Among the identified genes, 227 were upregulated and 236 were downregulated in beef breeds. The ontological analyses revealed that the largest group of genes similarly expressed in LIM and HER was involved in the processes of protein metabolism and development of muscle organ. In beef breeds, some genes involved in protein synthesis and proteolysis showed an upregulation, including ctsd, ctsf, fhl2, fhl3, fst, sirt1, and trim63, whereas some were downregulated, including bmpr1a, bmpr2, mstn, smad2, hspa8, gsk3β, and tgfβ2. The expression of the chosen genes was confirmed by RT-qPCR technique. Thus, it can be assumed that the identified genes involved in the regulation of growth and development of muscle tissue and the processes of protein metabolism in the examined cattle breeds may be responsible for the greater gain of muscle mass in beef-breed bulls.

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Pharmacological inhibition of GSK-3 in a guinea pig model of LPS-induced pulmonary inflammation: II. Effects on skeletal muscle atrophy

Cited by 19 publications

References 84 publications

Angiotensin-II-induced Muscle Wasting is Mediated by 25-Hydroxycholesterol via GSK3β Signaling Pathway

Angiotensin-II-induced Muscle Wasting is Mediated by 25-Hydroxycholesterol via GSK3β Signaling Pathway

Mechanisms of IGF-1-Mediated Regulation of Skeletal Muscle Hypertrophy and Atrophy

Transcriptomic profile of semitendinosus muscle of bulls of different breed and performance

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