Role(s) of nucleoli and phosphorylation of ribosomal protein S6 and/or HSP27 in the regulation of muscle mass

Kawano, Fuminori; Matsuoka, Yoshikazu; Oke, Yoshihiko; Higo, Yoko; Terada, Masahiro; Wang, X. D.; Nakai, Norihiro; Fukuda, Hirofumi; Imajoh‐Ohmi, Shinobu; Ohira, Yoshinobu

doi:10.1152/ajpcell.00297.2006

Cited by 50 publications

(59 citation statements)

References 39 publications

(76 reference statements)

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“…Taken together, these findings may suggest the possibility that PDK1-Akt(/mTOR) pathway plays a more important role in post-PH liver regeneration by cell growth, even though p70 S6K /S6 pathway is certainly involved in cell growth in other types of cells. 32,33 PDK1/Akt-Mediated Liver Regeneration by Cell Growth Rather than Cell Proliferation. To confirm the role of PDK1-Akt/mTOR pathway in liver regeneration, we employed the "pif-pocket" mutant of PDK1, which allows PDK1 to signal exclusively to Akt but not to p70 S6K or others.…”

Section: L-pdk1komentioning

confidence: 99%

The survival pathways phosphatidylinositol-3 kinase (PI3-K)/phosphoinositide-dependent protein kinase 1 (PDK1)/Akt modulate liver regeneration through hepatocyte size rather than proliferation

et al. 2008

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Liver regeneration comprises a series of complicated processes. The current study was designed to investigate the roles of phosphoinositide-dependent protein kinase 1 (PDK1)-associated pathways in liver regeneration after partial hepatectomy (PH) using liver-specific Pdk1-knockout (L-Pdk1KO) and Pdk1/STAT3 double KO (L-DKO) mice. There was no liver regeneration, and 70% PH was lethal in L-Pdk1KO mice. Liver regeneration was severely impaired equally in L-Pdk1KO and L-DKO mice, even after nonlethal 30% PH. There was no cell growth (measured as increase of cell size) after hepatectomy in L-Pdk1KO mice, although the post-PH mitotic response was the same as in controls. As expected, hepatectomy did not induce hepatic Akt-phosphorylation (Thr308) in L-Pdk1KO mice, and post-PH phosphorylation of Akt, mammalian target of rapamycin (mTOR), p70 ribosomal S6 kinase (p70 S6K ), and S6 were also reduced. To examine the specific role of PDK1-associated signals, a "pif-pocket" mutant of PDK1, which allows PDK1 only to phosphorylate Akt, was used.

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Section: L-pdk1komentioning

confidence: 99%

The survival pathways phosphatidylinositol-3 kinase (PI3-K)/phosphoinositide-dependent protein kinase 1 (PDK1)/Akt modulate liver regeneration through hepatocyte size rather than proliferation

et al. 2008

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“…9) and HSP27 (−63%, Fig. 10, Kawano et al, 2007), and with increased myonuclear size (+19%) and ubiquitination of MHC (+33%, p>0.05), was observed after unloading, which inhibited the mechanical load. Responses to deafferentation, which inhibited EMG level (−47%), were basically similar to those caused by hindlimb unloading, although the magnitudes were minor.…”

Section: Satellite Cellsmentioning

confidence: 90%

“…Nucleoli, ribosomal protein S6, and/or HSP27: Effects of 14 days of hindlimb unloading or overloading caused by ablation of synergists, with or without deafferentation, on the fiber CSA, myonuclear number, size, and domain, the number of nucleoli in a single myonucleus, and the levels in the phosphorylation of the ribosomal protein S6 (S6) and 27 kDa heat shock protein (HSP27) were studied in rat soleus (Kawano et al, 2007). Hypertrophy of fibers (+24%), associated with increased nucleolar number (from 1-2 to 3-5) within a myonucleus and myonuclear domain (+27%) compared to the preexperimental level, was induced by ablation of synergists.…”

Section: Satellite Cellsmentioning

confidence: 99%

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Role(s) of Mechanical Load and Satellite Cells in The Regulation of The Size of Soleus Muscle Fiber in Rats

et al. 2010

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Roles of mechanical load and satellite cells in the regulation of morphological properties of sol e us muscl e fib e rs we r e r evi e we d . G r avi t a t i o n a l unlo a din g by exp osur e to microgravity and/or by hindlimb suspension causes passive plantarflexion of ankle joints, which then shortens the length of muscle fibers and sarcomeres. Such phenomena cause the decrease of tension development. Atrophy of muscle fibers caused by inhibited protein synthesis is induced in association with decreased number and increased size of myonuclei. Distribution of satellite cells, which serve as a source of new myonuclei during regeneration after a muscle injury and /or atrophy, also decreases in response to lowered mechanical load. However, these responses are generally reversible, when the mechanical load applied to muscle fibers is increased, suggesting that satellite cells play important role (s) in the re gulation of muscle fib e r properties. The data also indicated that one of the satellite cell-related regulations of muscle fiber was mechanical load-dependent, which was influenced by the sarcomere length. ©2010 Jpn. Soc. Biol. Sci. Space; Article ID: 102403011

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“…Its phosphorylation at T317 allows MKK2 nuclear export in a complex containing p38 itself (Meng et al, 2002). Phosphorylation of heat shock protein 27 (HSP27), a substrate of MKK2, is increased in skeletal muscle hypertrophy and decreased during atrophy (Huey, 2006;Kawano et al, 2007), while HSP27…”

Section: Strategies To Correct Metabolic Alterationsmentioning

confidence: 99%

Mechanism-Based Therapeutic Approaches to Cachexia

et al. 2013

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Cachexia is a multifactorial syndrome characterized by body weight loss, depletion of adipose tissue and skeletal muscle mass, and marked alterations of the metabolic homeostasis.The occurrence of cachexia significantly impinges on patient's morbidity and mortality, and on quality of life. Inflammation, anorexia/malnutrition, alterations of protein and lipid metabolism are among the main mechanisms involved in the development of cachexia. While anorexia and malnutrition are long known contributing factors, the mechanisms leading to inflammation and metabolic alterations were clarified later on. On these premises, several therapeutic approaches were proposed. Most of them are in the pre-clinical phase, but some already reached the clinical experimentation. The present review will focus on treatment options proposed on the basis of mechanistic alterations. In this regard, in addition to nutritional and anti-inflammatory strategies, also approaches based on perturbation of specific signal transduction pathways are taken into consideration.

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Role(s) of nucleoli and phosphorylation of ribosomal protein S6 and/or HSP27 in the regulation of muscle mass

Cited by 50 publications

References 39 publications

The survival pathways phosphatidylinositol-3 kinase (PI3-K)/phosphoinositide-dependent protein kinase 1 (PDK1)/Akt modulate liver regeneration through hepatocyte size rather than proliferation

The survival pathways phosphatidylinositol-3 kinase (PI3-K)/phosphoinositide-dependent protein kinase 1 (PDK1)/Akt modulate liver regeneration through hepatocyte size rather than proliferation

Role(s) of Mechanical Load and Satellite Cells in The Regulation of The Size of Soleus Muscle Fiber in Rats

Mechanism-Based Therapeutic Approaches to Cachexia

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