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Article ; Online: Ribosomes 'muscle up' postnatal muscle growth.

Nader, Gustavo A

2014 Volume 592, Issue 23, Page(s) 5143

MeSH term(s)	Animal Nutritional Physiological Phenomena ; Animals ; Humans ; Infant ; Infant Nutrition Disorders/diet therapy ; Infant Nutrition Disorders/pathology ; Infant Nutrition Disorders/physiopathology ; Malnutrition/pathology ; Malnutrition/physiopathology ; Muscle, Skeletal/growth & development ; Muscle, Skeletal/physiology ; Nutritional Status ; Organ Size ; Ribosomes/physiology
Language	English
Publishing date	2014-12-01
Publishing country	England
Document type	Journal Article
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/jphysiol.2014.284828
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Article ; Online: Metastatic or xenograft colorectal cancer models induce divergent anabolic deficits and expression of pro-inflammatory effectors of muscle wasting in a tumor-type-dependent manner.

Kim, Hyo-Gun / Huot, Joshua R / Pin, Fabrizio / Belcher, Daniel J / Bonetto, Andrea / Nader, Gustavo A

Journal of applied physiology (Bethesda, Md. : 1985)

2022 Volume 133, Issue 6, Page(s) 1273–1283

Abstract: We investigated the impact of tumor burden on muscle wasting in metastatic (m) and xenograft (x) models of colorectal cancer (CRC). Male Nod SCID γ and CD2F1 mice were injected subcutaneously or intrasplenically with HCT116 or C26 tumor cells, ... ...

Abstract	We investigated the impact of tumor burden on muscle wasting in metastatic (m) and xenograft (x) models of colorectal cancer (CRC). Male Nod SCID γ and CD2F1 mice were injected subcutaneously or intrasplenically with HCT116 or C26 tumor cells, respectively. CRC tumors resulted in significant muscle wasting regardless of tumor type or model, although muscle loss was exacerbated in mHCT116 hosts. The mHCT116 model decreased ribosomal (r)RNA content and rDNA transcription, whereas the mC26 model showed no loss of rRNA and the upregulation of rDNA transcription. The xHCT116 model reduced mTOR, RPS6, and 4E-BP1 phosphorylation, whereas the mHCT116 model had a similar effect on RPS6 and 4E-BP1 without altering mTOR phosphorylation. The C26 models caused a reduction in 4E-BP1 phosphorylation independent of mTOR. Muscle interleukin (IL)-6 mRNA was elevated in all models except xHCT116, and the NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) mRNA was induced only in the mC26 model. IL-1β mRNA increased in all groups with greater expression in metastatic relative to the xenograft model regardless of tumor types. Our findings indicate that HCT116 tumor burden results in more drastic muscle wasting and anabolic deficits, whereas C26 tumor burden causes similar muscle wasting but exhibits a divergent proinflammatory phenotype. These results highlight potentially important divergence in the pathogenesis of muscle wasting among preclinical models of CRC and demonstrate that tumor burden plays a role in determining anabolic deficits and the expression of proinflammatory effectors of muscle wasting in a tumor-type-dependent manner.
MeSH term(s)	Mice ; Humans ; Male ; Animals ; Cachexia/metabolism ; Heterografts ; Muscle, Skeletal/metabolism ; Mice, SCID ; Muscular Atrophy/metabolism ; TOR Serine-Threonine Kinases/metabolism ; Disease Models, Animal ; Interleukin-6/metabolism ; Colorectal Neoplasms/complications ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/pathology ; RNA, Messenger/metabolism ; DNA, Ribosomal/metabolism ; DNA, Ribosomal/pharmacology
Chemical Substances	TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Interleukin-6 ; RNA, Messenger ; DNA, Ribosomal
Language	English
Publishing date	2022-10-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	219139-8
ISSN	1522-1601 ; 0021-8987 ; 0161-7567 ; 8750-7587
ISSN (online)	1522-1601
ISSN	0021-8987 ; 0161-7567 ; 8750-7587
DOI	10.1152/japplphysiol.00247.2022
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Article ; Online: Regulation of Ribosome Biogenesis During Skeletal Muscle Hypertrophy.

Kim, Hyo-Gun / Guo, Bin / Nader, Gustavo A

Exercise and sport sciences reviews

2019 Volume 47, Issue 2, Page(s) 91–97

Abstract: An increase in ribosomal capacity is a hallmark of the hypertrophying muscle. We review evidence demonstrating that transcription of ribosomal RNA genes is necessary for the increase in ribosomal capacity, and this is critical for muscle growth in human ... ...

Abstract	An increase in ribosomal capacity is a hallmark of the hypertrophying muscle. We review evidence demonstrating that transcription of ribosomal RNA genes is necessary for the increase in ribosomal capacity, and this is critical for muscle growth in human and animal models of hypertrophy.
MeSH term(s)	Animals ; Humans ; Muscle, Skeletal/growth & development ; Ribosomes/physiology ; TOR Serine-Threonine Kinases/physiology
Chemical Substances	TOR Serine-Threonine Kinases (EC 2.7.1.1)
Language	English
Publishing date	2019-01-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	187040-3
ISSN	1538-3008 ; 0091-6331
ISSN (online)	1538-3008
ISSN	0091-6331
DOI	10.1249/JES.0000000000000179
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Article ; Online: Chemotherapy agents reduce protein synthesis and ribosomal capacity in myotubes independent of oxidative stress.

Guo, Bin / Bennet, Devasier / Belcher, Daniel J / Kim, Hyo-Gun / Nader, Gustavo A

American journal of physiology. Cell physiology

2021 Volume 321, Issue 6, Page(s) C1000–C1009

Abstract: Chemotherapeutic agents (CAs) are first-line antineoplastic treatments against a wide variety of cancers. Despite their effectiveness in halting tumor progression, side effects associated with CAs promote muscle loss by incompletely understood mechanisms. ...

Abstract	Chemotherapeutic agents (CAs) are first-line antineoplastic treatments against a wide variety of cancers. Despite their effectiveness in halting tumor progression, side effects associated with CAs promote muscle loss by incompletely understood mechanisms. To address this problem, we first identified how oxidative stress impairs protein synthesis in C2C12 myotubes. Transient elevations in reactive oxygen species (ROS) resulted in protein synthesis deficits and reduced ribosomal (r)RNA levels. Oxidative stress did not reduce rRNA gene (rDNA) transcription, but it caused an increase in rRNA and protein oxidation. To determine whether CAs affect protein synthesis independent of oxidative stress, we exposed myotubes to Paclitaxel (PTX), Doxorubicin (DXR), or Marizomib (Mzb) at doses that did result in elevated ROS levels (sub-ROS). Exposure to CAs reduced protein synthesis and rRNA levels, but unlike oxidative stress, sub-ROS exposures impaired rDNA transcription. These results indicate that although oxidative stress disrupts protein synthesis by compromising ribosomal quantity and quality, CAs at sub-ROS doses compromise protein synthesis and ribosomal capacity, at least in part, by reducing rDNA transcription. Therefore, CAs negatively impact protein synthesis by causing oxidative stress in addition to directly reducing the ribosomal capacity of myotubes in a ROS-independent manner.
MeSH term(s)	Animals ; Antineoplastic Agents/toxicity ; Cell Line ; Hydrogen Peroxide/toxicity ; Mice ; Muscle Fibers, Skeletal/drug effects ; Muscle Fibers, Skeletal/metabolism ; Oxidative Stress/drug effects ; Oxidative Stress/physiology ; Protein Biosynthesis/drug effects ; Protein Biosynthesis/physiology ; Ribosomes/drug effects ; Ribosomes/metabolism
Chemical Substances	Antineoplastic Agents ; Hydrogen Peroxide (BBX060AN9V)
Language	English
Publishing date	2021-10-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00116.2021
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Article ; Online: Reduced rDNA transcription diminishes skeletal muscle ribosomal capacity and protein synthesis in cancer cachexia.

Kim, Hyo-Gun / Huot, Joshua R / Pin, Fabrizio / Guo, Bin / Bonetto, Andrea / Nader, Gustavo A

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2021 Volume 35, Issue 2, Page(s) e21335

Abstract: Muscle wasting in cancer is associated with deficits in protein synthesis, yet, the mechanisms underlying this anabolic impairment remain poorly understood. The capacity for protein synthesis is mainly determined by the abundance of muscle ribosomes, ... ...

Abstract	Muscle wasting in cancer is associated with deficits in protein synthesis, yet, the mechanisms underlying this anabolic impairment remain poorly understood. The capacity for protein synthesis is mainly determined by the abundance of muscle ribosomes, which is in turn regulated by transcription of the ribosomal (r)RNA genes (rDNA). In this study, we investigated whether muscle loss in a preclinical model of ovarian cancer is associated with a reduction in ribosomal capacity and was a consequence of impaired rDNA transcription. Tumor bearing resulted in a significant loss in gastrocnemius muscle weight and protein synthesis capacity, and was consistent with a significant reduction in rDNA transcription and ribosomal capacity. Despite the induction of the ribophagy receptor NUFIP1 mRNA and the loss of NUFIP1 protein, in vitro studies revealed that while inhibition of autophagy rescued NUFIP1, it did not prevent the loss of rRNA. Electrophoretic analysis of rRNA fragmentation from both in vivo and in vitro models showed no evidence of endonucleolytic cleavage, suggesting that rRNA degradation may not play a major role in modulating muscle ribosome abundance. Our results indicate that in this model of ovarian cancer-induced cachexia, the ability of skeletal muscle to synthesize protein is compromised by a reduction in rDNA transcription and consequently a lower ribosomal capacity. Thus, impaired ribosomal production appears to play a key role in the anabolic deficits associated with muscle wasting in cancer cachexia.
MeSH term(s)	Animals ; Cachexia/etiology ; Cachexia/genetics ; Cachexia/metabolism ; Cell Line, Tumor ; DNA, Ribosomal/genetics ; DNA, Ribosomal/metabolism ; Female ; Mice ; Muscle, Skeletal/metabolism ; Ovarian Neoplasms/complications ; Protein Biosynthesis ; RNA, Ribosomal/genetics ; RNA, Ribosomal/metabolism ; Ribosomes/metabolism ; Transcription, Genetic
Chemical Substances	DNA, Ribosomal ; RNA, Ribosomal
Language	English
Publishing date	2021-01-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202002257R
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Zs.A 2266: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: LP07 and LLC preclinical models of lung cancer induce divergent anabolic deficits and expression of pro-inflammatory effectors of muscle wasting.

Belcher, Daniel J / Guitart, Maria / Hain, Brian / Kim, Hyo-Gun / Waning, David / Barreiro, Esther / Nader, Gustavo A

Journal of applied physiology (Bethesda, Md. : 1985)

2022 Volume 133, Issue 6, Page(s) 1260–1272

Abstract: Preclinical models have been instrumental to elucidate the mechanisms underlying muscle wasting in lung cancer (LC). We investigated anabolic deficits and the expression of proinflammatory effectors of muscle wasting in the LP07 and Lewis lung carcinoma ( ...

Abstract	Preclinical models have been instrumental to elucidate the mechanisms underlying muscle wasting in lung cancer (LC). We investigated anabolic deficits and the expression of proinflammatory effectors of muscle wasting in the LP07 and Lewis lung carcinoma (LLC) tumor models. Tumor growth resulted in significant weakness in LP07 but not in LLC mice despite similar reductions in gastrocnemius muscle mass in both models. The LP07 tumors caused a reduction in ribosomal (r)RNA and a decrease in rRNA gene (rDNA) transcription elongation, whereas no changes in ribosomal capacity were evident in LLC tumor-bearing mice. Expression of RNA Polymerase I (Pol I) elongation-associated subunits Polr2f, PAF53, and Znrd1 mRNAs was significantly elevated in the LP07 model, whereas Pol I elongation-related factors FACT and Spt4/5 mRNAs were elevated in the LLC mice. Reductions in RPS6 and 4E-BP1 phosphorylation were similar in both models but were independent of mTOR phosphorylation in LP07 mice. Muscle inflammation was also tumor-specific, IL-6 and TNF-α mRNA increased with LLC tumors, and upregulation of NLRP3 mRNA was independent of tumor type. In summary, although both models caused muscle wasting, only the LP07 model displayed muscle weakness with reductions in ribosomal capacity. Intracellular signaling diverged at the mTOR level with similar reductions in RPS6 and 4E-BP1 phosphorylation regardless of tumor type. The increase in proinflammatory factors was more pronounced in the LLC model. Our results demonstrate novel divergent anabolic deficits and expression of proinflammatory effectors of muscle wasting in the LP07 and LLC preclinical models of lung cancer.
MeSH term(s)	Mice ; Animals ; Carcinoma, Lewis Lung/genetics ; Carcinoma, Lewis Lung/metabolism ; Carcinoma, Lewis Lung/pathology ; Cachexia/etiology ; Muscular Atrophy/metabolism ; Muscle, Skeletal/metabolism ; Lung Neoplasms/complications ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; TOR Serine-Threonine Kinases/metabolism ; RNA, Messenger/metabolism ; Mice, Inbred C57BL
Chemical Substances	TOR Serine-Threonine Kinases (EC 2.7.11.1) ; RNA, Messenger
Language	English
Publishing date	2022-10-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	219139-8
ISSN	1522-1601 ; 0021-8987 ; 0161-7567 ; 8750-7587
ISSN (online)	1522-1601
ISSN	0021-8987 ; 0161-7567 ; 8750-7587
DOI	10.1152/japplphysiol.00246.2022
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Article: Muscle growth learns new tricks from an old dog.

Nader, Gustavo A

Nature medicine

2007 Volume 13, Issue 9, Page(s) 1016–1018

MeSH term(s)	Adenylate Kinase/metabolism ; Animals ; Humans ; Hypertrophy ; Mice ; Mitochondria, Muscle/physiology ; Models, Animal ; Muscle, Skeletal/enzymology ; Muscle, Skeletal/growth & development ; Muscle, Skeletal/pathology
Chemical Substances	Adenylate Kinase (EC 2.7.4.3)
Language	English
Publishing date	2007-09
Publishing country	United States
Document type	News
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/nm0907-1016
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Article: Concurrent strength and endurance training: from molecules to man.

Nader, Gustavo A

Medicine and science in sports and exercise

2006 Volume 38, Issue 11, Page(s) 1965–1970

Abstract: Strength and endurance training produce widely diversified adaptations, with little overlap between them. Strength training typically results in increases in muscle mass and muscle strength. In contrast, endurance training induces increases in maximal ... ...

Abstract	Strength and endurance training produce widely diversified adaptations, with little overlap between them. Strength training typically results in increases in muscle mass and muscle strength. In contrast, endurance training induces increases in maximal oxygen uptake and metabolic adaptations that lead to an increased exercise capacity. In many sports, a combination of strength and endurance training is required to improve performance, but in some situations when strength and endurance training are performed simultaneously, a potential interference in strength development takes place, making such a combination seemingly incompatible. The phenomenon of concurrent training, or simultaneously training for strength and endurance, was first described in the scientific literature in 1980 by Robert C. Hickson, and although work that followed provided evidence for and against it, the interference effect seems to hold true in specific situations. At the molecular level, there seems to be an explanation for the interference of strength development during concurrent training; it is now clear that different forms of exercise induce antagonistic intracellular signaling mechanisms that, in turn, could have a negative impact on the muscle's adaptive response to this particular form of training. That is, activation of AMPK by endurance exercise may inhibit signaling to the protein-synthesis machinery by inhibiting the activity of mTOR and its downstream targets. The purpose of this review is to briefly describe the problem of concurrent strength and endurance training and to examine new data highlighting potential molecular mechanisms that may help explain the inhibition of strength development when strength and endurance training are performed simultaneously.
MeSH term(s)	Adaptation, Physiological ; Glycogen/metabolism ; Humans ; Muscle Fibers, Skeletal/physiology ; Muscle Strength/physiology ; Muscle, Skeletal/physiology ; Physical Endurance/physiology ; Protein Biosynthesis/physiology ; Signal Transduction/physiology
Chemical Substances	Glycogen (9005-79-2)
Language	English
Publishing date	2006-11
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	603994-7
ISSN	1530-0315 ; 0195-9131 ; 0025-7990
ISSN (online)	1530-0315
ISSN	0195-9131 ; 0025-7990
DOI	10.1249/01.mss.0000233795.39282.33
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Article ; Online: Ursolic acid directly promotes protein accretion in myotubes but does not affect myoblast proliferation.

Figueiredo, Vandré Casagrande / Nader, Gustavo A

Cell biochemistry and function

2012 Volume 30, Issue 5, Page(s) 432–437

Abstract: Ursolic acid (UA) has been recently proposed as a potential candidate for the treatment of muscle wasting conditions because of its protein sparring/anabolic effects. Despite this finding, it is unknown whether this response is the consequence of a ... ...

Abstract	Ursolic acid (UA) has been recently proposed as a potential candidate for the treatment of muscle wasting conditions because of its protein sparring/anabolic effects. Despite this finding, it is unknown whether this response is the consequence of a direct effect on the muscle fibre or if it is mediated by neural or other systemic factors. In the present study, we sought to determine if UA has direct effects in skeletal muscle cells, whether it can increase myoblast proliferation and whether UA can become myotoxic at higher doses. Our results demonstrate that UA directly promoted protein accretion in cultured myotubes but did not modulate myoblast proliferation. At higher doses, UA compromised cell viability in both myoblasts and myotubes. We conclude that the anabolic properties of UA seen in vivo and in vitro are likely a direct effect on the muscle cell, but at higher doses, the benefits decline in favour of a myotoxic outcome.
MeSH term(s)	Cell Proliferation ; Cell Survival/drug effects ; Cells, Cultured ; Dose-Response Relationship, Drug ; Humans ; Muscle Fibers, Skeletal/cytology ; Muscle Fibers, Skeletal/drug effects ; Muscle Fibers, Skeletal/metabolism ; Muscle Proteins/metabolism ; Myoblasts/cytology ; Myoblasts/drug effects ; Time Factors ; Triterpenes/pharmacology ; Ursolic Acid
Chemical Substances	Muscle Proteins ; Triterpenes
Language	English
Publishing date	2012-03-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	283643-9
ISSN	1099-0844 ; 0263-6484
ISSN (online)	1099-0844
ISSN	0263-6484
DOI	10.1002/cbf.2821
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Article ; Online: Mechanisms of mechanical overload-induced skeletal muscle hypertrophy: current understanding and future directions.

Roberts, Michael D / McCarthy, John J / Hornberger, Troy A / Phillips, Stuart M / Mackey, Abigail L / Nader, Gustavo A / Boppart, Marni D / Kavazis, Andreas N / Reidy, Paul T / Ogasawara, Riki / Libardi, Cleiton A / Ugrinowitsch, Carlos / Booth, Frank W / Esser, Karyn A

Physiological reviews

2023 Volume 103, Issue 4, Page(s) 2679–2757

Abstract: Mechanisms underlying mechanical overload-induced skeletal muscle hypertrophy have been extensively researched since the landmark report by Morpurgo (1897) of "work-induced hypertrophy" in dogs that were treadmill trained. Much of the preclinical rodent ... ...

Abstract	Mechanisms underlying mechanical overload-induced skeletal muscle hypertrophy have been extensively researched since the landmark report by Morpurgo (1897) of "work-induced hypertrophy" in dogs that were treadmill trained. Much of the preclinical rodent and human resistance training research to date supports that involved mechanisms include enhanced mammalian/mechanistic target of rapamycin complex 1 (mTORC1) signaling, an expansion in translational capacity through ribosome biogenesis, increased satellite cell abundance and myonuclear accretion, and postexercise elevations in muscle protein synthesis rates. However, several lines of past and emerging evidence suggest that additional mechanisms that feed into or are independent of these processes are also involved. This review first provides a historical account of how mechanistic research into skeletal muscle hypertrophy has progressed. A comprehensive list of mechanisms associated with skeletal muscle hypertrophy is then outlined, and areas of disagreement involving these mechanisms are presented. Finally, future research directions involving many of the discussed mechanisms are proposed.
MeSH term(s)	Humans ; Animals ; Dogs ; Muscle, Skeletal/metabolism ; Signal Transduction ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Protein Biosynthesis ; Hypertrophy/metabolism ; Mammals/metabolism
Chemical Substances	Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
Language	English
Publishing date	2023-06-29
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	209902-0
ISSN	1522-1210 ; 0031-9333
ISSN (online)	1522-1210
ISSN	0031-9333
DOI	10.1152/physrev.00039.2022
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