Mechanisms Regulating Muscle Protein Synthesis in CKD.
Adult
Aged
Animals
Cell Line
DNA, Ribosomal
Dioxygenases
/ genetics
Disease Models, Animal
Epigenesis, Genetic
Female
Gene Expression
Histone Demethylases
/ genetics
Histones
/ genetics
Humans
Interferon-gamma
/ pharmacology
Interleukin-6
/ genetics
Jumonji Domain-Containing Histone Demethylases
/ genetics
Male
Mice
Mice, Knockout
Middle Aged
Muscle Fibers, Skeletal
/ metabolism
Muscle Proteins
/ genetics
NF-kappa B
/ metabolism
Nephrectomy
Protein Biosynthesis
/ genetics
RNA, Messenger
/ metabolism
Renal Dialysis
Renal Insufficiency, Chronic
/ complications
SKP Cullin F-Box Protein Ligases
/ genetics
Signal Transduction
Tripartite Motif Proteins
/ genetics
Tumor Necrosis Factor-alpha
/ pharmacology
Ubiquitin-Protein Ligases
/ genetics
chronic kidney disease
epigenetics
muscle wasting
protein metabolism
protein synthesis
ribosomal RNA transcription
Journal
Journal of the American Society of Nephrology : JASN
ISSN: 1533-3450
Titre abrégé: J Am Soc Nephrol
Pays: United States
ID NLM: 9013836
Informations de publication
Date de publication:
11 2020
11 2020
Historique:
received:
10
12
2019
accepted:
21
06
2020
pubmed:
9
8
2020
medline:
10
3
2021
entrez:
9
8
2020
Statut:
ppublish
Résumé
CKD induces loss of muscle proteins partly by suppressing muscle protein synthesis. Muscles of mice with CKD have increased expression of nucleolar protein 66 (NO66), as do muscle biopsy specimens from patients with CKD or those undergoing hemodialysis. Inflammation stimulates NO66 expression and changes in NF- Subtotal nephrectomy created a mouse model of CKD with BUN >80 mg/dl. Crossing NO66 Muscle-specific NO66 knockout in mice blocks CKD-induced loss of muscle mass and improves protein synthesis. NO66 suppression of ribosomal biogenesis CKD suppresses muscle protein synthesis
Sections du résumé
BACKGROUND
CKD induces loss of muscle proteins partly by suppressing muscle protein synthesis. Muscles of mice with CKD have increased expression of nucleolar protein 66 (NO66), as do muscle biopsy specimens from patients with CKD or those undergoing hemodialysis. Inflammation stimulates NO66 expression and changes in NF-
METHODS
Subtotal nephrectomy created a mouse model of CKD with BUN >80 mg/dl. Crossing NO66
RESULTS
Muscle-specific NO66 knockout in mice blocks CKD-induced loss of muscle mass and improves protein synthesis. NO66 suppression of ribosomal biogenesis
CONCLUSIONS
CKD suppresses muscle protein synthesis
Identifiants
pubmed: 32764136
pii: ASN.2019121277
doi: 10.1681/ASN.2019121277
pmc: PMC7608956
doi:
Substances chimiques
DNA, Ribosomal
0
Histones
0
IL6 protein, human
0
Interleukin-6
0
Muscle Proteins
0
NF-kappa B
0
RNA, Messenger
0
Tripartite Motif Proteins
0
Tumor Necrosis Factor-alpha
0
histone H3 trimethyl Lys4
0
Interferon-gamma
82115-62-6
Dioxygenases
EC 1.13.11.-
Histone Demethylases
EC 1.14.11.-
Jumonji Domain-Containing Histone Demethylases
EC 1.14.11.-
nucleolar protein 66, mouse
EC 1.14.11.-
RIOX1 protein, human
EC 1.14.11.27
FBXO32 protein, human
EC 2.3.2.27
SKP Cullin F-Box Protein Ligases
EC 2.3.2.27
TRIM63 protein, human
EC 2.3.2.27
Ubiquitin-Protein Ligases
EC 2.3.2.27
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2573-2587Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK037175
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL147108
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK079638
Pays : United States
Commentaires et corrections
Type : CommentIn
Type : ErratumIn
Informations de copyright
Copyright © 2020 by the American Society of Nephrology.
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