Mitochondrial adaptations in skeletal muscle to hindlimb unloading

Akira Wagatsuma, Naoki Kotake, Takayuki Kawachi, Masataka Shiozuka, Shigeru Yamada, Ryoichi Matsuda

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

To gain insight into the regulation of mitochondrial adaptations to hindlimb unloading (HU), the activity of mitochondrial enzymes and the expression of nuclear-encoded genes which control mitochondrial properties in mouse gastrocnemius muscle were investigated. Biochemical and enzyme histochemical analysis showed that subsarcolemmal mitochondria were lost largely than intermyofibrillar mitochondria after HU. Gene expression analysis revealed disturbed or diminished gene expression patterns. The three main results of this analysis are as follows. First, in contrast to peroxisome proliferator-activated receptor γ coactivator 1 β (PGC-1β) and PGC-1-related coactivator, which were down-regulated by HU, PGC-1α was up-regulated concomitant with decreased expression of its DNA binding transcription factors, PPARα, and estrogen-related receptor α (ERRα). Moreover, there was no alteration in expression of nuclear respiratory factor 1, but its downstream target gene, mitochondrial transcription factor A, was down-regulated. Second, both mitofusin 2 and fission 1, which control mitochondrial morphology, were down-regulated. Third, ATP-dependent Lon protease, which participates in mitochondrial-protein degradation, was also down-regulated. These findings suggest that HU may induce uncoordinated expression of PGC-1 family coactivators and DNA binding transcription factors, resulting in reducing ability of mitochondrial biogenesis. Furthermore, down-regulation of mitochondrial morphology-related genes associated with HU may be also involved in alterations in intracellular mitochondrial distribution.

Original languageEnglish
Pages (from-to)1-11
Number of pages11
JournalMolecular and cellular biochemistry
Volume350
Issue number1-2
DOIs
Publication statusPublished - Apr 1 2011
Externally publishedYes

Fingerprint

Hindlimb Suspension
Unloading
Muscle
Skeletal Muscle
Peroxisome Proliferator-Activated Receptors
Mitochondria
Genes
Gene expression
Nuclear Respiratory Factor 1
Transcription Factors
Protease La
ATP-Dependent Proteases
Gene Expression
Aptitude
Mitochondrial Proteins
DNA
Organelle Biogenesis
Enzymes
Estrogen Receptors
Proteolysis

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

Cite this

Mitochondrial adaptations in skeletal muscle to hindlimb unloading. / Wagatsuma, Akira; Kotake, Naoki; Kawachi, Takayuki; Shiozuka, Masataka; Yamada, Shigeru; Matsuda, Ryoichi.

In: Molecular and cellular biochemistry, Vol. 350, No. 1-2, 01.04.2011, p. 1-11.

Research output: Contribution to journalArticle

Wagatsuma, Akira ; Kotake, Naoki ; Kawachi, Takayuki ; Shiozuka, Masataka ; Yamada, Shigeru ; Matsuda, Ryoichi. / Mitochondrial adaptations in skeletal muscle to hindlimb unloading. In: Molecular and cellular biochemistry. 2011 ; Vol. 350, No. 1-2. pp. 1-11.
@article{9baf552655d4411486b8f5417b413a0d,
title = "Mitochondrial adaptations in skeletal muscle to hindlimb unloading",
abstract = "To gain insight into the regulation of mitochondrial adaptations to hindlimb unloading (HU), the activity of mitochondrial enzymes and the expression of nuclear-encoded genes which control mitochondrial properties in mouse gastrocnemius muscle were investigated. Biochemical and enzyme histochemical analysis showed that subsarcolemmal mitochondria were lost largely than intermyofibrillar mitochondria after HU. Gene expression analysis revealed disturbed or diminished gene expression patterns. The three main results of this analysis are as follows. First, in contrast to peroxisome proliferator-activated receptor γ coactivator 1 β (PGC-1β) and PGC-1-related coactivator, which were down-regulated by HU, PGC-1α was up-regulated concomitant with decreased expression of its DNA binding transcription factors, PPARα, and estrogen-related receptor α (ERRα). Moreover, there was no alteration in expression of nuclear respiratory factor 1, but its downstream target gene, mitochondrial transcription factor A, was down-regulated. Second, both mitofusin 2 and fission 1, which control mitochondrial morphology, were down-regulated. Third, ATP-dependent Lon protease, which participates in mitochondrial-protein degradation, was also down-regulated. These findings suggest that HU may induce uncoordinated expression of PGC-1 family coactivators and DNA binding transcription factors, resulting in reducing ability of mitochondrial biogenesis. Furthermore, down-regulation of mitochondrial morphology-related genes associated with HU may be also involved in alterations in intracellular mitochondrial distribution.",
author = "Akira Wagatsuma and Naoki Kotake and Takayuki Kawachi and Masataka Shiozuka and Shigeru Yamada and Ryoichi Matsuda",
year = "2011",
month = "4",
day = "1",
doi = "10.1007/s11010-010-0677-1",
language = "English",
volume = "350",
pages = "1--11",
journal = "Molecular and Cellular Biochemistry",
issn = "0300-8177",
publisher = "Springer Netherlands",
number = "1-2",

}

TY - JOUR

T1 - Mitochondrial adaptations in skeletal muscle to hindlimb unloading

AU - Wagatsuma, Akira

AU - Kotake, Naoki

AU - Kawachi, Takayuki

AU - Shiozuka, Masataka

AU - Yamada, Shigeru

AU - Matsuda, Ryoichi

PY - 2011/4/1

Y1 - 2011/4/1

N2 - To gain insight into the regulation of mitochondrial adaptations to hindlimb unloading (HU), the activity of mitochondrial enzymes and the expression of nuclear-encoded genes which control mitochondrial properties in mouse gastrocnemius muscle were investigated. Biochemical and enzyme histochemical analysis showed that subsarcolemmal mitochondria were lost largely than intermyofibrillar mitochondria after HU. Gene expression analysis revealed disturbed or diminished gene expression patterns. The three main results of this analysis are as follows. First, in contrast to peroxisome proliferator-activated receptor γ coactivator 1 β (PGC-1β) and PGC-1-related coactivator, which were down-regulated by HU, PGC-1α was up-regulated concomitant with decreased expression of its DNA binding transcription factors, PPARα, and estrogen-related receptor α (ERRα). Moreover, there was no alteration in expression of nuclear respiratory factor 1, but its downstream target gene, mitochondrial transcription factor A, was down-regulated. Second, both mitofusin 2 and fission 1, which control mitochondrial morphology, were down-regulated. Third, ATP-dependent Lon protease, which participates in mitochondrial-protein degradation, was also down-regulated. These findings suggest that HU may induce uncoordinated expression of PGC-1 family coactivators and DNA binding transcription factors, resulting in reducing ability of mitochondrial biogenesis. Furthermore, down-regulation of mitochondrial morphology-related genes associated with HU may be also involved in alterations in intracellular mitochondrial distribution.

AB - To gain insight into the regulation of mitochondrial adaptations to hindlimb unloading (HU), the activity of mitochondrial enzymes and the expression of nuclear-encoded genes which control mitochondrial properties in mouse gastrocnemius muscle were investigated. Biochemical and enzyme histochemical analysis showed that subsarcolemmal mitochondria were lost largely than intermyofibrillar mitochondria after HU. Gene expression analysis revealed disturbed or diminished gene expression patterns. The three main results of this analysis are as follows. First, in contrast to peroxisome proliferator-activated receptor γ coactivator 1 β (PGC-1β) and PGC-1-related coactivator, which were down-regulated by HU, PGC-1α was up-regulated concomitant with decreased expression of its DNA binding transcription factors, PPARα, and estrogen-related receptor α (ERRα). Moreover, there was no alteration in expression of nuclear respiratory factor 1, but its downstream target gene, mitochondrial transcription factor A, was down-regulated. Second, both mitofusin 2 and fission 1, which control mitochondrial morphology, were down-regulated. Third, ATP-dependent Lon protease, which participates in mitochondrial-protein degradation, was also down-regulated. These findings suggest that HU may induce uncoordinated expression of PGC-1 family coactivators and DNA binding transcription factors, resulting in reducing ability of mitochondrial biogenesis. Furthermore, down-regulation of mitochondrial morphology-related genes associated with HU may be also involved in alterations in intracellular mitochondrial distribution.

UR - http://www.scopus.com/inward/record.url?scp=79953696779&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79953696779&partnerID=8YFLogxK

U2 - 10.1007/s11010-010-0677-1

DO - 10.1007/s11010-010-0677-1

M3 - Article

C2 - 21165677

AN - SCOPUS:79953696779

VL - 350

SP - 1

EP - 11

JO - Molecular and Cellular Biochemistry

JF - Molecular and Cellular Biochemistry

SN - 0300-8177

IS - 1-2

ER -