Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

Difference between revisions of "Remels 2010 Mol Cell Endocrinol"

From Bioblast
Β 
(7 intermediate revisions by 6 users not shown)
Line 1: Line 1:
{{Publication
{{Publication
|title=Remels AH, Langen RC, Schrauwen P, Schaart G, Schols AM, Gosker HR (2010) Regulation of mitochondrial biogenesis during myogenesis. Mol Cell Endocrinol 315: 113-120.
|title=Remels AH, Langen RC, Schrauwen P, Schaart G, Schols AM, Gosker HR (2010) Regulation of mitochondrial biogenesis during myogenesis. Mol Cell Endocrinol 315:113-20.
|info=[http://peer.ccsd.cnrs.fr/docs/00/54/76/58/PDF/PEER_stage2_10.1016%252Fj.mce.2009.09.029.pdf PMID: 19804813 pdf]
|info=[http://www.ncbi.nlm.nih.gov/pubmed/19804813 PMID:19804813]
|authors=Remels AH, Langen RC, Schrauwen P, Schaart G, Schols AM, Gosker HR
|authors=Remels AH, Langen RC, Schrauwen P, Schaart G, Schols AM, Gosker HR
|year=2010
|year=2010
|journal=Mol Cell Endocrinol
|journal=Mol Cell Endocrinol
|abstract=Pathways involved in mitochondrial biogenesis associated with myogenic differentiation are poorly defined. Therefore, C(2)C(12) myoblasts were differentiated into multi-nucleated myotubes and parameters/regulators of mitochondrial biogenesis were investigated. Mitochondrial respiration, citrate synthase- and beta-hydroxyacyl-CoA dehydrogenase activity as well as protein content of complexes I, II, III and V of the mitochondrial respiratory chain increased 4-8-fold during differentiation. Additionally, an increase in the ratio of myosin heavy chain (MyHC) slow vs MyHC fast protein content was observed. PPAR transcriptional activity and transcript levels of PPAR-alpha, the PPAR co-activator [[PGC-1alpha]], mitochondrial transcription factor A and nuclear respiratory factor 1 increased during differentiation while expression levels of PPAR-gamma decreased. In conclusion, expression and activity levels of genes known for their regulatory role in skeletal muscle oxidative capabilities parallel the increase in oxidative parameters during the myogenic program. In particular, [[PGC-1alpha]] and PPAR-alpha may be involved in the regulation of mitochondrial biogenesis during myogenesis.
|abstract=Pathways involved in mitochondrial biogenesis associated with myogenic differentiation are poorly defined. Therefore, C(2)C(12) myoblasts were differentiated into multi-nucleated myotubes and parameters/regulators of mitochondrial biogenesis were investigated. Mitochondrial respiration, citrate synthase- and beta-hydroxyacyl-CoA dehydrogenase activity as well as protein content of complexes I, II, III and V of the mitochondrial respiratory chain increased 4-8-fold during differentiation. Additionally, an increase in the ratio of myosin heavy chain (MyHC) slow vs MyHC fast protein content was observed. PPAR transcriptional activity and transcript levels of PPAR-alpha, the PPAR co-activator [[PGC-1alpha]], mitochondrial transcription factor A and nuclear respiratory factor 1 increased during differentiation while expression levels of PPAR-gamma decreased. In conclusion, expression and activity levels of genes known for their regulatory role in skeletal muscle oxidative capabilities parallel the increase in oxidative parameters during the myogenic program. In particular, [[PGC-1alpha]] and PPAR-alpha may be involved in the regulation of mitochondrial biogenesis during myogenesis.
|keywords=Peroxisome, proliferator-activated, receptors, myogenesis, mitochondrial transcription factor A, nuclear respiratory factor 1, skeletal muscle
|keywords=Peroxisome, Proliferator-activated, Receptors, Myogenesis, Mitochondrial transcription factor A, Nuclear respiratory factor 1, Skeletal muscle, C2C12 cells, L6 muscle cells
|mipnetlab=NL Maastricht Schrauwen P
|mipnetlab=NL Maastricht Schrauwen P
}}
}}
{{Labeling
{{Labeling
|area=Respiration
|organism=Mouse, Rat
|tissues=Skeletal muscle, Other cell lines
|preparations=Permeabilized cells
|couplingstates=ROUTINE, OXPHOS, ET
|pathways=F
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|tissues=Skeletal muscle
|preparations=Intact Cell; Cultured; Primary
|couplingstates=OXPHOS
}}
}}

Latest revision as of 15:46, 13 November 2017

Publications in the MiPMap
Remels AH, Langen RC, Schrauwen P, Schaart G, Schols AM, Gosker HR (2010) Regulation of mitochondrial biogenesis during myogenesis. Mol Cell Endocrinol 315:113-20.

Β» PMID:19804813

Remels AH, Langen RC, Schrauwen P, Schaart G, Schols AM, Gosker HR (2010) Mol Cell Endocrinol

Abstract: Pathways involved in mitochondrial biogenesis associated with myogenic differentiation are poorly defined. Therefore, C(2)C(12) myoblasts were differentiated into multi-nucleated myotubes and parameters/regulators of mitochondrial biogenesis were investigated. Mitochondrial respiration, citrate synthase- and beta-hydroxyacyl-CoA dehydrogenase activity as well as protein content of complexes I, II, III and V of the mitochondrial respiratory chain increased 4-8-fold during differentiation. Additionally, an increase in the ratio of myosin heavy chain (MyHC) slow vs MyHC fast protein content was observed. PPAR transcriptional activity and transcript levels of PPAR-alpha, the PPAR co-activator PGC-1alpha, mitochondrial transcription factor A and nuclear respiratory factor 1 increased during differentiation while expression levels of PPAR-gamma decreased. In conclusion, expression and activity levels of genes known for their regulatory role in skeletal muscle oxidative capabilities parallel the increase in oxidative parameters during the myogenic program. In particular, PGC-1alpha and PPAR-alpha may be involved in the regulation of mitochondrial biogenesis during myogenesis. β€’ Keywords: Peroxisome, Proliferator-activated, Receptors, Myogenesis, Mitochondrial transcription factor A, Nuclear respiratory factor 1, Skeletal muscle, C2C12 cells, L6 muscle cells

β€’ O2k-Network Lab: NL Maastricht Schrauwen P


Labels: MiParea: Respiration 


Organism: Mouse, Rat  Tissue;cell: Skeletal muscle, Other cell lines  Preparation: Permeabilized cells 


Coupling state: ROUTINE, OXPHOS, ET  Pathway:HRR: Oxygraph-2k