Local GHR roles in regulation of mitochondrial function through mitochondrial biogenesis during myoblast differentiation.

Proto-Oncogene Proteins c-akt / metabolism Organelle Biogenesis Phosphatidylinositol 3-Kinases / metabolism Mitochondria / metabolism DNA, Mitochondrial / genetics Myoblasts / metabolism
GHR IGF1 Mitochondrial biogenesis Mitochondrial function Myoblast differentiation

Journal

Cell communication and signaling : CCS
ISSN: 1478-811X
Titre abrégé: Cell Commun Signal
Pays: England
ID NLM: 101170464

Informations de publication

Date de publication:
19 06 2023
Historique:
received: 06 03 2023
accepted: 13 05 2023
medline: 21 6 2023
pubmed: 20 6 2023
entrez: 19 6 2023
Statut: epublish

Résumé

Myoblast differentiation requires metabolic reprogramming driven by increased mitochondrial biogenesis and oxidative phosphorylation. The canonical GH-GHR-IGFs axis in liver exhibits a great complexity in response to somatic growth. However, the underlying mechanism of whether local GHR acts as a control valve to regulate mitochondrial function through mitochondrial biogenesis during myoblast differentiation remains unknown. We manipulated the GHR expression in chicken primary myoblast to investigate its roles in mitochondrial biogenesis and function during myoblast differentiation. We reported that GHR is induced during myoblast differentiation. Local GHR promoted mitochondrial biogenesis during myoblast differentiation, as determined by the fluorescence intensity of Mito-Tracker Green staining and MitoTimer reporter system, the expression of mitochondrial biogenesis markers (PGC1α, NRF1, TFAM) and mtDNA encoded gene (ND1, CYTB, COX1, ATP6), as well as mtDNA content. Consistently, local GHR enhanced mitochondrial function during myoblast differentiation, as determined by the oxygen consumption rate, mitochondrial membrane potential, ATP level and ROS production. We next revealed that the regulation of mitochondrial biogenesis and function by GHR depends on IGF1. In terms of the underlying mechanism, we demonstrated that IGF1 regulates mitochondrial biogenesis via PI3K/AKT/CREB pathway. Additionally, GHR knockdown repressed myoblast differentiation. In conclusion, our data corroborate that local GHR acts as a control valve to enhance mitochondrial function by promoting mitochondrial biogenesis via IGF1-PI3K/AKT/CREB pathway during myoblast differentiation. Video Abstract.

Sections du résumé

BACKGROUND
Myoblast differentiation requires metabolic reprogramming driven by increased mitochondrial biogenesis and oxidative phosphorylation. The canonical GH-GHR-IGFs axis in liver exhibits a great complexity in response to somatic growth. However, the underlying mechanism of whether local GHR acts as a control valve to regulate mitochondrial function through mitochondrial biogenesis during myoblast differentiation remains unknown.
METHODS
We manipulated the GHR expression in chicken primary myoblast to investigate its roles in mitochondrial biogenesis and function during myoblast differentiation.
RESULTS
We reported that GHR is induced during myoblast differentiation. Local GHR promoted mitochondrial biogenesis during myoblast differentiation, as determined by the fluorescence intensity of Mito-Tracker Green staining and MitoTimer reporter system, the expression of mitochondrial biogenesis markers (PGC1α, NRF1, TFAM) and mtDNA encoded gene (ND1, CYTB, COX1, ATP6), as well as mtDNA content. Consistently, local GHR enhanced mitochondrial function during myoblast differentiation, as determined by the oxygen consumption rate, mitochondrial membrane potential, ATP level and ROS production. We next revealed that the regulation of mitochondrial biogenesis and function by GHR depends on IGF1. In terms of the underlying mechanism, we demonstrated that IGF1 regulates mitochondrial biogenesis via PI3K/AKT/CREB pathway. Additionally, GHR knockdown repressed myoblast differentiation.
CONCLUSIONS
In conclusion, our data corroborate that local GHR acts as a control valve to enhance mitochondrial function by promoting mitochondrial biogenesis via IGF1-PI3K/AKT/CREB pathway during myoblast differentiation. Video Abstract.

Identifiants

DOI: 10.1186/s12964-023-01166-5 PMID: 37337300 PMC: PMC10278349
pubmed: 37337300
doi: 10.1186/s12964-023-01166-5
pii: 10.1186/s12964-023-01166-5
pmc: PMC10278349
doi:

Substances chimiques

Proto-Oncogene Proteins c-akt EC 2.7.11.1
Phosphatidylinositol 3-Kinases EC 2.7.1.-
DNA, Mitochondrial 0

Types de publication

Video-Audio Media Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

148

Informations de copyright

© 2023. The Author(s).

Références

Cell Struct Funct. 1997 Aug;22(4):421-31
pubmed: 9368716
Front Cell Dev Biol. 2021 Mar 18;9:630248
pubmed: 33816476
J Cell Physiol. 2006 Apr;207(1):75-86
pubmed: 16261590
Proc Natl Acad Sci U S A. 2006 May 9;103(19):7315-20
pubmed: 16670201
Poult Sci. 2016 Jun 1;95(6):1396-402
pubmed: 26944971
Cell Death Dis. 2014 Jul 17;5:e1347
pubmed: 25032870
Mol Cell Endocrinol. 2010 Feb 5;315(1-2):113-20
pubmed: 19804813
Cell Prolif. 2006 Apr;39(2):127-45
pubmed: 16542348
Am J Physiol Cell Physiol. 2016 Aug 1;311(2):C190-200
pubmed: 27281480
Autophagy. 2016;12(2):369-80
pubmed: 26566717
Proc Natl Acad Sci U S A. 1999 Jun 22;96(13):7324-9
pubmed: 10377413
Eur J Cell Biol. 1993 Aug;61(2):400-8
pubmed: 8223726
J Cell Mol Med. 2021 Mar;25(5):2450-2458
pubmed: 33492754
PLoS One. 2011;6(9):e24714
pubmed: 21931825
Free Radic Biol Med. 2011 Sep 15;51(6):1106-15
pubmed: 21762777
Diabetes. 2007 Jun;56(6):1592-9
pubmed: 17351150
J Biol Chem. 1998 Dec 4;273(49):32377-9
pubmed: 9829964
Mol Genet Metab. 2000 Sep-Oct;71(1-2):293-314
pubmed: 11001823
Nat Rev Endocrinol. 2018 May;14(5):285-300
pubmed: 29546874
Int J Mol Sci. 2019 Mar 31;20(7):
pubmed: 30935132
J Biol Chem. 2001 Oct 19;276(42):39264-70
pubmed: 11500504
FEBS J. 2015 Feb;282(4):647-72
pubmed: 25495651
Development. 2017 Jun 15;144(12):2104-2122
pubmed: 28634270
Growth Horm IGF Res. 2022 Aug;65:101478
pubmed: 35717687
J Cell Mol Med. 2020 May;24(9):4892-4899
pubmed: 32279443
Biosci Rep. 2015 May 19;35(3):
pubmed: 26182383
Autophagy. 2019 Sep;15(9):1606-1619
pubmed: 30859901
Int J Mol Sci. 2016 Feb 24;17(3):276
pubmed: 26927061
Endocrinology. 1997 Oct;138(10):4301-7
pubmed: 9322943
Autophagy. 2019 Jul;15(7):1182-1198
pubmed: 30741592
Nature. 2001 Sep 13;413(6852):179-83
pubmed: 11557984
Endocrinology. 2005 Feb;146(2):851-60
pubmed: 15498882
Dev Cell. 2018 Jul 16;46(2):135-143
pubmed: 30016618
J Biol Chem. 2014 Apr 25;289(17):12005-12015
pubmed: 24644293
Trends Endocrinol Metab. 2012 Sep;23(9):459-66
pubmed: 22817841
Oncotarget. 2016 Nov 8;7(45):73607-73617
pubmed: 27713155
Endocrinology. 1987 Feb;120(2):651-8
pubmed: 3803295
Physiol Rev. 2008 Apr;88(2):611-38
pubmed: 18391175
J Clin Invest. 2010 Nov;120(11):4007-20
pubmed: 20921627
Int J Biochem Cell Biol. 2008;40(10):1984-9
pubmed: 17888716
J Bone Miner Res. 2019 Jan;34(1):106-122
pubmed: 30216544
Mitochondrion. 2019 Nov;49:156-165
pubmed: 31419493
Cell Mol Life Sci. 2021 May;78(10):4653-4675
pubmed: 33751143
Eur J Neurosci. 2012 Oct;36(7):2899-905
pubmed: 22817531
Nat Rev Endocrinol. 2013 Jun;9(6):366-376
pubmed: 23591370
Biochim Biophys Acta. 2015 Jun-Jul;1847(6-7):544-57
pubmed: 25766847
Biochim Biophys Acta. 1993 Mar 24;1181(1):63-7
pubmed: 7681329
Annu Rev Cell Biol. 1988;4:289-333
pubmed: 2461720
Exp Cell Res. 2004 Sep 10;299(1):27-35
pubmed: 15302570
Endocr Rev. 1995 Feb;16(1):3-34
pubmed: 7758431
PLoS One. 2013 May 21;8(5):e62235
pubmed: 23704876
J Biol Chem. 2017 Oct 13;292(41):16983-16998
pubmed: 28821609
J Physiol. 2003 Oct 15;552(Pt 2):335-44
pubmed: 14561818
Gen Comp Endocrinol. 1996 Jan;101(1):43-52
pubmed: 8713643
Autophagy. 2013 Nov 1;9(11):1663-76
pubmed: 23787782
J Biol Chem. 2000 Jan 28;275(4):2733-44
pubmed: 10644737
Am J Physiol Cell Physiol. 2006 Apr;290(4):C1119-27
pubmed: 16531567
Science. 1992 Jan 17;255(5042):306-12
pubmed: 1549776
J Biol Chem. 1993 Apr 5;268(10):7358-64
pubmed: 8385105
Proc Natl Acad Sci U S A. 1999 Jun 8;96(12):7088-92
pubmed: 10359843
Am J Physiol Endocrinol Metab. 2007 Jun;292(6):E1647-55
pubmed: 17284572
Gen Comp Endocrinol. 2015 Jun-Jul;217-218:1-9
pubmed: 25957918
J Gerontol A Biol Sci Med Sci. 2011 Oct;66(10):1062-76
pubmed: 21788651
Oxid Med Cell Longev. 2019 Dec 24;2019:7838754
pubmed: 31949883
Anat Embryol (Berl). 2003 Jul;207(1):73-84
pubmed: 12743812
Exp Gerontol. 2009 Jan-Feb;44(1-2):10-9
pubmed: 18675334
Mol Metab. 2020 Jun;36:100978
pubmed: 32277923
Mol Cell Biol. 2005 Feb;25(4):1354-66
pubmed: 15684387
Cell Signal. 2003 Jun;15(6):615-23
pubmed: 12681449
Comp Biochem Physiol A Comp Physiol. 1991;99(1-2):207-14
pubmed: 1675947
Science. 1956 Feb 24;123(3191):309-14
pubmed: 13298683

Auteurs

Bowen Hu (B)

State Key Laboratory of Livestock and Poultry Breeding, South China Agricultural University, Guangzhou, Guangdong, China.
State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources and Lingnan Guangdong Laboratory of Agriculture, South China Agricultural University, Guangzhou, Guangdong, China.
Department of Animal Genetics, Breeding and Reproduction, College of Animal Science, South China Agricultural University, Guangzhou, Guangdong, China.

Changbin Zhao (C)

State Key Laboratory of Livestock and Poultry Breeding, South China Agricultural University, Guangzhou, Guangdong, China.
State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources and Lingnan Guangdong Laboratory of Agriculture, South China Agricultural University, Guangzhou, Guangdong, China.
Department of Animal Genetics, Breeding and Reproduction, College of Animal Science, South China Agricultural University, Guangzhou, Guangdong, China.

Xiangchun Pan (X)

Department of Animal Genetics, Breeding and Reproduction, College of Animal Science, South China Agricultural University, Guangzhou, Guangdong, China.

Haohui Wei (H)

State Key Laboratory of Livestock and Poultry Breeding, South China Agricultural University, Guangzhou, Guangdong, China.
State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources and Lingnan Guangdong Laboratory of Agriculture, South China Agricultural University, Guangzhou, Guangdong, China.
Department of Animal Genetics, Breeding and Reproduction, College of Animal Science, South China Agricultural University, Guangzhou, Guangdong, China.

Guodong Mo (G)

State Key Laboratory of Livestock and Poultry Breeding, South China Agricultural University, Guangzhou, Guangdong, China.
State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources and Lingnan Guangdong Laboratory of Agriculture, South China Agricultural University, Guangzhou, Guangdong, China.
Department of Animal Genetics, Breeding and Reproduction, College of Animal Science, South China Agricultural University, Guangzhou, Guangdong, China.

Mingjian Xian (M)

State Key Laboratory of Livestock and Poultry Breeding, South China Agricultural University, Guangzhou, Guangdong, China.
State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources and Lingnan Guangdong Laboratory of Agriculture, South China Agricultural University, Guangzhou, Guangdong, China.
Department of Animal Genetics, Breeding and Reproduction, College of Animal Science, South China Agricultural University, Guangzhou, Guangdong, China.

Wen Luo (W)

State Key Laboratory of Livestock and Poultry Breeding, South China Agricultural University, Guangzhou, Guangdong, China.
State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources and Lingnan Guangdong Laboratory of Agriculture, South China Agricultural University, Guangzhou, Guangdong, China.
Department of Animal Genetics, Breeding and Reproduction, College of Animal Science, South China Agricultural University, Guangzhou, Guangdong, China.

Qinghua Nie (Q)

State Key Laboratory of Livestock and Poultry Breeding, South China Agricultural University, Guangzhou, Guangdong, China.
State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources and Lingnan Guangdong Laboratory of Agriculture, South China Agricultural University, Guangzhou, Guangdong, China.
Department of Animal Genetics, Breeding and Reproduction, College of Animal Science, South China Agricultural University, Guangzhou, Guangdong, China.

Hongmei Li (H)

State Key Laboratory of Livestock and Poultry Breeding, South China Agricultural University, Guangzhou, Guangdong, China.
State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources and Lingnan Guangdong Laboratory of Agriculture, South China Agricultural University, Guangzhou, Guangdong, China.
Department of Animal Genetics, Breeding and Reproduction, College of Animal Science, South China Agricultural University, Guangzhou, Guangdong, China.

Xiquan Zhang (X)

State Key Laboratory of Livestock and Poultry Breeding, South China Agricultural University, Guangzhou, Guangdong, China. xqzhang@scau.edu.cn.
State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources and Lingnan Guangdong Laboratory of Agriculture, South China Agricultural University, Guangzhou, Guangdong, China. xqzhang@scau.edu.cn.
Department of Animal Genetics, Breeding and Reproduction, College of Animal Science, South China Agricultural University, Guangzhou, Guangdong, China. xqzhang@scau.edu.cn.

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Classifications MeSH

questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines tumorales › Protéines oncogènes › Protéines proto-oncogènes › Protéines proto-oncogènes c-akt › Local GHR roles in regulation of mitochondrial...
questionsmedicales.fr › Phénomènes biologiques › Biogenèse des organelles › Local GHR roles in regulation of mitochondrial...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines et peptides de signalisation intracellulaire › Phosphatidylinositol 3-kinases › Local GHR roles in regulation of mitochondrial...
questionsmedicales.fr › Cellules › Structures cellulaires › Fractions subcellulaires › Mitochondries › Local GHR roles in regulation of mitochondrial...
questionsmedicales.fr › Acides nucléiques, nucléotides et nucléosides › Acides nucléiques › ADN › ADN mitochondrial › Local GHR roles in regulation of mitochondrial...
questionsmedicales.fr › Cellules › Cellules souches › Myoblastes › Local GHR roles in regulation of mitochondrial...