Tags

Type your tag names separated by a space and hit enter

Erythropoietin enhances mitochondrial biogenesis in cardiomyocytes exposed to chronic hypoxia through Akt/eNOS signalling pathway.
Cell Biol Int. 2014 Mar; 38(3):335-42.CB

Abstract

Adaptation of cardiomyocytes to chronic hypoxia in cyanotic patients remains unclear. Mitochondrial biogenesis is enhanced in myocardium from cyanotic patients, which is possibly an adaptive response. Erythropoietin (EPO) in blood and its receptor (EPOR) on cardiomyocytes are upregulated by chronic hypoxia, suggesting that EPO-EPOR interaction is increased, which is inferred to positively regulate mitochondrial biogenesis through protein kinase B (Akt)/endothelial nitric oxide synthase (eNOS) signalling pathway. H9c2 cardiomyocytes were exposed to hypoxia (1% O(2)) for 1 week and treated with different doses of recombinant human erythropoietin (rhEPO). Mitochondrial number, mitochondrial DNA (mtDNA) copy number and peroxisome proliferator activated receptor gamma coactivator alpha (PGC-1α) mRNA expression increased in a dose-dependent manner induced by rhEPO. Akt and eNOS were significantly phosphorylated by rhEPO. Both blocking Akt with Wortmannin and silencing eNOS expression with shRNA plasmid decreased the mtDNA copy number and PGC-1α mRNA expression induced by rhEPO. Blocking Akt was associated with the decreased phosphorylation of Akt and eNOS. RNA interference led to a reduction in the total and phosphorylated proteins of eNOS. Thus EPO enhances mitochondrial biogenesis in cardiomyocytes exposed to chronic hypoxia, at least partly through Akt/eNOS signalling, which might be an adaptive mechanism of cardiomyocytes associated with the increased EPO-EPOR interaction in patients with cyanotic congenital heart disease (CCHD).

Authors+Show Affiliations

Department of Cardiovascular Surgery, Xinqiao Hospital, The Third Military Medical University, Chongqing, China.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

24436050

Citation

Qin, Chuan, et al. "Erythropoietin Enhances Mitochondrial Biogenesis in Cardiomyocytes Exposed to Chronic Hypoxia Through Akt/eNOS Signalling Pathway." Cell Biology International, vol. 38, no. 3, 2014, pp. 335-42.
Qin C, Zhou S, Xiao Y, et al. Erythropoietin enhances mitochondrial biogenesis in cardiomyocytes exposed to chronic hypoxia through Akt/eNOS signalling pathway. Cell Biol Int. 2014;38(3):335-42.
Qin, C., Zhou, S., Xiao, Y., & Chen, L. (2014). Erythropoietin enhances mitochondrial biogenesis in cardiomyocytes exposed to chronic hypoxia through Akt/eNOS signalling pathway. Cell Biology International, 38(3), 335-42. https://doi.org/10.1002/cbin.10205
Qin C, et al. Erythropoietin Enhances Mitochondrial Biogenesis in Cardiomyocytes Exposed to Chronic Hypoxia Through Akt/eNOS Signalling Pathway. Cell Biol Int. 2014;38(3):335-42. PubMed PMID: 24436050.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Erythropoietin enhances mitochondrial biogenesis in cardiomyocytes exposed to chronic hypoxia through Akt/eNOS signalling pathway. AU - Qin,Chuan, AU - Zhou,Shengkai, AU - Xiao,Yingbin, AU - Chen,Lin, Y1 - 2014/01/16/ PY - 2013/08/21/received PY - 2013/10/27/accepted PY - 2014/1/18/entrez PY - 2014/1/18/pubmed PY - 2014/10/15/medline KW - caridiomyocyte KW - chronic hypoxia KW - endothelial nitric oxide synthase KW - erythropoietin KW - protein kinase B SP - 335 EP - 42 JF - Cell biology international JO - Cell Biol. Int. VL - 38 IS - 3 N2 - Adaptation of cardiomyocytes to chronic hypoxia in cyanotic patients remains unclear. Mitochondrial biogenesis is enhanced in myocardium from cyanotic patients, which is possibly an adaptive response. Erythropoietin (EPO) in blood and its receptor (EPOR) on cardiomyocytes are upregulated by chronic hypoxia, suggesting that EPO-EPOR interaction is increased, which is inferred to positively regulate mitochondrial biogenesis through protein kinase B (Akt)/endothelial nitric oxide synthase (eNOS) signalling pathway. H9c2 cardiomyocytes were exposed to hypoxia (1% O(2)) for 1 week and treated with different doses of recombinant human erythropoietin (rhEPO). Mitochondrial number, mitochondrial DNA (mtDNA) copy number and peroxisome proliferator activated receptor gamma coactivator alpha (PGC-1α) mRNA expression increased in a dose-dependent manner induced by rhEPO. Akt and eNOS were significantly phosphorylated by rhEPO. Both blocking Akt with Wortmannin and silencing eNOS expression with shRNA plasmid decreased the mtDNA copy number and PGC-1α mRNA expression induced by rhEPO. Blocking Akt was associated with the decreased phosphorylation of Akt and eNOS. RNA interference led to a reduction in the total and phosphorylated proteins of eNOS. Thus EPO enhances mitochondrial biogenesis in cardiomyocytes exposed to chronic hypoxia, at least partly through Akt/eNOS signalling, which might be an adaptive mechanism of cardiomyocytes associated with the increased EPO-EPOR interaction in patients with cyanotic congenital heart disease (CCHD). SN - 1095-8355 UR - https://www.unboundmedicine.com/medline/citation/24436050/Erythropoietin_enhances_mitochondrial_biogenesis_in_cardiomyocytes_exposed_to_chronic_hypoxia_through_Akt/eNOS_signalling_pathway_ L2 - https://doi.org/10.1002/cbin.10205 DB - PRIME DP - Unbound Medicine ER -