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Transfection by eukaryotic expression vector pcDNA3-HERG inhibits the cultured neonatal rabbit ventricular myocyte hypertrophy induced by phenylephrine.
Cardiovasc Pathol. 2012 Jul-Aug; 21(4):339-45.CP

Abstract

OBJECTIVE

Prolonged action potential and decreased outward K(+) currents are consistent findings in hypertrophic myocardium. The relation between action potential prolongation and myocyte hypertrophy has remained unclear. The present study investigated the temporal relation between action potential prolongation and myocyte hypertrophy, and the effect of enhancing repolarization on myocyte hypertrophy induced by phenylephrine.

METHODS

Neonatal rabbit ventricular myocytes were cultured and treated with 10 μmol/l phenylephrine. At 6 and 48 h after phenylephrine stimulation, myocyte hypertrophic parameters (including myocyte volume, total protein content, and membrane capacitance), action potential duration (APD), and calcineurin activity were measured; meanwhile, the effect of human-ether-a-go-go-related gene (HERG; encoding the αsubunit of rapidly activating delayed rectifier potassium channel) transfection on the above parameters at 48 h of phenylephrine stimulation was also measured.

RESULTS

At 6 h after phenylephrine treatment, APD at 90% repolarization of neonatal rabbit ventricular myocytes was prolonged by 14.3% (P<.05), but myocyte hypertrophy was not found. At 48 h after phenylephrine stimulation, APD at 90% repolarization of neonatal rabbit ventricular myocytes was furthermore prolonged by 18.8% (P<.05); at the same time, myocyte volume, total protein content, membrane capacitance, and calcineurin activity were increased by 40.0%, 41.8%, 36.4%, and 124.1%, respectively (P<.01). Neonatal rabbit ventricular myocytes transfected by pcDNA3-HERG overexpressed I(HERG,tail) current, which was about fourfold higher than I(Kr) (rapidly activating delayed rectifier K(+) current) of neonatal rabbit ventricular myocytes without transfection of HERG. HERG overexpression could accelerate repolarization and shorten APD at 90% repolarization prolonged by phenylephrine and partially inhibit myocyte hypertrophy and calcineurin activation.

CONCLUSIONS

During the myocyte hypertrophy induced by phenylephrine, prolongation of APD at 90% repolarization is not secondary to but precedes myocyte hypertrophy. HERG overexpression could enhance the repolarization and inhibit the calcineurin activation and myocyte hypertrophy induced by phenylephrine.

Authors+Show Affiliations

Department of Cardiology, Henan Provincial People's Hospital, Zhengzhou 450003, PR China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

22100990

Citation

Zhao, Yonghui, et al. "Transfection By Eukaryotic Expression Vector pcDNA3-HERG Inhibits the Cultured Neonatal Rabbit Ventricular Myocyte Hypertrophy Induced By Phenylephrine." Cardiovascular Pathology : the Official Journal of the Society for Cardiovascular Pathology, vol. 21, no. 4, 2012, pp. 339-45.
Zhao Y, Xu Y, Cui C, et al. Transfection by eukaryotic expression vector pcDNA3-HERG inhibits the cultured neonatal rabbit ventricular myocyte hypertrophy induced by phenylephrine. Cardiovasc Pathol. 2012;21(4):339-45.
Zhao, Y., Xu, Y., Cui, C., Li, Y., & Zeng, Y. (2012). Transfection by eukaryotic expression vector pcDNA3-HERG inhibits the cultured neonatal rabbit ventricular myocyte hypertrophy induced by phenylephrine. Cardiovascular Pathology : the Official Journal of the Society for Cardiovascular Pathology, 21(4), 339-45. https://doi.org/10.1016/j.carpath.2011.09.006
Zhao Y, et al. Transfection By Eukaryotic Expression Vector pcDNA3-HERG Inhibits the Cultured Neonatal Rabbit Ventricular Myocyte Hypertrophy Induced By Phenylephrine. Cardiovasc Pathol. 2012 Jul-Aug;21(4):339-45. PubMed PMID: 22100990.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Transfection by eukaryotic expression vector pcDNA3-HERG inhibits the cultured neonatal rabbit ventricular myocyte hypertrophy induced by phenylephrine. AU - Zhao,Yonghui, AU - Xu,Yu, AU - Cui,Changcong, AU - Li,Yu, AU - Zeng,Yanjun, Y1 - 2011/11/18/ PY - 2010/08/06/received PY - 2011/08/11/revised PY - 2011/09/26/accepted PY - 2011/11/22/entrez PY - 2011/11/22/pubmed PY - 2012/11/14/medline SP - 339 EP - 45 JF - Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology JO - Cardiovasc Pathol VL - 21 IS - 4 N2 - OBJECTIVE: Prolonged action potential and decreased outward K(+) currents are consistent findings in hypertrophic myocardium. The relation between action potential prolongation and myocyte hypertrophy has remained unclear. The present study investigated the temporal relation between action potential prolongation and myocyte hypertrophy, and the effect of enhancing repolarization on myocyte hypertrophy induced by phenylephrine. METHODS: Neonatal rabbit ventricular myocytes were cultured and treated with 10 μmol/l phenylephrine. At 6 and 48 h after phenylephrine stimulation, myocyte hypertrophic parameters (including myocyte volume, total protein content, and membrane capacitance), action potential duration (APD), and calcineurin activity were measured; meanwhile, the effect of human-ether-a-go-go-related gene (HERG; encoding the αsubunit of rapidly activating delayed rectifier potassium channel) transfection on the above parameters at 48 h of phenylephrine stimulation was also measured. RESULTS: At 6 h after phenylephrine treatment, APD at 90% repolarization of neonatal rabbit ventricular myocytes was prolonged by 14.3% (P<.05), but myocyte hypertrophy was not found. At 48 h after phenylephrine stimulation, APD at 90% repolarization of neonatal rabbit ventricular myocytes was furthermore prolonged by 18.8% (P<.05); at the same time, myocyte volume, total protein content, membrane capacitance, and calcineurin activity were increased by 40.0%, 41.8%, 36.4%, and 124.1%, respectively (P<.01). Neonatal rabbit ventricular myocytes transfected by pcDNA3-HERG overexpressed I(HERG,tail) current, which was about fourfold higher than I(Kr) (rapidly activating delayed rectifier K(+) current) of neonatal rabbit ventricular myocytes without transfection of HERG. HERG overexpression could accelerate repolarization and shorten APD at 90% repolarization prolonged by phenylephrine and partially inhibit myocyte hypertrophy and calcineurin activation. CONCLUSIONS: During the myocyte hypertrophy induced by phenylephrine, prolongation of APD at 90% repolarization is not secondary to but precedes myocyte hypertrophy. HERG overexpression could enhance the repolarization and inhibit the calcineurin activation and myocyte hypertrophy induced by phenylephrine. SN - 1879-1336 UR - https://www.unboundmedicine.com/medline/citation/22100990/Transfection_by_eukaryotic_expression_vector_pcDNA3_HERG_inhibits_the_cultured_neonatal_rabbit_ventricular_myocyte_hypertrophy_induced_by_phenylephrine_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1054-8807(11)00109-8 DB - PRIME DP - Unbound Medicine ER -