5 Citations (Scopus)

Abstract

This study investigated how lycopene affected urotensin-II- (U-II-) induced cardiomyocyte hypertrophy and the possible implicated mechanisms. Neonatal rat cardiomyocytes were exposed to U-II (1 nM) either exclusively or following 6 h of lycopene pretreatment (1-10 μM). The lycopene (3-10 μM) pretreatment significantly inhibited the U-II-induced cardiomyocyte hypertrophy, decreased the production of U-II-induced reactive oxygen species (ROS), and reduced the level of NAD(P)H oxidase-4 expression. Lycopene further inhibited the U-II-induced phosphorylation of the redox-sensitive extracellular signal-regulated kinases. Moreover, lycopene treatment prevented the increase in the phosphorylation of serine-threonine kinase Akt and glycogen synthase kinase-3beta (GSK-3β) caused by U-II without affecting the protein levels of the phosphatase and tensin homolog deleted on chromosome 10 (PTEN). However, lycopene increased the PTEN activity level, suggesting that lycopene prevents ROS-induced PTEN inactivation. These findings imply that lycopene yields antihypertrophic effects that can prevent the activation of the Akt/GSK-3β hypertrophic pathway by modulating PTEN inactivation through U-II treatment. Thus, the data indicate that lycopene prevented U-II-induced cardiomyocyte hypertrophy through a mechanism involving the inhibition of redox signaling. These findings provide novel data regarding the molecular mechanisms by which lycopene regulates cardiomyocyte hypertrophy.

Original languageEnglish
Article number724670
JournalEvidence-based Complementary and Alternative Medicine
Volume2014
DOIs
Publication statusPublished - 2014

Fingerprint

Cardiac Myocytes
Hypertrophy
Glycogen Synthase Kinases
Oxidation-Reduction
Reactive Oxygen Species
Phosphorylation
lycopene
urotensin II
Chromosomes, Human, Pair 10
NADPH Oxidase
Phosphoprotein Phosphatases
Protein-Serine-Threonine Kinases
Extracellular Signal-Regulated MAP Kinases

ASJC Scopus subject areas

  • Complementary and alternative medicine

Cite this

Lycopene inhibits urotensin-II-induced cardiomyocyte hypertrophy in neonatal rat cardiomyocytes. / Chao, Hung Hsing; Sung, Li-Chin; Chen, Cheng Hsien; Liu, Ju Chi; Chen, Jin Jer; Cheng, Tzu-Hurng.

In: Evidence-based Complementary and Alternative Medicine, Vol. 2014, 724670, 2014.

Research output: Contribution to journalArticle

@article{da3a277a8f2444e49461783aa043b72c,
title = "Lycopene inhibits urotensin-II-induced cardiomyocyte hypertrophy in neonatal rat cardiomyocytes",
abstract = "This study investigated how lycopene affected urotensin-II- (U-II-) induced cardiomyocyte hypertrophy and the possible implicated mechanisms. Neonatal rat cardiomyocytes were exposed to U-II (1 nM) either exclusively or following 6 h of lycopene pretreatment (1-10 μM). The lycopene (3-10 μM) pretreatment significantly inhibited the U-II-induced cardiomyocyte hypertrophy, decreased the production of U-II-induced reactive oxygen species (ROS), and reduced the level of NAD(P)H oxidase-4 expression. Lycopene further inhibited the U-II-induced phosphorylation of the redox-sensitive extracellular signal-regulated kinases. Moreover, lycopene treatment prevented the increase in the phosphorylation of serine-threonine kinase Akt and glycogen synthase kinase-3beta (GSK-3β) caused by U-II without affecting the protein levels of the phosphatase and tensin homolog deleted on chromosome 10 (PTEN). However, lycopene increased the PTEN activity level, suggesting that lycopene prevents ROS-induced PTEN inactivation. These findings imply that lycopene yields antihypertrophic effects that can prevent the activation of the Akt/GSK-3β hypertrophic pathway by modulating PTEN inactivation through U-II treatment. Thus, the data indicate that lycopene prevented U-II-induced cardiomyocyte hypertrophy through a mechanism involving the inhibition of redox signaling. These findings provide novel data regarding the molecular mechanisms by which lycopene regulates cardiomyocyte hypertrophy.",
author = "Chao, {Hung Hsing} and Li-Chin Sung and Chen, {Cheng Hsien} and Liu, {Ju Chi} and Chen, {Jin Jer} and Tzu-Hurng Cheng",
year = "2014",
doi = "10.1155/2014/724670",
language = "English",
volume = "2014",
journal = "Evidence-based Complementary and Alternative Medicine",
issn = "1741-427X",
publisher = "Hindawi Publishing Corporation",

}

TY - JOUR

T1 - Lycopene inhibits urotensin-II-induced cardiomyocyte hypertrophy in neonatal rat cardiomyocytes

AU - Chao, Hung Hsing

AU - Sung, Li-Chin

AU - Chen, Cheng Hsien

AU - Liu, Ju Chi

AU - Chen, Jin Jer

AU - Cheng, Tzu-Hurng

PY - 2014

Y1 - 2014

N2 - This study investigated how lycopene affected urotensin-II- (U-II-) induced cardiomyocyte hypertrophy and the possible implicated mechanisms. Neonatal rat cardiomyocytes were exposed to U-II (1 nM) either exclusively or following 6 h of lycopene pretreatment (1-10 μM). The lycopene (3-10 μM) pretreatment significantly inhibited the U-II-induced cardiomyocyte hypertrophy, decreased the production of U-II-induced reactive oxygen species (ROS), and reduced the level of NAD(P)H oxidase-4 expression. Lycopene further inhibited the U-II-induced phosphorylation of the redox-sensitive extracellular signal-regulated kinases. Moreover, lycopene treatment prevented the increase in the phosphorylation of serine-threonine kinase Akt and glycogen synthase kinase-3beta (GSK-3β) caused by U-II without affecting the protein levels of the phosphatase and tensin homolog deleted on chromosome 10 (PTEN). However, lycopene increased the PTEN activity level, suggesting that lycopene prevents ROS-induced PTEN inactivation. These findings imply that lycopene yields antihypertrophic effects that can prevent the activation of the Akt/GSK-3β hypertrophic pathway by modulating PTEN inactivation through U-II treatment. Thus, the data indicate that lycopene prevented U-II-induced cardiomyocyte hypertrophy through a mechanism involving the inhibition of redox signaling. These findings provide novel data regarding the molecular mechanisms by which lycopene regulates cardiomyocyte hypertrophy.

AB - This study investigated how lycopene affected urotensin-II- (U-II-) induced cardiomyocyte hypertrophy and the possible implicated mechanisms. Neonatal rat cardiomyocytes were exposed to U-II (1 nM) either exclusively or following 6 h of lycopene pretreatment (1-10 μM). The lycopene (3-10 μM) pretreatment significantly inhibited the U-II-induced cardiomyocyte hypertrophy, decreased the production of U-II-induced reactive oxygen species (ROS), and reduced the level of NAD(P)H oxidase-4 expression. Lycopene further inhibited the U-II-induced phosphorylation of the redox-sensitive extracellular signal-regulated kinases. Moreover, lycopene treatment prevented the increase in the phosphorylation of serine-threonine kinase Akt and glycogen synthase kinase-3beta (GSK-3β) caused by U-II without affecting the protein levels of the phosphatase and tensin homolog deleted on chromosome 10 (PTEN). However, lycopene increased the PTEN activity level, suggesting that lycopene prevents ROS-induced PTEN inactivation. These findings imply that lycopene yields antihypertrophic effects that can prevent the activation of the Akt/GSK-3β hypertrophic pathway by modulating PTEN inactivation through U-II treatment. Thus, the data indicate that lycopene prevented U-II-induced cardiomyocyte hypertrophy through a mechanism involving the inhibition of redox signaling. These findings provide novel data regarding the molecular mechanisms by which lycopene regulates cardiomyocyte hypertrophy.

UR - http://www.scopus.com/inward/record.url?scp=84902121569&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84902121569&partnerID=8YFLogxK

U2 - 10.1155/2014/724670

DO - 10.1155/2014/724670

M3 - Article

AN - SCOPUS:84902121569

VL - 2014

JO - Evidence-based Complementary and Alternative Medicine

JF - Evidence-based Complementary and Alternative Medicine

SN - 1741-427X

M1 - 724670

ER -