Abstract:
OBJECTIVE:To investigate whether the glycoprotein (gp130)-mediated survival pathway, which protects cardiomyocytes from apoptosis, is depressed in left ventricular hypertrophy hypertensive patients with chronic heart failure. METHODS:Transvenous endomyocardial biopsies were obtained in 52 hypertensive patients with left ventricular hypertrophy: 28 without heart failure and 24 with heart failure. gp130 and gp130-dependent antiapoptotic pathways p42/44 mitogen-activated protein kinase (MAPK) and phosphatidylinositol-3 kinase (PI3K)/protein kinase B (Akt) as well as gp130 agonist cardiotrophin-1 were analyzed by reverse transcriptase-polymerase chain reaction and western blot. Apoptosis was assessed by DNA end-labeling (TUNEL), caspase-3 immunostaining and caspase substrate poly(ADP-ribose) polymerase cleavage. RESULTS:gp130 protein expression (P < 0.05) and p42/44 MAPK and PI3K/Akt activation (P < 0.01) were decreased in heart-failure hypertensive patients compared with nonheart-failure hypertensive individuals. No changes in gp130 mRNA expression were found between the two groups. Cardiotrophin-1 was increased (P < 0.05) at both the mRNA and protein levels in heart-failure hypertensive individuals compared with nonheart-failure hypertensive individuals. Cardiomyocyte apoptosis was increased (P < 0.01) in heart-failure hypertensive individuals compared with nonheart-failure hypertensive individuals. Inverse correlations (P < 0.01) occurred between cardiomyocyte apoptosis and p42/44 MAPK and PI3K/Akt activation in all hypertensive patients. Cardiotrophin-1 correlated inversely (r = -0.554, P < 0.05) with gp130 in all hypertensive individuals. In cultured HL-1 cardiomyocytes, cardiotrophin-1 decreased (P < 0.05) the gp130:phosphorylated gp130 (at Ser782) ratio and increased (P < 0.05) gp130ubiquitination. CONCLUSIONS:An association exists between depression of the gp130 cytoprotective pathway and stimulation of cardiomyocyte apoptosis in hypertensive patients that develop heart failure. Whether the excess of cardiotrophin-1 induces ligand-induced receptor down-regulation in these patients requires further study.
journal_name
J Hypertensjournal_title
Journal of hypertensionauthors
González A,Ravassa S,Loperena I,López B,Beaumont J,Querejeta R,Larman M,Díez Jdoi
10.1097/HJH.0b013e32828626e2subject
Has Abstractpub_date
2007-10-01 00:00:00pages
2148-57issue
10eissn
0263-6352issn
1473-5598pii
00004872-200710000-00027journal_volume
25pub_type
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journal_title:Journal of hypertension
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pub_type: 杂志文章
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更新日期:2000-02-01 00:00:00
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doi:10.1097/HJH.0b013e32834f9dd3
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journal_title:Journal of hypertension
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更新日期:2009-07-01 00:00:00
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pub_type: 杂志文章,多中心研究
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更新日期:1998-05-01 00:00:00
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journal_title:Journal of hypertension
pub_type: 杂志文章
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更新日期:1984-10-01 00:00:00
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journal_title:Journal of hypertension
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更新日期:2010-06-01 00:00:00
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