Loss of myocardial LIF receptor in experimental heart failure reduces cardiotrophin-1 cytoprotection. A role for neurohumoral agonists?

Cardiomyocyte loss is involved in the transition from compensatory left ventricular hypertrophy (LVH) to heart failure (HF). Our aim was to investigate the status of the leukaemia inhibitory factor receptor (LIFR)/gp130 survival pathway and its cytoprotective activity in intact cardiac tissue and in...

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Bibliographic Details
Published in:Cardiovascular research 2007-08, Vol.75 (3), p.536-545
Main Authors: LOPEZ, Natalia, VARO, Nerea, DIEZ, Javier, FORTUNO, Maria Antonia
Format: Article
Language:English
Subjects:
Aldosterone - pharmacology
Angiotensin II - pharmacology
Animals
Apoptosis
Arterial hypertension. Arterial hypotension
Biological and medical sciences
Blood and lymphatic vessels
Cardiology. Vascular system
Cells, Cultured
Cytokines - pharmacology
Cytokines - physiology
Cytoprotection
Endothelin-1 - pharmacology
Heart
Heart Failure - metabolism
Heart failure, cardiogenic pulmonary edema, cardiac enlargement
In Situ Nick-End Labeling
Leukemia Inhibitory Factor - metabolism
Medical sciences
Myocardium - metabolism
Myocytes, Cardiac - metabolism
Norepinephrine - pharmacology
Rats
Rats, Inbred SHR
Rats, Inbred WKY
Receptors, OSM-LIF - analysis
Receptors, OSM-LIF - antagonists & inhibitors
Receptors, OSM-LIF - metabolism
RNA, Messenger - analysis
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Summary:Cardiomyocyte loss is involved in the transition from compensatory left ventricular hypertrophy (LVH) to heart failure (HF). Our aim was to investigate the status of the leukaemia inhibitory factor receptor (LIFR)/gp130 survival pathway and its cytoprotective activity in intact cardiac tissue and in cardiomyocytes obtained from adult spontaneously hypertensive rats (SHR) with LVH (non-failing SHR) and from aged SHR with overt HF (failing SHR). Cardiac morphometry was assayed by planimetry in an image analysis system. mRNA and protein expression were quantified by real time RT-PCR and Western blotting. Receptors were localized by immunocytochemistry. Trypan blue staining, TUNEL, and MTT cell viability assays were employed to study the cytoprotective activity of cardiotrophin-1 (CT-1) in isolated caridomyocytes. Compared to non-failing SHR, failing SHR exhibited enhanced myocardial cell death (p
ISSN:0008-6363
1755-3245
DOI:10.1016/j.cardiores.2007.04.025