Full metadata record
DC Field | Value | Language |
---|---|---|
dc.creator | Lopez, N. (Natalia) | - |
dc.creator | Diez-Martinez, J. (Javier) | - |
dc.creator | Fortuño, M.A. (María Antonia) | - |
dc.date.accessioned | 2012-05-02T14:35:04Z | - |
dc.date.available | 2012-05-02T14:35:04Z | - |
dc.date.issued | 2006 | - |
dc.identifier.citation | Lopez N, Diez J, Fortuno MA. Differential hypertrophic effects of cardiotrophin-1 on adult cardiomyocytes from normotensive and spontaneously hypertensive rats. J Mol Cell Cardiol 2006 Nov;41(5):902-913. | es_ES |
dc.identifier.issn | 1095-8584 | - |
dc.identifier.uri | https://hdl.handle.net/10171/21876 | - |
dc.description.abstract | Cardiotrophin-1 (CT-1) produces longitudinal elongation of neonatal cardiomyocytes, but its effects in adult cardiomyocytes are not known. Recent observations indicate that CT-1 may be involved in pressure overload left ventricular hypertrophy (LVH). We investigated whether the hypertrophic effects of CT-1 are different in cardiomyocytes isolated from adult normotensive and spontaneously hypertensive rats (SHR). Hypertrophy was evaluated by planimetry and confocal microscopy, contractile proteins were quantified by Western blotting and real-time RT-PCR, and intracellular pathways were analyzed with specific chemical inhibitors. CT-1 increased c-fos and ANP expression (p<0.01) and cell area (p<0.01) in cardiomyocytes from both rat strains. In Wistar cells, CT-1 augmented cell length (p<0.01) but did not modify either the transverse diameter or cell depth. In SHR cells, CT-1 increased cell length (p<0.05), cell width (p<0.01) and cell depth, augmented the expression of myosin light chain-2v (MLC-2v) and skeletal alpha-actin (p<0.01) and enhanced MLC-2v phosphorylation (p<0.01). The blockade of gp130 or LIFR abolished CT-1-induced growth in the two cell types. All distinct effects observed in cardiomyocytes from SHR were mediated by STAT3. Baseline angiotensinogen expression was higher in SHR cells, and CT-1 induced a 1.7-fold and 3.2-fold increase of angiotensinogen mRNA in cardiomyocytes from Wistar rats and SHR respectively. In addition, AT1 blockade inhibited the specific effects of CT-1 in SHR cells. Finally, ex vivo determinations revealed that adult SHR exhibited enhanced myocardial CT-1 (mRNA and protein, p<0.01), increased cell width (p<0.01) and concentric LVH compared with pre-hypertensive SHR. These findings reveal a specific cell-broadening effect of CT-1 in cardiomyocytes from adult SHR and suggest that the hypertensive phenotype of these cells may influence the hypertrophic effects of CT-1, probably by means of an exaggerated induction of angiotensinogen expression. We suggest that CT-1 might facilitate LVH in genetic hypertension through a cross-talk with the renin-angiotensin system. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Elsevier | es_ES |
dc.rights | info:eu-repo/semantics/openAccess | es_ES |
dc.subject | Adult cardiomyocytes | es_ES |
dc.subject | Angiotensinogen | es_ES |
dc.subject | Cardiac hypertrophy cardiotrophin-1 | es_ES |
dc.subject | Hypertension | es_ES |
dc.subject | Myofibrils | es_ES |
dc.subject | Sarcomere | es_ES |
dc.subject | STATs | es_ES |
dc.title | Differential hypertrophic effects of cardiotrophin-1 on adult cardiomyocytes from normotensive and spontaneously hypertensive rats | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.relation.publisherversion | http://www.sciencedirect.com/science/article/pii/S0022282806007607 | es_ES |
dc.type.driver | info:eu-repo/semantics/article | es_ES |
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