Is plasma cardiotrophin-1 a marker of hypertensive heart disease?

López, Begoña; González, Arantxa; Lasarte, Juan José; Sarobe, Pablo; Borrás, Francisco; Díaz, Agnes; Barba, J; Tomás, Lourdes; Lozano, Elisa; Serrano, Manuel Ríos; Varo, Nerea; Beloqui, Óscar; Fortuño, María Antonia; Díez, Javier

doi:10.1097/01.hjh.0000160221.09468.d3

Cited by 72 publications

(81 citation statements)

References 48 publications

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“…Moreover, left ventricular CT-1 expression is increased in different experimental models of hypertensive LVH [5,14]. In addition, an association between LVH and high plasma levels of CT-1 has recently been observed in essential hypertensive patients [6]. Furthermore, regression of LVH and diminution of plasma levels of CT-1 are associated in treated hypertensive patients [15].…”

Section: Introductionmentioning

confidence: 90%

“…Following the enrichment step with 4% BSA, cells recovered from the pellet consisted of 90% rod-shaped viable cardiomyocytes. The average number of cardiomyocytes obtained was 2.5 × 10 6 . Cells were plated in laminin-precoated (0.5 μg/cm 2 ) culture plates at a density of 10 4 cells/ cm 2 in serum-free medium 199 with Hanks' salts supplemented with 26 mmol/L NaHCO 3 , 10…”

Section: Adult Cardiomyocyte Isolation and Culturementioning

confidence: 99%

“…At cellular level, the growth of cardiomyocytes is the main determinant of LVH, although other factors such as exaggerated collagen accumulation are also involved [2,3]. Recent experimental and clinical evidence indicates that interleukin-6-related cytokines may participate in the development of hypertensive LVH [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

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Differential hypertrophic effects of cardiotrophin-1 on adult cardiomyocytes from normotensive and spontaneously hypertensive rats

López

Dı́ez

Fortuño

2006

Journal of Molecular and Cellular Cardiology

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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 α-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.

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Section: Introductionmentioning

confidence: 90%

Section: Adult Cardiomyocyte Isolation and Culturementioning

confidence: 99%

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Differential hypertrophic effects of cardiotrophin-1 on adult cardiomyocytes from normotensive and spontaneously hypertensive rats

López

Dı́ez

Fortuño

2006

Journal of Molecular and Cellular Cardiology

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“…Indeed, the release of CT-1 was found to be stimulated by ventricular stretch [109]. Comparable to systemic levels, the increase in local myocardial CT-1 in hypertensive patients [40,86,126] as well as in patients with dilative cardiomyopathy is furthermore significantly correlated with the left ventricular mass index, suggesting that CT-1 might play a role in structural left ventricular remodeling in these patients [149]. On the other hand myocardial levels of IL-6 and LIF receptor appear to be reduced in patients with dilative cardiomyopathy [28,67].…”

Section: General Overview On Gp130 Signalingmentioning

confidence: 99%

Survival pathways in hypertrophy and heart failure: The gp130-STAT3 axis

2007

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■ Abstract Circulating levels of interleukin (IL)-6 and related cytokines are elevated in patients with congestive heart failure and after myocardial infarction. Serum IL-6 concentrations are related to decreasing functional status of these patients and provide important prognostic information. Moreover, in the failing human heart, multiple components of the IL-6-glycoprotein (gp)130 receptor system are impaired, implicating an important role of this system in cardiac pathophysiology.Experimental studies have shown that the common receptor subunit of IL-6 cytokines is phosphorylated in response to pressure overload and myocardial infarction and that it subsequently activates at least three different downstream signaling pathways, the signal transducers and activators of transcription 1 and 3 (STAT1/3), the Src-homology tyrosine phosphatase 2 (SHP2)-Ras-ERK, and the PI3K-Akt system. Gp130 receptor mediated signaling promotes cardiomyocyte survival, induces hypertrophy, modulates cardiac extracellular matrix and cardiac function. In this regard, the gp130 receptor system and its main downstream mediator STAT3 play a key role in cardioprotection.This review summarizes the current knowledge of IL-6 cytokines, gp130 receptor and STAT3 signaling in the heart exposed to physiological (aging, pregnancy) and pathophysiological stress (ischemia, pressure overload, inflammation and cardiotoxic agents) with a special focus on the potential role of individual IL-6 cytokines.

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“…Changes associated with LVH include cardiac fibrosis and remodeling, as well as cardiomyocyte hypertrophy [2]. LVH typically arises as a compensatory mechanism against a chronic increase in cardiac workload, though neurochemical and hormonal stimuli have also been implicated, including mediators such as cardiotrophin -1 and parathyroid hormone [3][4][5]. These mechanical stresses placed on the heart may be pressure or volume-mediated [6].…”

Section: Introductionmentioning

confidence: 99%

Accuracy of the Electrocardiograph in Detecting Cardiac Left Ventricular Hypertrophy in Pediatric Patients with Aortic Valve Disease

Mondal¹

2015

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Is plasma cardiotrophin-1 a marker of hypertensive heart disease?

Cited by 72 publications

References 48 publications

Differential hypertrophic effects of cardiotrophin-1 on adult cardiomyocytes from normotensive and spontaneously hypertensive rats

Differential hypertrophic effects of cardiotrophin-1 on adult cardiomyocytes from normotensive and spontaneously hypertensive rats

Survival pathways in hypertrophy and heart failure: The gp130-STAT3 axis

Accuracy of the Electrocardiograph in Detecting Cardiac Left Ventricular Hypertrophy in Pediatric Patients with Aortic Valve Disease

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