Evaluation of Myocyte Proliferation in Alcoholic Cardiomyopathy: Telomerase Enzyme Activity (TERT) Compared with Ki-67 Expression

Lluís, Meritxell; Fernández‐Solà, Joaquim; Castellví–Bel, Sergi; Sacanella, Emilio; Estruch, Ramón; Urbano-Márquez, Á

doi:10.1093/alcalc/agr071

Cited by 8 publications

(5 citation statements)

References 57 publications

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“…This results in the marked proliferation of VSMCs to form the neointima, which leads to stenosis of the vascular lumen. The proliferating cell nuclear antigen, Ki67, is considered to be an ideal indicator for detecting cell proliferation (38). In the present study, PTX intervention was associated with a significant decrease in expression of Ki67, and its expression was decreased when compared with the model group.…”

Section: Discussionmentioning

confidence: 99%

Effects of paclitaxel intervention on pulmonary vascular remodeling in rats with pulmonary hypertension

Zhao

Yang

et al. 2018

Exp Ther Med

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The aim of the present study was to investigate the effects of paclitaxel (PTX), at a non-cytotoxic concentration, on pulmonary vascular remodeling (PVR) in rats with pulmonary hypertension (PAH), and to explore the mechanisms underlying the PTX-mediated reversal of PVR in PAH. A total of 36 rats were divided into control group (n=12), model group (n=12) receiving a subcutaneous injection of monocrotaline (60 mg/kg) in the back on day 7 following left pneumonectomy and PTX group (n=12) with PTX (2 mg/kg) injection via the caudal vein 3 weeks following establishing the model. The degree of PVR among all groups, as well as the expression levels of Ki67, p27Kip1 and cyclin B1, were compared. The mean pulmonary artery pressure, right ventricular hypertrophy index [right ventricle/(left ventricle + septum) ratio] and the thickness of the pulmonary arterial tunica media in the model group were 58.34±2.01 mmHg, 0.64±0.046 and 65.3±3.3%, respectively, which were significantly higher when compared with 23.30±1.14 mmHg, 0.32±0.028 and 16.2±1.3% in the control group, respectively (P<0.01). The mean pulmonary artery pressure, right ventricular hypertrophy index and thickness of the pulmonary arterial tunica media in the PTX group were 42.35±1.53 mmHg, 0.44±0.029 and 40.5±2.6%, respectively, which were significantly lower when compared with the model group (P<0.01). Compared with the control group, the expression levels of Ki67 and cyclin B1 in the model group were significantly increased (P<0.01), while p27Kip1 expression was significantly reduced (P<0.01). Following PTX intervention, the expression levels of Ki67 and cyclin B1 were significantly reduced when compared with the model group (P<0.01), while p27Kip1 expression was significantly increased (P<0.01). The results of the present study suggest that PTX, administered at a non-cytotoxic concentration, may reduce PAH in rats, and prevent the effects of PVR in PAH. These effects of PTX may be associated with increased expression of p27Kip1 and decreased expression of cyclin B1.

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Section: Discussionmentioning

confidence: 99%

Effects of paclitaxel intervention on pulmonary vascular remodeling in rats with pulmonary hypertension

Zhao

Yang

et al. 2018

Exp Ther Med

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“…After myocyte apoptosis or necrosis, the heart tries to repair and regenerate this tissue damage [39,123], but the heart regenerative capacity is low as a result of the ethanol aggressive damage and develops ineffective repair mechanisms such as progressive fibrosis [124,125]. In fact, ethanol itself decreases the myocyte regeneration capacity and increases the fibrogenic process [52,126]. Subendocardial and interstitial fibrosis progressively appear in the course of ACM, usually in advanced stages [52,56].…”

Section: Ethanol-induced Heart Fibrosismentioning

confidence: 99%

The Effects of Ethanol on the Heart: Alcoholic Cardiomyopathy

Fernández‐Solà

2020

Nutrients

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109

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Alcoholic-dilated Cardiomyopathy (ACM) is the most prevalent form of ethanol-induced heart damage. Ethanol induces ACM in a dose-dependent manner, independently of nutrition, vitamin, or electrolyte disturbances. It has synergistic effects with other heart risk factors. ACM produces a progressive reduction in myocardial contractility and heart chamber dilatation, leading to heart failure episodes and arrhythmias. Pathologically, ethanol induces myocytolysis, apoptosis, and necrosis of myocytes, with repair mechanisms causing hypertrophy and interstitial fibrosis. Myocyte ethanol targets include changes in membrane composition, receptors, ion channels, intracellular [Ca2+] transients, and structural proteins, and disrupt sarcomere contractility. Cardiac remodeling tries to compensate for this damage, establishing a balance between aggression and defense mechanisms. The final process of ACM is the result of dosage and individual predisposition. The ACM prognosis depends on the degree of persistent ethanol intake. Abstinence is the preferred goal, although controlled drinking may still improve cardiac function. New strategies are addressed to decrease myocyte hypertrophy and interstitial fibrosis and try to improve myocyte regeneration, minimizing ethanol-related cardiac damage. Growth factors and cardiomyokines are relevant molecules that may modify this process. Cardiac transplantation is the final measure in end-stage ACM but is limited to those subjects able to achieve abstinence.

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“…An increase of the index of cardiomyocyte proliferative activity was detected in acute myocardial infarction in the zone adjacent to the necrotic zone [13], in cardiomyopathies of various origin (2.5-3 times higher; [10]), and in donor hearts during unfolding rejection reaction [12]. An increase of cardiomyocyte proliferative activity was demonstrated (by detection of Ki-67 antigen) in rats after acute myocardial infarction [9], intense exercise [15], injection of growth hormone [7].…”

Section: Resultsmentioning

confidence: 99%

Stimulation of Cardiomyocyte Regeneratory Reactions under Conditions of Cytopathic Hypercholesterolemia

et al. 2015

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The regeneratory reactions of cardiomyocytes in the heart under conditions of cytopathic exposure to hypercholesterolemia and during verapamil treatment were studied by immunohistochemical detection of proliferation marker Ki-67 and evaluation of cardiomyocyte count. A 30-day exposure of rats to atherogenic diet led to an increase of Ki-67+ cardiomyocytes by 14.5-16.7 times (p<0.05). The Ki-67 label index in cardiomyocytes remained higher than normally (8-9-fold; p<0.05) after 64 days. It remained elevated (8-11-fold; p<0.05) after verapamil treatment. Evaluation of cardiomyocyte count and of their nuclear status detected various regeneratory strategies: increase of the total cardiomyocyte count, with increase of the percentage of mononuclear cardiomyocytes (particularly in response to verapamil in group 1 rats); decrease of total cardiomyocyte count with increase of the percentage of multinuclear cardiomyocytes (particularly in group 2 rats in response to verapamil).

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Evaluation of Myocyte Proliferation in Alcoholic Cardiomyopathy: Telomerase Enzyme Activity (TERT) Compared with Ki-67 Expression

Cited by 8 publications

References 57 publications

Effects of paclitaxel intervention on pulmonary vascular remodeling in rats with pulmonary hypertension

Effects of paclitaxel intervention on pulmonary vascular remodeling in rats with pulmonary hypertension

The Effects of Ethanol on the Heart: Alcoholic Cardiomyopathy

Stimulation of Cardiomyocyte Regeneratory Reactions under Conditions of Cytopathic Hypercholesterolemia

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