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Increased myostatin activity and decreased myocyte proliferation in chronic alcoholic cardiomyopathy.

BACKGROUNDApoptosis mediates in alcohol-induced heart damage leading to cardiomyopathy (CMP). Myocyte proliferation may compensate for myocyte loss. Myostatin is upregulated after cardiac damage and by alcohol consumption thereby decreasing myocyte renewal. We assess the potential role of alcohol in... Full description

Journal Title: Alcoholism clinical and experimental research, July 2011, Vol.35(7), pp.1220-1229
Main Author: Fernández-Solà, Joaquim
Other Authors: Lluis, Meritxell , Sacanella, Emilio , Estruch, Ramón , Antúnez, Emilia , Urbano-Márquez, Alvaro
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1530-0277 ; DOI: 10.1111/j.1530-0277.2011.01456.x
Link: http://search.proquest.com/docview/872440347/?pq-origsite=primo
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title: Increased myostatin activity and decreased myocyte proliferation in chronic alcoholic cardiomyopathy.
format: Article
creator:
  • Fernández-Solà, Joaquim
  • Lluis, Meritxell
  • Sacanella, Emilio
  • Estruch, Ramón
  • Antúnez, Emilia
  • Urbano-Márquez, Alvaro
subjects:
  • Adult–Metabolism
  • Aged–Pathology
  • Alcoholism–Metabolism
  • Cardiomyopathy, Alcoholic–Pathology
  • Cell Proliferation–Metabolism
  • Chronic Disease–Pathology
  • Female–Metabolism
  • Humans–Pathology
  • Hypertension–Metabolism
  • Male–Pathology
  • Middle Aged–Biosynthesis
  • Myocardium–Metabolism
  • Myocytes, Cardiac–Physiology
  • Myostatin–Physiology
  • Up-Regulation–Physiology
  • Myostatin
ispartof: Alcoholism, clinical and experimental research, July 2011, Vol.35(7), pp.1220-1229
description: BACKGROUNDApoptosis mediates in alcohol-induced heart damage leading to cardiomyopathy (CMP). Myocyte proliferation may compensate for myocyte loss. Myostatin is upregulated after cardiac damage and by alcohol consumption thereby decreasing myocyte renewal. We assess the potential role of alcohol in inducing myocyte apoptosis as well as in inhibiting myocyte proliferation. METHODSHeart samples were obtained from organ donors, including 22 high alcohol consumers, 22 with hypertension, 8 with other causes of CMP, and 10 healthy donors. Evaluation included medical record with data on daily, recent and lifetime ethanol consumption, chest X-ray, left ventricular (LV) function assessed by two-dimensional echocardiography, and LV histology and immunohistochemistry. Apoptosis was evaluated by TUNEL, BAX, and BCL-2 assays. Myocyte proliferation was evaluated with Ki-67 assay. Myostatin activity was measured with a specific immunohistochemical assay. CMP was assessed by functional and histological criteria. RESULTSAlcoholic and hypertensive donors with CMP showed higher apoptotic indices than did their partners without CMP. Myostatin activity was higher in alcoholics than in controls, mainly in those with CMP. The increase in myostatin expression in alcoholic CMP was higher than in other groups. The Ki-67 proliferation index increased in all groups with CMP compared to those without CMP, with alcoholics showing a lower increase in this proliferation response. CONCLUSIONSAlcohol produces cardiac myocyte loss through apoptosis but also partially inhibits myocyte proliferation through myostatin up-regulation. The final result may suppose an imbalance in myocyte homeostasis, with a net loss in total ventricular myocyte mass and progressive ventricular dysfunction.
language: eng
source:
identifier: E-ISSN: 1530-0277 ; DOI: 10.1111/j.1530-0277.2011.01456.x
fulltext: fulltext
issn:
  • 15300277
  • 1530-0277
url: Link


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titleIncreased myostatin activity and decreased myocyte proliferation in chronic alcoholic cardiomyopathy.
creatorFernández-Solà, Joaquim ; Lluis, Meritxell ; Sacanella, Emilio ; Estruch, Ramón ; Antúnez, Emilia ; Urbano-Márquez, Alvaro
contributorFernández-Solà, Joaquim (correspondence author) ; Fernández-Solà, Joaquim (record owner)
ispartofAlcoholism, clinical and experimental research, July 2011, Vol.35(7), pp.1220-1229
identifierE-ISSN: 1530-0277 ; DOI: 10.1111/j.1530-0277.2011.01456.x
subjectAdult–Metabolism ; Aged–Pathology ; Alcoholism–Metabolism ; Cardiomyopathy, Alcoholic–Pathology ; Cell Proliferation–Metabolism ; Chronic Disease–Pathology ; Female–Metabolism ; Humans–Pathology ; Hypertension–Metabolism ; Male–Pathology ; Middle Aged–Biosynthesis ; Myocardium–Metabolism ; Myocytes, Cardiac–Physiology ; Myostatin–Physiology ; Up-Regulation–Physiology ; Myostatin
descriptionBACKGROUNDApoptosis mediates in alcohol-induced heart damage leading to cardiomyopathy (CMP). Myocyte proliferation may compensate for myocyte loss. Myostatin is upregulated after cardiac damage and by alcohol consumption thereby decreasing myocyte renewal. We assess the potential role of alcohol in inducing myocyte apoptosis as well as in inhibiting myocyte proliferation. METHODSHeart samples were obtained from organ donors, including 22 high alcohol consumers, 22 with hypertension, 8 with other causes of CMP, and 10 healthy donors. Evaluation included medical record with data on daily, recent and lifetime ethanol consumption, chest X-ray, left ventricular (LV) function assessed by two-dimensional echocardiography, and LV histology and immunohistochemistry. Apoptosis was evaluated by TUNEL, BAX, and BCL-2 assays. Myocyte proliferation was evaluated with Ki-67 assay. Myostatin activity was measured with a specific immunohistochemical assay. CMP was assessed by functional and histological criteria. RESULTSAlcoholic and hypertensive donors with CMP showed higher apoptotic indices than did their partners without CMP. Myostatin activity was higher in alcoholics than in controls, mainly in those with CMP. The increase in myostatin expression in alcoholic CMP was higher than in other groups. The Ki-67 proliferation index increased in all groups with CMP compared to those without CMP, with alcoholics showing a lower increase in this proliferation response. CONCLUSIONSAlcohol produces cardiac myocyte loss through apoptosis but also partially inhibits myocyte proliferation through myostatin up-regulation. The final result may suppose an imbalance in myocyte homeostasis, with a net loss in total ventricular myocyte mass and progressive ventricular dysfunction.
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titleIncreased myostatin activity and decreased myocyte proliferation in chronic alcoholic cardiomyopathy.
descriptionBACKGROUNDApoptosis mediates in alcohol-induced heart damage leading to cardiomyopathy (CMP). Myocyte proliferation may compensate for myocyte loss. Myostatin is upregulated after cardiac damage and by alcohol consumption thereby decreasing myocyte renewal. We assess the potential role of alcohol in inducing myocyte apoptosis as well as in inhibiting myocyte proliferation. METHODSHeart samples were obtained from organ donors, including 22 high alcohol consumers, 22 with hypertension, 8 with other causes of CMP, and 10 healthy donors. Evaluation included medical record with data on daily, recent and lifetime ethanol consumption, chest X-ray, left ventricular (LV) function assessed by two-dimensional echocardiography, and LV histology and immunohistochemistry. Apoptosis was evaluated by TUNEL, BAX, and BCL-2 assays. Myocyte proliferation was evaluated with Ki-67 assay. Myostatin activity was measured with a specific immunohistochemical assay. CMP was assessed by functional and histological criteria. RESULTSAlcoholic and hypertensive donors with CMP showed higher apoptotic indices than did their partners without CMP. Myostatin activity was higher in alcoholics than in controls, mainly in those with CMP. The increase in myostatin expression in alcoholic CMP was higher than in other groups. The Ki-67 proliferation index increased in all groups with CMP compared to those without CMP, with alcoholics showing a lower increase in this proliferation response. CONCLUSIONSAlcohol produces cardiac myocyte loss through apoptosis but also partially inhibits myocyte proliferation through myostatin up-regulation. The final result may suppose an imbalance in myocyte homeostasis, with a net loss in total ventricular myocyte mass and progressive ventricular dysfunction.
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titleIncreased myostatin activity and decreased myocyte proliferation in chronic alcoholic cardiomyopathy.
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abstractBACKGROUNDApoptosis mediates in alcohol-induced heart damage leading to cardiomyopathy (CMP). Myocyte proliferation may compensate for myocyte loss. Myostatin is upregulated after cardiac damage and by alcohol consumption thereby decreasing myocyte renewal. We assess the potential role of alcohol in inducing myocyte apoptosis as well as in inhibiting myocyte proliferation. METHODSHeart samples were obtained from organ donors, including 22 high alcohol consumers, 22 with hypertension, 8 with other causes of CMP, and 10 healthy donors. Evaluation included medical record with data on daily, recent and lifetime ethanol consumption, chest X-ray, left ventricular (LV) function assessed by two-dimensional echocardiography, and LV histology and immunohistochemistry. Apoptosis was evaluated by TUNEL, BAX, and BCL-2 assays. Myocyte proliferation was evaluated with Ki-67 assay. Myostatin activity was measured with a specific immunohistochemical assay. CMP was assessed by functional and histological criteria. RESULTSAlcoholic and hypertensive donors with CMP showed higher apoptotic indices than did their partners without CMP. Myostatin activity was higher in alcoholics than in controls, mainly in those with CMP. The increase in myostatin expression in alcoholic CMP was higher than in other groups. The Ki-67 proliferation index increased in all groups with CMP compared to those without CMP, with alcoholics showing a lower increase in this proliferation response. CONCLUSIONSAlcohol produces cardiac myocyte loss through apoptosis but also partially inhibits myocyte proliferation through myostatin up-regulation. The final result may suppose an imbalance in myocyte homeostasis, with a net loss in total ventricular myocyte mass and progressive ventricular dysfunction.
doi10.1111/j.1530-0277.2011.01456.x
urlhttp://search.proquest.com/docview/872440347/
issn01456008
date2011-07-01