title: Cells involved in extracellular matrix remodeling after acute myocardial infarction.
abstract: OBJECTIVE
  Evaluate the effects of VEGF165 gene transfer in the process of remodeling of the extracellular matrix after an acute myocardial infarct.
  
  
  METHODS
  Wistar rats were submitted to myocardial infarction, after the ligation of the left descending artery, and the left ventricle ejection fraction was used to classify the infarcts into large and small. The animals were divided into groups of ten, according to the size of infarcted area (large or small), and received or not VEGF165 treatment. Evaluation of different markers was performed using immunohistochemistry and digital quantification. The primary antibodies used in the analysis were anti-fibronectin, anti-vimentin, anti-CD44, anti-E-cadherin, anti-CD24, anti-alpha-1-actin, and anti-PCNA. The results were expressed as mean and standard error, and analyzed by ANOVA, considering statistically significant if p≤0.05.
  
  
  RESULTS
  There was a significant increase in the expression of undifferentiated cell markers, such as fibronectin (protein present in the extracellular matrix) and CD44 (glycoprotein present in the endothelial cells). However, there was decreased expression of vimentin and PCNA, indicating a possible decrease in the process of cell proliferation after treatment with VEGF165. Markers of differentiated cells, E-cadherin (adhesion protein between myocardial cells), CD24 (protein present in the blood vessels), and alpha-1-actin (specific myocyte marker), showed higher expression in the groups submitted to gene therapy, compared to non-treated group. The value obtained by the relation between alpha-1-actin and vimentin was approximately three times higher in the groups treated with VEGF165, suggesting greater tissue differentiation.
  
  
  CONCLUSIONS
  The results demonstrated the important role of myocytes in the process of tissue remodeling, confirming that VEGF165 seems to provide a protective effect in the treatment of acute myocardial infarct.
authors.affiliation: Faculdade de Medicina do ABC, Santo André, SP, Brazil.
authors.forename: Larissa Ferraz
authors.initials: LF
authors.lastname: Garcia
authors.affiliation: Universidade Federal de São Paulo, São Paulo, SP, Brazil.
authors.forename: Fábio D'Aguiar
authors.initials: FD
authors.lastname: Mataveli
authors.affiliation: Faculdade de Medicina do ABC, Santo André, SP, Brazil.
authors.forename: Ana Maria Amaral Antônio
authors.initials: AM
authors.lastname: Mader
authors.affiliation: Faculdade de Medicina do ABC, Santo André, SP, Brazil.
authors.forename: Thérèse Rachell
authors.initials: TR
authors.lastname: Theodoro
authors.affiliation: Universidade Federal de São Paulo, São Paulo, SP, Brazil.
authors.forename: Giselle Zenker
authors.initials: GZ
authors.lastname: Justo
authors.affiliation: Universidade Federal de São Paulo, São Paulo, SP, Brazil.
authors.forename: Maria Aparecida da Silva
authors.initials: MA
authors.lastname: Pinhal
mesh_terms: D000199:Actins / Q000032:analysis; D000818:Animals; D051927:CD24 Antigen / Q000032:analysis; D015820:Cadherins / Q000032:analysis; D049109:Cell Proliferation / Q000502:physiology; D004195:Disease Models, Animal; D005109:Extracellular Matrix / Q000502:physiology*; D005260:Female; D005353:Fibronectins / Q000032:analysis; D018014:Gene Transfer Techniques; D015316:Genetic Therapy / Q000379:methods; D018960:Hyaluronan Receptors / Q000032:analysis; D007150:Immunohistochemistry; D009203:Myocardial Infarction / Q000628:therapy*; D032383:Myocytes, Cardiac / Q000502:physiology; D017208:Rats, Wistar; D015203:Reproducibility of Results; D016896:Treatment Outcome; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics / Q000627:therapeutic use*; D014746:Vimentin / Q000032:analysis
chemical_list: D000199:Actins; D051927:CD24 Antigen; D015820:Cadherins; C476399:Cd44 protein, mouse; D005353:Fibronectins; D018960:Hyaluronan Receptors; D042461:Vascular Endothelial Growth Factor A; D014746:Vimentin; C467498:vascular endothelial growth factor A, rat