Clinical on molecular basis of atrial fibrosis in patients with atrial fibrillation investigation / 中华心血管病杂志
Chinese Journal of Cardiology
;
(12): 459-463, 2005.
Artigo
em Chinês
| WPRIM
| ID: wpr-334682
ABSTRACT
<p><b>OBJECTIVE</b>To determine the molecular mechanisms involved in atrial fibrosis which occurs in patients with atrial fibrillation (AF) and to investigate their effects on the initiation and maintenance of AF.</p><p><b>METHODS</b>The right atrial tissue samples were taken from 73 patients with rheumatic heart disease who underwent heart valve replacement surgery. 34 patients had no history of AF (sinus rhythm group), 9 patients had paroxysmal AF and 30 patients had persistent AF. The mRNA content of collagen type I, collagen type III, MMP-2, TIMP-1, TIMP-2, TIMP-3 and TIMP-4 was measured by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and normalized to beta-actin or GAPDH.</p><p><b>RESULTS</b>Compared to sinus rhythm group, the mRNA of collagen type I and MMP-2 increased significantly in the persistent AF group (all, P < 0.01), followed by the paroxysmal AF group (all, P < 0.05). The mRNA of collagen type III was slightly higher in both AF groups than in the sinus rhythm group, but the differences were not statistically significant (P > 0.05). The mRNA of TIMP-1, TIMP-2 and TIMP-3 was down-regulated in the persistent AF group (all, P < 0.01, respectively), however, the trends of reduction did not reach statistical significance in the paroxysmal AF group (P > 0.05). The mRNA of TIMP-4 remained compatible in each group. The mRNA of collagen type I was significantly correlated with left atrial dimension (r = 0.336, P = 0.004) and AF duration (r = 0.339, P = 0.003). The mRNA of MMP-2 was significantly correlated with the mRNA of TIMP-2 (r = -0.326, P = 0.006), the mRNA of collagen type I (r = 0.322, P = 0.006), left atrial dimension (r = 0.300, P = 0.011) and AF duration (r = 0.300, P = 0.010).</p><p><b>CONCLUSION</b>The increased level of collagen type I associated with selective downregulation of TIMP-2 and upregulation of MMP-2 gene expression in atrium could be one of the molecular mechanisms of atrial fibrosis during atrial fibrillation, which correlates with the initiation and maintenance of AF.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Patologia
/
Fibrilação Atrial
/
Fibrose
/
RNA Mensageiro
/
Inibidores Teciduais de Metaloproteinases
/
Inibidor Tecidual de Metaloproteinase-2
/
Metaloproteinase 2 da Matriz
/
Colágeno Tipo I
/
Genética
/
Metabolismo
Limite:
Adolescente
/
Adulto
/
Feminino
/
Humanos
/
Masculino
Idioma:
Chinês
Revista:
Chinese Journal of Cardiology
Ano de publicação:
2005
Tipo de documento:
Artigo
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