[Calpain-I, calpastatin, caspase-3 and apoptosis in the human left atrium in rheumatic atrial fibrillation].
OBJECTIVE
The aim of the present study was to detect the expression of calpain-I, calpastatin, caspase-3 and apoptosis in the left atria of patients with rheumatic heart disease (RHD), and to find the association of these factors. Also, it was intended to investigate the effect of the above factors on the mechanism of atrial fibrillation (AF).


METHODS
43 patients with RHD undergoing valve-replacement were included, 15 patients with regular sinus rhythm (Group RSR), 8 patients with paroxysmal AF (Group AF1) and 20 patients with permanent AF (Group AF2). Western blot was used to examine the content of calpain-I, caspase-3 and calpastatin. The apoptosis index (AI) was measured by TUNEL.


RESULTS
(1) Expression of calpain-I in group AF2 was increased to (344.0 +/- 101.9)%, and caspase-3 was increased to (394.0 +/- 99.4)% compared to group RSR (P < 0.01, respectively). Amount of calpastatin was reduced to (27.0 +/- 12.8)% (P < 0.01). The expressions of these proteins were unchanged in group AF1. (2) AI in group AF2 was higher than that in groups RSR and AF1 (P < 0.01). (3) In group AF2, the levels of calpain-I, caspase-3 and AI were positively relative to left atrial dimension and AF duration, P < 0.05 - 0.01, respectively, whereas calpastatin was negatively correlated with left atrial dimension and AF duration (P = 0.007 and P = 0.001, respectively). (4) The protein content of calpain-I was positively related with that of caspase-3 and AI (P < 0.01, respectively), and the content of calpastatin was negatively related with that of calpain-I and caspase-3 (P < 0.01, respectively).


CONCLUSIONS
Apoptosis of atrial cell increased in left atria and the protein contents of calpain-I, caspase-3 and calpastatin significantly altered during AF in humans with RHD. The observed interactions suggest that these factors compose a system to cause the structural remodeling and dysfunction of atria. The course may play a key role in promoting the onset and maintenance of AF.
Chen
Yun-qing
YQ
Department of Cardiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Wang
Lin
L
Su
Xi
X
Tao
Liang
L
Chen
Xu-fa
XF
D000328:Adult; D017209:Apoptosis; D001281:Atrial Fibrillation / Q000209:etiology / Q000378:metabolism*; D016275:Atrial Function; D002135:Calcium-Binding Proteins / Q000378:metabolism*; D002154:Calpain / Q000378:metabolism*; D053148:Caspase 3 / Q000378:metabolism*; D005260:Female; D006325:Heart Atria / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D032383:Myocytes, Cardiac / Q000378:metabolism; D012214:Rheumatic Heart Disease / Q000150:complications / Q000378:metabolism*
D002135:Calcium-Binding Proteins; C033668:calpastatin; D002154:Calpain; D053148:Caspase 3