PMID- 18692064
OWN - NLM
STAT- MEDLINE
DCOM- 20090122
LR  - 20230120
IS  - 1095-8584 (Electronic)
IS  - 0022-2828 (Linking)
VI  - 45
IP  - 6
DP  - 2008 Dec
TI  - Upregulation of matrix metalloproteinase-9 and tissue inhibitors of 
      metalloproteinases in rapid atrial pacing-induced atrial fibrillation.
PG  - 742-53
LID - 10.1016/j.yjmcc.2008.07.007 [doi]
AB  - Remodeling of atrial extracellular matrix (ECM) in atrial fibrillation (AF) 
      involves changes in the expression of matrix metalloproteinases (MMPs) and tissue 
      inhibitors of MMPs (TIMPs). The contributions of MMPs and TIMPs to the 
      pathogenesis of AF development have not been clearly defined. This study 
      evaluated the in situ activity and expression of gelatinases (MMP-2 and MMP-9) 
      and their relationship with TIMP-1 or TIMP-3 in atria undergoing rapid atrial 
      pacing for the induction of AF (4 weeks' pacing followed by 2 weeks of maintained 
      AF) in pigs. In AF atria, in situ gelatinase activity was mainly localized in the 
      interstitium of atrial myocardium, and was significantly larger than that of 
      sinus rhythm control (i.e., sham control). The significant increase of MMP-9 in 
      its pro-form and mRNA level, but not MMP-2, was shown to be responsible for the 
      increased gelatinase activity in atria with AF. The inhibitory activities of 
      glycosylated TIMP-1 and TIMP-3, but not TIMP-2, in AF tissues were markedly 
      elevated and also localized in the atrial interstitium. TIMP-1 was found to be 
      mostly colocalized with gelatinase activity over the AF tissues, implying the 
      coexistence of gelatinase activity and TIMP-1, but TIMP-3 appeared only partially 
      colocalized and discontinued the gelatinase activity surrounding the 
      cardiomyocytes. TIMP-1 and TIMP-3 may play differential roles in the inhibition 
      of gelatinase activity in vivo. Together with the survey of several MMPs 
      transcripts and the level of transforming growth factor-beta1 (TGF-beta1), we 
      proposed that the increased activity of gelatinase (i.e., MMP-9), TIMP-1 and 
      TIMP-3 and their interaction may contribute to atrial ECM remodeling of AF.
FAU - Chen, Chien-Lung
AU  - Chen CL
AD  - Department of Biological Science and Technology, National Chiao Tung University, 
      Hsinchu, Taiwan.
FAU - Huang, Shoei K Stephen
AU  - Huang SK
FAU - Lin, Jiunn-Lee
AU  - Lin JL
FAU - Lai, Ling-Ping
AU  - Lai LP
FAU - Lai, Shao-Chuan
AU  - Lai SC
FAU - Liu, Chia-Wei
AU  - Liu CW
FAU - Chen, Wen-Chi
AU  - Chen WC
FAU - Wen, Cheng-Hao
AU  - Wen CH
FAU - Lin, Chih-Sheng
AU  - Lin CS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20080723
PL  - England
TA  - J Mol Cell Cardiol
JT  - Journal of molecular and cellular cardiology
JID - 0262322
RN  - 0 (RNA, Messenger)
RN  - 0 (Tissue Inhibitor of Metalloproteinase-1)
RN  - 0 (Tissue Inhibitor of Metalloproteinase-3)
RN  - 0 (Transforming Growth Factor beta1)
RN  - EC 3.4.24.35 (Matrix Metalloproteinase 9)
SB  - IM
MH  - Animals
MH  - Atrial Fibrillation/*metabolism/pathology
MH  - Extracellular Matrix/*metabolism/pathology
MH  - Heart Atria/metabolism/pathology
MH  - Humans
MH  - Matrix Metalloproteinase 9/*biosynthesis
MH  - RNA, Messenger/biosynthesis
MH  - Swine
MH  - Time Factors
MH  - Tissue Inhibitor of Metalloproteinase-1/*biosynthesis
MH  - Tissue Inhibitor of Metalloproteinase-3/*biosynthesis
MH  - Transforming Growth Factor beta1/metabolism
MH  - *Up-Regulation
EDAT- 2008/08/12 09:00
MHDA- 2009/01/23 09:00
CRDT- 2008/08/12 09:00
PHST- 2008/01/23 00:00 [received]
PHST- 2008/06/27 00:00 [revised]
PHST- 2008/07/03 00:00 [accepted]
PHST- 2008/08/12 09:00 [pubmed]
PHST- 2009/01/23 09:00 [medline]
PHST- 2008/08/12 09:00 [entrez]
AID - S0022-2828(08)00515-4 [pii]
AID - 10.1016/j.yjmcc.2008.07.007 [doi]
PST - ppublish
SO  - J Mol Cell Cardiol. 2008 Dec;45(6):742-53. doi: 10.1016/j.yjmcc.2008.07.007. Epub 
      2008 Jul 23.