This Article Full Text Full Text (PDF) All Versions of this Article: jhc.5A6804.2005v1 54/5/515    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Zhang, Q.-Y. Articles by Tse, H.-F. Search for Related Content PubMed PubMed Citation Articles by Zhang, Q.-Y. Articles by Tse, H.-F. Social Bookmarking                      What's this?

Mast Cell Contributes to Cardiomyocyte Apoptosis after Coronary Microembolization

Qing-Yong Zhang, Jun-Bo Ge, Jun-Zhu Chen, Jian-Hua Zhu, Liang-Hui Zhang, Chu-Pak Lau and Hung-Fat Tse

The First Affiliate Hospital of Zhejiang University, HangZhou, People's Republic of China (Q-YZ,J-ZC,J-HZ); Cardiology Division, Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, China (Q-YZ,C-PL,H-FT); The No. 6 People's Hospital, Jiao Tong University, Shanghai, China (Q-YZ); and Institute of Cardiovascular Disease, Zhongshan Hospital, Fudan University, Shanghai, China (J-BG,L-HZ)

Correspondence to: Hung-Fat Tse, MD, Cardiology Division, Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, China. E-mail: hftse{at}hkucc.hku.hk

Coronary microembolization (CME) is associated with progressive myocardial dysfunction despite restoration of coronary flow reserve (CFR). The potential pathophysiological role of mast cells (MCs) remains unclear. Therefore, we induced CME in 18 miniswines and determined whether MC accumulation occurs and their effects on local cytokine secretion [interleukin (IL)-6, IL-8, tumor necrosis factor- (TNF-)]; cardiomyocyte apoptosis; and collagen formation at day 1 (D1), day 7 (D7), and day 30 (D30) after CME. Four sham-operated animals without CME (controls) and six animals treated with a MC stabilization agent (tranilast) for 30 days after CME were also studied. CFR decreased at D1 but returned to baseline level at D7 and D30. Coronary sinus levels of IL-6, IL-8, and TNF- increased significantly at D1 and D7 (p<0.01 vs baseline). Levels of IL-6 and IL-8 at D30 returned to baseline level, but not those of TNF-. The numbers of total and degranulating MCs, % apoptotic cardiomyocytes, and collagen volume fraction (CVF) over CME myocardium at D1, D7, and D30 were significantly higher than controls (p<0.01). Treatment with tranilast significantly reduced the serum level of TNF-, numbers of total and degranulating MCs, % apoptotic cardiomyocytes, and CVF at D30 (all p<0.05). There was a significant positive correlation between the numbers of MCs with % apoptotic cardiomyocytes (r = 0.77, p<0.001) and CVF (r = 0.75, p<0.001) over the CME myocardium. Despite restoration of CFR, cardiomyocyte apoptosis persisted after CME and was positively correlated with the number of MCs but was prevented with tranilast treatment. These findings suggest that MCs contribute to cardiomyocyte apoptosis after CME. (J Histochem Cytochem &!squf;54:515–523, 2006)

Key Words: apoptosis • coronary mircoembolization • mast cell

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

Guidelines | Subscriptions | About | exPRESS - Current - Archive | Business Information | Contact

The Journal of Histochemistry & Cytochemistry is owned, published, and licensed by The Histochemical Society © 2006