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Isolation of Functional Cardiac Immune Cells
Published on: December 5, 2011
[Cardiac mast cells accumulation and degranulation contribute to collagen deposition after coronary
Qing-yong Zhang1, Zhi-hua Wang, Xiao-bo Li
1Department of Cardiology, The No.6 People's Hospital, Shanghai Jiaotong University, Shanghai 200233, China. yeakcardio@yahoo.com.cn
Objective:
To investigate potential pathophysiological role of cardiac mast cells accumulation and degranulation on the collagen deposition after coronary microembolization (CME).
Methods:
CME was induced in miniswine by selective infusion of 15X10(4) microspheres (diameter, 45 mum) into the left anterior descending artery groups (CME group, n=8). Some CME-induced animals were pretreated with the MC stabilizer tranilast (50 mg/kg, twice daily), beginning 2 weeks before CME and thereafter throughout the experimental period (CME +tranilast group, n=8), while some animals received tranilast without CME (tranilast group, n=8). Eight sham-operated animals without CME served as controls. After 30 days, the total number of MC and degranulating MCs and collagen deposition was assessed by histological and electronic microscopy studies.
Results:
The numbers of total and degranulating MCs and collagen volume fraction (CVF) at day 30 in CME group were significantly higher than those in controls (P <0.01). Treatment with tranilast significantly reduced the numbers of total and degranulating MCs and CVF at day 30 (all P <0.01). There was a significant positive correlation of the CVF with the number of total MCs (r=0.91, P <0.001) and degranulating MCs (r=0.92, P <0.001) over the CME myocardium.
Conclusion:
MCs accumulation and degranulating contribute to myocardial fibrosis collagen deposition.
Insights
Cardiac mast cells (MCs) accumulation and degranulation contribute to myocardial fibrosis. Tranilast treatment reduced MCs and collagen deposition, suggesting a therapeutic target for cardiac fibrosis.
Area of Science:
- Cardiovascular Research
- Immunology
- Pathology
Context:
- Coronary microembolization (CME) is a model for studying myocardial injury.
- Cardiac mast cells (MCs) are implicated in inflammatory responses and tissue remodeling.
- The role of MCs in post-injury collagen deposition requires further elucidation.
Purpose:
- To investigate the pathophysiological role of cardiac mast cell accumulation and degranulation in collagen deposition following coronary microembolization (CME).
Summary:
- Coronary microembolization (CME) in miniswine led to increased cardiac mast cells (MCs) and collagen deposition.
- Pretreatment with tranilast, an MC stabilizer, significantly reduced MC numbers, degranulation, and collagen volume fraction (CVF).
- A strong positive correlation was observed between MCs and CVF, supporting their role in myocardial fibrosis.
Impact:
- Demonstrates that cardiac mast cell accumulation and degranulation contribute to myocardial fibrosis.
- Highlights tranilast as a potential therapeutic agent for mitigating cardiac fibrosis by stabilizing mast cells.
- Provides a mechanistic link between mast cell activity and collagen deposition in the heart.
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