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Published on: February 20, 2015
Endothelial microparticles are increased in congenital heart diseases and contribute to endothelial dysfunction
Ze-Bang Lin1,2,3, Hong-Bo Ci1,2,3, Yan Li1,2,3
1Division of Cardiac Surgery, The First Affiliated Hospital of Sun Yat-sen University, 58 Zhong Shan Er Road, Guangzhou, 510080, People's Republic of China.
Background:
We previously demonstrated that endothelial microparticles (EMPs) are increased in mitral valve diseases and impair valvular endothelial cell function. Perioperative systemic inflammation is an important risk factor and complication of cardiac surgery. In this study, we investigate whether EMPs increase in congenital heart diseases to promote inflammation and endothelial dysfunction.
Methods:
The level of plasma EMPs in 20 patients with atrial septal defect (ASD), 23 patients with ventricular septal defect (VSD), and 30 healthy subjects were analyzed by flow cytometry. EMPs generated from human umbilical vascular endothelial cells (HUVECs) were injected into C57BL6 mice, or cultured with HUVECs without or with siRNAs targeting P38 MAPK. The expression and/or phosphorylation of endothelial nitric oxide synthase (eNOS), P38 MAPK, and caveolin-1 in mouse heart and/or in cultured HUVECs were determined. We evaluated generation of nitric oxide (NO) in mouse hearts, and levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in cultured HUVECs and in mice.
Results:
EMPs were significantly elevated in patients with ASD and VSD, especially in those with pulmonary hypertension when compared with controls. EMPs increased caveolin-1 expression and P38 MAPK phosphorylation and decreased eNOS phosphorylation and NO production in mouse hearts. EMPs stimulated P38 MAPK expression, TNF-α and IL-6 production, which were all inhibited by siRNAs targeting P38 MAPK in cultured HUVECs.
Conclusions:
EMPs were increased in adult patients with congenital heart diseases and may contribute to increased inflammation leading to endothelial dysfunction via P38 MAPK-dependent pathways. This novel data provides a potential therapeutic target to address important complications of surgery of congenial heart disease.
Insights
Endothelial microparticles (EMPs) are elevated in congenital heart disease patients, promoting inflammation and endothelial dysfunction through P38 MAPK pathways. This finding suggests EMPs as a potential therapeutic target for surgical complications.
Area of Science:
- Cardiovascular Science
- Immunology
- Cell Biology
Background:
- Endothelial microparticles (EMPs) are implicated in mitral valve diseases.
- Perioperative systemic inflammation is a risk factor in cardiac surgery.
- This study investigates EMPs in congenital heart diseases (CHDs) and their role in inflammation and endothelial dysfunction.
Purpose of the Study:
- To determine if EMPs are elevated in patients with congenital heart diseases.
- To investigate the mechanism by which EMPs may promote inflammation and endothelial dysfunction in CHDs.
- To explore the role of P38 MAPK signaling in EMP-induced effects.
Main Methods:
- Plasma EMP levels were measured using flow cytometry in patients with atrial septal defect (ASD) and ventricular septal defect (VSD) compared to healthy controls.
- In vitro and in vivo models were used, involving EMP injection into mice and co-culture with endothelial cells.
- Key molecular markers including P38 MAPK, eNOS, caveolin-1, nitric oxide (NO), TNF-α, and IL-6 were assessed.
Main Results:
- EMPs were significantly higher in ASD and VSD patients, particularly those with pulmonary hypertension.
- In mouse hearts, EMPs increased caveolin-1, P38 MAPK phosphorylation, and decreased eNOS phosphorylation and NO production.
- In endothelial cells, EMPs induced P38 MAPK, TNF-α, and IL-6, effects reversed by P38 MAPK inhibition.
Conclusions:
- Elevated EMPs in adult CHD patients contribute to inflammation and endothelial dysfunction.
- The P38 MAPK pathway is a key mediator of EMP-induced effects in CHDs.
- EMPs represent a potential therapeutic target for managing complications associated with CHD surgery.
