Coronary artery remodeling in a model of left ventricular pressure overload is influenced by platelets and inflammatory cells

Autor: Juliana Odetunde, Jessica Caicedo, Paul Mueller, Ahmed Abdel-Latif, Fanmuyi Yang, Alyssa Moore Sutton, Anping Dong, Yuri M. Klyachkin, Susan S. Smyth, Cordelia J. Barrick
Jazyk: angličtina
Rok vydání: 2012
Předmět:
Pathology
Mouse
Cardiac fibrosis
T-Lymphocytes
lcsh:Medicine
030204 cardiovascular system & hematology
Cardiovascular
Left ventricular hypertrophy
Polymerase Chain Reaction
Sudden cardiac death
Mice
0302 clinical medicine
Fibrosis
lcsh:Science
0303 health sciences
Multidisciplinary
T Cells
Animal Models
Hematology
Flow Cytometry
Coronary Vessels
Echocardiography
Doppler
3. Good health
medicine.anatomical_structure
Hypertension
Ventricular pressure
Cardiology
Medicine
Cardiomyopathies
Research Article
Platelets
Blood Platelets
medicine.medical_specialty
Immune Cells
Heart Ventricles
Immunology
Mice
Transgenic
Models
Biological
03 medical and health sciences
Model Organisms
Internal medicine
medicine
Animals
Ventricular remodeling
Biology
030304 developmental biology
Heart Failure
Inflammation
Pressure overload
business.industry
Macrophages
lcsh:R
Immunity
medicine.disease
Coronary arteries
Clinical Immunology
lcsh:Q
business
Zdroj: PLoS ONE, Vol 7, Iss 8, p e40196 (2012)
PLoS ONE
ISSN: 1932-6203
Popis: Left ventricular hypertrophy (LVH) is usually accompanied by intensive interstitial and perivascular fibrosis, which may contribute to arrhythmogenic sudden cardiac death. The mechanisms underlying the development of cardiac fibrosis are incompletely understood. To investigate the role of perivascular inflammation in coronary artery remodeling and cardiac fibrosis during hypertrophic ventricular remodeling, we used a well-established mouse model of LVH (transverse aortic constriction [TAC]). Three days after pressure overload, macrophages and T lymphocytes accumulated around and along left coronary arteries in association with luminal platelet deposition. Consistent with these histological findings, cardiac expression of IL-10 was upregulated and in the systemic circulation, platelet white blood cell aggregates tended to be higher in TAC animals compared to sham controls. Since platelets can dynamically modulate perivascular inflammation, we investigated the impact of thrombocytopenia on the response to TAC. Immunodepletion of platelets decreased early perivascular T lymphocytes' accumulation and altered subsequent coronary artery remodeling. The contribution of lymphocytes were examined in Rag1(-/-) mice, which displayed significantly more intimal hyperplasia and perivascular fibrosis compared to wild-type mice following TAC. Collectively, our studies support a role of early perivascular accumulation of platelets and T lymphocytes in pressure overload-induced inflammation.
Databáze: OpenAIRE
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