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Proteomic analysis of smooth muscle cells derived from carotid plaque reveals differences between symptomatic & asymptomatic plaques

Chronic Ischaemic Heart Disease (IHD)




Louise Full
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Full, Louise
(United Kingdom)
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List of Authors:

L.E. Full, A.H. Davies, R. Wait, C. Monaco;

Abstract:


Rationale: Smooth muscle cells (SMC) are key players in atherosclerotic disease. The proteome of SMC in human carotid disease and its relationship with plaque-related symptomatology are still ill defined. Rationale Smooth muscle cells (SMC) are key players in atherosclerotic disease. The proteome of SMC in human carotid disease and its relationship with plaque-related symptomatology are still ill defined.

Methodology: Carotid endarterectomies were collected from 10 consenting patients (6 symptomatic, 4 asymptomatic). Plaque SMC were isolated via enzymatic dissociation of endarterectomy specimens and using immunomagnetic beads (Miltenyi). Commercially available aortic medial SMC from 6 healthy donors were purchased from Promocell. Cells were used consistently at passage 3. We used 2-dimensional electrophoresis with digital image analysis (SameSpots, Non-linear Dynamics) and tandem mass spectrometry, to detect changes in the proteome of atherosclerotic SMC.

Results: Analysis of 2D gel images revealed 29 proteins with a statistically significant difference in expression between medial and plaque SMC (P<0.05). Plaque SMC had decreased expression of mitochondrial protein ATP Synthase subunit-beta but an increase in the oxidised form of peroxiredoxin-4, suggesting decreased mitochondrial function, possibly due to oxidative stress. Furthermore, differences in protein expression between SMC from symptomatic and asymptomatic patients were also found. Plaque SMC from symptomatic patients exhibited decreased levels of the anti-inflammatory protein Annexin I (P<0.05), compatible with a pro-inflammatory behaviour. These findings were confirmed by immunoblotting.

Conclusions: Our data demonstrate that plaque-derived SMC are exposed to higher levels of oxidative stress compared to control SMC. Differences between SMC from symptomatic and asymptomatic patients appear to reflect pro-inflammatory changes associated with plaque instability.

References


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The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.