Key result
Cultured circulating T-cells from patients with unstable angina showed markedly increased ACE gene expression and enzymatic activity compared to controls (p<0.001), leading to enhanced de novo Angiotensin II production.
Why the study?
Does in vitro Angiotensin II stimulation increase T-cell ACE gene expression and activity in patients with unstable angina compared to controls?
Observational (n=36)
No
Does in vitro Angiotensin II stimulation increase T-cell ACE gene expression and activity in patients with unstable angina compared to controls?
Circulating T-cells in unstable angina patients exhibit upregulated ACE gene expression and activity, suggesting they may autonomously synthesize Angiotensin II and contribute to local inflammation and plaque vulnerability.
T-cell ACE expression may link to ACS inflammation; hypothesis-generating and should not yet change practice.
: T-cells are endowed with a functional cell-based renin angiotensin system (RAS), related with and by circulating RAS that can autonomously synthesize angiotensin (Ang) II. Angiotensing converting (ACE) is the key step for the regulation of the synthesis of Ang II by RAS and T-cell ACE gene expression reported to be up-regulated in hypertensives with low grade inflammation. Ang II and T-cells play a major role in systemic inflammation that occurs in unstable angina patients, but whether T-cell based RAS is directly involved unknown .This study was aimed at measuring ACE gene expression and enzymatic activity in the cell pellet and in the of human cultured circulating T-cells obtained from control subjects, hypertensive or unstable angina . C reactive protein (CRP) levels as a marker of systemic inflammation were also investigated.
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Coppo et al. (2016) conducted an observational in Unstable Angina and Hypertension (n=36). Unstable angina vs. Healthy controls and hypertensive patients was evaluated on T-cell ACE gene expression and enzymatic activity (p=<0.001). Cultured circulating T-cells from patients with unstable angina showed markedly increased ACE gene expression and enzymatic activity compared to controls (p<0.001), leading to enhanced de novo Angiotensin II production.
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