Dataset related to the article "12(S)-Hydroxyeicosatetraenoic acid downregulates monocyte-derived macrophage efferocytosis: new insights in atherosclerosis"

<p>This record contains raw data related to the article&nbsp;&nbsp;&ldquo;12(S)-Hydroxyeicosatetraenoic acid downregulates monocyte-derived macrophage efferocytosis: new insights in atherosclerosis&quot;</p> <p>Abstract:The involvement of 12(S)-hydroxyeicosatetraenoic acid (12(S)-HETE), a 12-lipooxygenase product of arachidonic acid, has been suggested in atherosclerosis. However,its effecton macrophage functions is not completely&nbsp;understood, so far. The uptake of apoptotic cells (efferocytosis) by macrophages is an anti-inflammatory process, impaired in advanced atherosclerotic lesions. This process induces the release of the anti-inflammatory cytokine interleukin-10 (IL-10), and it is regulated by Rho-GTPases, whose activation involves the isoprenylation, a modification inhibited by statins. We assessed 12-HETE levels in serum of coronary artery disease (CAD) patients, and explored12(S)-HETE invitro effect on monocyte-derived macrophage (MDM) efferocytosis.Sixty-four CAD patients and 24 healthy subjects (HS) were enrolled. Serum12-HETE levels were measured using a tandem mass spectrometry method. MDMs, obtained from a spontaneous differentiation of adherent monocytes, were treated with12(S)-HETE (10&ndash;50&nbsp; ng/mL). Efferocytosis and RhoA activation were evaluated by flow cytometry. IL-10 was measured by ELISA. CAD patients showed increased 12-HETE serum levels compared to HS (665.2 [438.1&ndash;896.2] ng/mL and 525.1 [380.1&ndash;750.1] ng/mL, respectively, p &lt; 0.05) and reduced levels of IL-10. MDMs expressed the12(S)-HETE cognate receptor GPR31. CAD-derived MDMs displayed defective efferocytosis vs HS-MDMs (9.4 [7.7&ndash;11.3]% and 11.1 [9.6&ndash;14.1]% of MDMs that have engulfed apoptotic cells, respectively, p &lt; 0.01). This reduction is marked in MDMs obtained from patients not treated with statin (9.3 [7.4&ndash;10.6]% statin-free CAD vs HS, p=0.01; and 9.9 [8.6&ndash;11.6]% statin-treated CAD vs HS, p=0.07). The in vitro treatment of MDMs with12 (S)-HETE (20ng/mL) induced 20% decrease of efferocytosis (p &lt; 0.01) and 71% increase of RhoA activated form(p &lt; 0.05). Atorvastatin (0.1&mu;M) counteracted these 12(S)-HETE-mediated effects.These results show a12(S)-HETE pro-inflammatory effect and suggest a new potential contribution of this mediator in the development of atherosclerosis.</p> <p>&nbsp;</p>