1.
Exercise training improves high-density lipoprotein-mediated transcription of proangiogenic microRNA in endothelial cells.
Riedel, S, Radzanowski, S, Bowen, TS, Werner, S, Erbs, S, Schuler, G, Adams, V
European journal of preventive cardiology. 2015;(7):899-903
Abstract
BACKGROUND The functional properties of endothelial cells (ECs) for regulating nitric oxide (NO) bioavailability are important for normal endothelial function. Micro-RNAs (miRs) and especially angiomiRs regulate vascular integrity and angiogenesis. Besides regulation of reverse cholesterol transport, high-density lipoprotein (HDL) also stimulates NO generation by ECs. This function is impaired in patients with chronic heart failure (CHF) and can be attenuated by exercise training. The aim of the present study was to evaluate if HDL-induced miR expression is altered in CHF and if exercise training has an impact. METHODS HDL was isolated from CHF patients in NYHA-IIIb (HDLNYHA) and healthy subjects (HDLHealthy) before and after exercise training. Subsequently ECs were incubated for 24 h with the isolated HDL and miR expression was quantified by RT-PCR. RESULTS HDL-induced expression of miR-126, miR-21 and miR-222 was significantly reduced in ECs incubated with HDLNYHA when compared to HDLHealthy. Exercise training attenuated this HDL-induced reduction of miR-126 and miR-21. HDL-induced expression of miR-221 and miR-214 was not altered in CHF compared to controls and no impact of exercise training was noted. CONCLUSION In conclusion, the present study shows that HDL isolated from CHF patients (NYHA-III) reduces the expression of pro-angiogenic miRs (i.e. miR-126 and miR-21), which may contribute to atherogenesis and endothelial dysfunction. However, exercise training was able to attenuate the HDL-induced reduction in pro-angiogenic miRs expression.
2.
Radioidine therapy temporarily increases circulating endothelial cells and decreases endothelial progenitor cells.
Palumbo, B, Palumbo, R, Sinzinger, H
Nuclear medicine review. Central & Eastern Europe. 2003;(2):123-6
Abstract
BACKGROUND Radiotherapy can cause vascular injury. No data on radioiodine therapy and vascular damage are available. MATERIAL AND METHODS We examined the number of circulating endothelial cells (CEC) and circulating endothelial progenitor cells (CEPC) before therapy 1, 2, 3 and 5 days as well as 1, 2, 3, 4, 6, 8, 10, and 12 weeks after therapy with (131)I at doses ranging from 5-200 mCi. The individual number of CEC and CEPC is associated with the presence of risk factors. RESULTS Irrespective of prevalues, CEC exhibited a significant dose-dependent temporary increase reaching the maximum in weeks 1 and 2. In contrast, CEPC show a decrease at the same time. CONCLUSIONS These results indicate that (131)I-therapy induces a dose-dependent radiation injury at the vascular wall level enhancing endothelial desquamation and reducing reendothelialization and thereby a proatherogenic stage. The clinical consequence of these findings still needs to be assessed.