World over the air travel is the fastest growing source of greenhouse gases leading towards global climate change. Estimates show that each long distance flight of a 747 adds approximately 400 tons of CO₂ to the atmosphere. Like elsewhere in Libya too with the expected threefold increase in air travel over the next 30 years, the reliability and environmental impact of aviation are becoming critical issues for the future of flight in the country.

This paper is designed to present greener sky initiative indicating how Civil Aviation Technical College based at Sbia Libya in its march towards sustainable aviation is focusing on critical technologies like: (a) Integrated modeling of vehicles, atmospheric impact, and noise (b) optimization of new aircraft concepts and operations including environmental impact and (c) distributed, adaptive sensing and control. It treats sustainability is the way forward for aviation to …

Abstract

Our previous study showed that circulating microvesicles (cMVs) of diabetic mice have negative effects on the function of endothelial progenitor cells (EPCs). Whether this is true in diabetic patients deserves further study. In this study, the effects of cMVs and EPC-derived MVs (EPC-MVs) on EPC migration, apoptosis, and reactive oxygen species (ROS) production in healthy controls, well-controlled, and uncontrolled diabetic patients were investigated. The levels of miR-126 and vascular endothelial growth factor receptor 2 (VEGFR2) in cMVs, EPC-MVs, and/or EPCs were analyzed. Moreover, miR-126 inhibitor or mimic was applied to EPCs to modulate the miR-126 level in EPC-MVs. We found the following: 1) the circulating EPC level was reduced but the circulating EPC-MV level increased in uncontrolled diabetic patients; 2) the cMVs and EPC-MVs of healthy controls had beneficial effects on EPCs (migration, apoptosis, ROS), whereas the effects were reversely changed in the cMVs and EPC-MVs of uncontrolled diabetic patients; and 3) the cMVs and EPC-MVs of uncontrolled diabetic patients carried less miR-126 and had downregulated VEGFR2 expression in EPCs. Manipulating the miR-126 level in EPC-MVs with inhibitor or mimic changed their function. The effects of cMVs and EPC-MVs are compromised in diabetes due to the reduction of their carried miR-126, which might provide a therapy target for diabetic vascular complications.

diabetes mellitus (DM) is considered one of the major risk factors for various cardiovascular complications. Endothelium dysfunction is a key initiator for vascular disease, which results from increased oxidative stress in the vascular cells (39). Endothelial progenitor cells (EPCs) are known to play important roles in maintaining vascular function and structure by repairing or replacing dysfunctional or injured endothelial cells (ECs) (33). Impaired EPC proliferation, differentiation, adhesion, mobilization, and survival have been reported in DM (1, 26). Our previous study has demonstrated that the circulating EPC level is decreased and the function of EPCs impaired in db/db diabetic mice (8). Moreover, we found that the circulating microvesicles (cMVs) of db/db diabetic mice compromised the functions of EPCs. Investigation on the regulatory effects of cMVs on EPCs in diabetic patients could provide novel therapeutic avenues for vascular complications of diabetes.

Extracellular MVs are submicrometric fragments released from the cells in response to activation and apoptosis (22, 37). cMVs are the MVs released from the cells in the blood and from the vascular wall. An elevation of cMV levels has been reported in vascular diseases such as thrombotic diseases, diabetes, and cardiovascular diseases (2, 8, 25). Furthermore, one study has shown that the level of cMVs could predict the severity of vascular diseases (30). MVs released from EPCs (EPC-MVs) have been reported to serve as an index for EPC loss and functional incompetence (27). Moreover, the level of circulating EPC-MVs can predict aortic stiffness in atherosclerotic patients (27). Therefore, circulating MV and EPC-MV levels could serve as biomarkers and predictors for vascular diseases. On the other hand, accumulating evidence suggests that MVs mediate cell-cell communication via transferring proteins, mRNAs, and miroRNAs (miRs) from their parent cells to the target cells (5, 17, 29). The functions of MVs are complex and multifactorial, depending on the stimulator and origin. Previously, we demonstrated that cMVs of diabetic mice impair the function of EPCs, whereas cMVs of healthy controls do not have detrimental effects on EPCs (8). However, whether this is true in diabetic patients remains unclear.

Previous studies have shown that miR-126 governs vascular integrity (35) and is a biomarker or mediator of vascular diseases (11, 32). Downregulation of miR-126 impairs EPC function (23). EPC-MVs have been shown to improve ischemia-reperfusion injury of hindlimb and kidney through the transfer of miR-126 to target cells (6, 28). In the meantime, miR-126 has been reported to regulate angiogenic process and EC/EPC function by modulating vascular endothelial growth factor receptor 2 (VEGFR2) (13, 15). Our previous study found that EPC-MVs affect EC functions and apoptosis via their carried miR-126 (34). However, it is unknown whether EPC-MVs, as one type of MVs, would affect EPC functions through the miR-126 and its downstream VEGFR2 pathway.

In the present study, we determined the effects of cMVs and EPC-MVs of diabetic patients on EPC survival and functions and explored whether miR-126/VEGFR2 is involved in the mechanism.