Cell-derived microparticles and the lung

Dario Nieri, Tommaso Neri, Silvia Petrini, Barbara Vagaggini, Pierluigi Paggiaro, Alessandro Celi, Dario Nieri, Tommaso Neri, Silvia Petrini, Barbara Vagaggini, Pierluigi Paggiaro, Alessandro Celi

Abstract

Cell-derived microparticles are small (0.1-1 μm) vesicles shed by most eukaryotic cells upon activation or during apoptosis. Microparticles carry on their surface, and enclose within their cytoplasm, molecules derived from the parental cell, including proteins, DNA, RNA, microRNA and phospholipids. Microparticles are now considered functional units that represent a disseminated storage pool of bioactive effectors and participate both in the maintenance of homeostasis and in the pathogenesis of diseases. The mechanisms involved in microparticle generation include intracellular calcium mobilisation, cytoskeleton rearrangement, kinase phosphorylation and activation of the nuclear factor-κB. The role of microparticles in blood coagulation and inflammation, including airway inflammation, is well established in in vitro and animal models. The role of microparticles in human pulmonary diseases, both as pathogenic determinants and biomarkers, is being actively investigated. Microparticles of endothelial origin, suggestive of apoptosis, have been demonstrated in the peripheral blood of patients with emphysema, lending support to the hypothesis that endothelial dysfunction and apoptosis are involved in the pathogenesis of the disease and represent a link with cardiovascular comorbidities. Microparticles also have potential roles in patients with asthma, diffuse parenchymal lung disease, thromboembolism, lung cancer and pulmonary arterial hypertension.

Conflict of interest statement

Conflict of interest: Disclosures can be found alongside the online version of this article at err.ersjournals.com

Copyright ©ERS 2016.

Figures

FIGURE 1
FIGURE 1
Schematic representations of a) the three types of extracellular vesicles and b) microparticle generation in more detail.
FIGURE 2
FIGURE 2
Simplified scheme of the “extrinsic” pathway of blood coagulation. F: factor.
FIGURE 3
FIGURE 3
Proposed interactions among the environment, lungs, endothelium, bone marrow and adipose tissue in the pathogenesis of chronic obstructive pulmonary disease and its comorbidities. Reproduced and modified from [82] with permission.

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