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Review
. 2019 Aug 29;8(9):1345.
doi: 10.3390/jcm8091345.

Exosomal miRNAs in Lung Diseases: From Biologic Function to Therapeutic Targets

Julien Guiot  1   2 , Ingrid Struman  3   4 , Edouard Louis  3   5 , Renaud Louis  6   3 , Michel Malaise  3   7 , Makon-Sébastien Njock  8   9   10   11
Affiliations
Review

Exosomal miRNAs in Lung Diseases: From Biologic Function to Therapeutic Targets

"V体育安卓版" Julien Guiot et al. J Clin Med. .

Abstract (VSports手机版)

Increasing evidence suggests the potential role of extracellular vesicles (EVs) in many lung diseases. According to their subcellular origin, secretion mechanism, and size, EVs are currently classified into three subpopulations: exosomes, microvesicles, and apoptotic bodies. Exosomes are released in most biofluids, including airway fluids, and play a key role in intercellular communication via the delivery of their cargo (e. g. , microRNAs (miRNAs)) to target cell. In a physiological context, lung exosomes present protective effects against stress signals which allow them to participate in the maintenance of lung homeostasis. The presence of air pollution alters the composition of lung exosomes (dysregulation of exosomal miRNAs) and their homeostatic property VSports手机版. Indeed, besides their potential as diagnostic biomarkers for lung diseases, lung exosomes are functional units capable of dysregulating numerous pathophysiological processes (including inflammation or fibrosis), resulting in the promotion of lung disease progression. Here, we review recent studies on the known and potential role of lung exosomes/exosomal miRNAs, in the maintaining of lung homeostasis on one hand, and in promoting lung disease progression on the other. We will also discuss using exosomes as prognostic/diagnostic biomarkers as well as therapeutic tools for lung diseases. .

Keywords: acute lung injury/acute respiratory distress syndrome; asthma; chronic obstructive pulmonary disease; diagnostic biomarkers; exosomes; idiopathic pulmonary fibrosis; lung diseases; microRNAs; therapeutics V体育安卓版. .

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"V体育安卓版" Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Lung extracellular vesicles (EVs) participate in the maintenance of lung homeostasis. (1) In a physiological context, bronchial epithelial cells (EC)-derived exosomes contain mucin (MUC) protein, which give them a neutralizing effect on human influenza virus and participate in innate mucosal defense [33,34]. (2) In the alveolar space, alveolar macrophage-derived exosomes are able to modulate inflammatory signaling by the transfer of suppressor of cytokine signaling (SOCS) proteins [35] or (3) miR-223 in various respiratory cells, including alveolar ECs and monocytes [36]. (4) Endothelial-derived EVs could also participate in lung homeostasis by delivering anti-inflammatory miR-10a to respiratory cells [28].
Figure 2
Figure 2
Role of lung EVs in the pathogenesis of Chronic Obstructive Pulmonary Disease (COPD). In the context of COPD, bronchial ECs-derived EVs are able to induce myofibroblast differentiation by the delivery of (1) miR-21 [30] and (2) miR-210 [31] to lung fibroblasts. (3) Furthermore, endothelial-derived EVs are able to inhibit the clearance of apoptotic cells by delivering let-7d, miR-191, miR-126, and miR-125a in lung macrophages [17].
Figure 3
Figure 3
Role of lung EVs in the pathogenesis of asthma. (1) In the context of asthma, elevated levels of three sputum microRNAs (miRNAs), miR-629-3p, miR-223-3p, and miR-142-3p, in the sputum of patients with severe asthma, have been reported [47]. The delivery of miR-629-3p in lung ECs could participate in lung inflammation (release of pro-inflammatory cytokines, interleukin (IL)-6 and IL-8, by ECs) [47]. (2) The levels of EV-derived miRNAs selectively expressed by immune cells, including miR-223 and miR-142a, increased in bronchoalveolar lavage fluid (BALF) from allergen-treated mice [32]. It would be interesting to study the impact of these exosomal miRNAs on lungs.
Figure 4
Figure 4
Role of lung EVs in the pathogenesis of Acute Lung Injury/Acute Respiratory Distress Syndrome (ALI/ARDS) (1–5). In the context of ALI/ARDS, EVs released by bronchial ECs and alveolar macrophages contribute to lung inflammation. Indeed, these vesicles are able to activate macrophages and promote the infiltration of immune cells (macrophages, neutrophils) in the lung in a miRNA transfer-dependent manner (delivery of (1) miR-17/miR-221 [51] and (3) miR-320a/miR-221 [53] in alveolar macrophages via epithelial EVs) or (2) caspase-3-dependent manner [52]. (4) In addition, the alveolar macrophages-derived EVs are able to promote the proliferation of lung ECs by delivering miR-221/222 [54]. (5) After bacterial lung infection, alveolar EC-derived EVs contribute to innate immune responses by delivering miRNAs into alveolar macrophages, subsequently promoting inflammasome activation, neutrophil recruitment, and M1-macrophage polarization [55].
Figure 5
Figure 5
Role of lung EVs in the pathogenesis of Idiopathic Pulmonary Fibrosis (IPF). (1) In the context of IPF, macrophage-derived EVs promote the progression of pulmonary fibrosis by delivering miR-328 to pulmonary interstitial fibroblasts which enhances their proliferation [65]. (2) Altered levels of three exosomal miRNAs (miR-142-3p, miR-33a-5p, let-7d-5p) in the sputum of IPF patients have been reported [25]. These exosomal miRNAs could play a crucial role in the IPF progression.
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