Table 1.
Source of EVs | Key characteristics | Functions | References | ||
---|---|---|---|---|---|
Size | Markers | Contents | |||
Embryo/embryonic stem cells | 50–200 nm | CD9, CD63, ALIX, HLA-G | mRNAs of the pluripotency genes such as Oct4, Sox2, Klf4, c-Myc, Nanog and mi RNAs | Mediates embryo growth Promotes embryo implantation |
[17–21] |
Oviduct epithelium | 30–100 nm, > 100 nm | OVGP1 | Total of 315 proteins with varying distribution among the in vivo and in vitro derived EVs | Promotes early embryonic development | [27] |
Endometrial epithelial cells | 40–150 nm | Tetraspanins, CD9, CD63 | 254 proteins and 227 miRNAs | Control trophoblast physiology which can promote embryo implantation | [32–34] |
Endometrial stromal cells | 30–120 nm | Tetraspanin-6, disintegrin, metalloproteinase domain-containing protein 10 | 250 proteins and several miRNAs including miR-21, miR-126 | Control angiogenesis Promote Cell proliferation Crucial role in embryonic and fetal survival |
[37–39] |
Placenta | 50–150 nm | NKGD2 ligands, FasL, TRAIL, syncytin, placental alkaline phosphatase TGF-β | mRNA, miRNA and proteins | Feto-maternal tolerance Pro-inflammatory, anti-angiogenic and procoagulant activity |
[41–49] |
Endothelial and adipose tissue | 150–200 nm | TNF-α, CD63, HSP-TNF-α HPS70 CD63 | 231 proteins and miRNAs and proteins | Contribute to the systemic inflammation and insulin resistance seen in obese gestational diabetic pregnancies | [50–52] |
Microbial (group B Streptococcus) | < 50 nm, 150–300 nm | Unknown | cAMP factor, Hyaluronate lyase, PcsB protein, DNA, RNA | Degradation of amniotic membranes Mechanical weakening resembling preterm premature rupture membrane (PPROM) Fetal death and preterm delivery |
[61] |