From: Physiological and pathological consequences of exosomes at the blood–brain-barrier interface
Exosomal cargo | Mechanisms | Target cell | Function | References |
---|---|---|---|---|
Annexin A2 | Making of plasmin | Macrophages and ECs | Pro-angiogenesis | [115] |
Angiopoietin-2 | Tie2-unrelated route | HUVECs | Pro-angiogenesis | [116] |
Alcohol acetyltransferase II, Metastasis Associated 1, Seryl-TRNA Synthetase 1, Rho-associated coiled-coil containing protein kinase 1/2 | Increased VEGF and HIF-1 expression | HUVECs | Pro-angiogenesis | [117] |
Carbonic anhydrase 9 | Enhancing the transcription of MMP-2 | HUVECs | Pro-angiogenesis | [118] |
SRC Proto-Oncogene, Non-Receptor Tyrosine Kinase, insulin-like growth factor 1 receptor, Focal adhesion kinase | VEGF overexpression | Endothelial cells | Pro-angiogenesis | [119] |
The cluster of differentiation 147 | increase in VEGF and MMP | HUVECs | Pro-angiogenesis | [120] |
Delta Like Canonical Notch Ligand 4 | Stopping notch indication | U373 and HUVECs | Pro-angiogenesis | [121] |
EGF Like Repeats And Discoidin Domains 3 | encourage cell migration and expansion | Pro-angiogenesis | [122] | |
Epidermal growth factor receptor III | By initiating the MAPK and Akt paths, the interpretation of the VEGF gene is increased | U373 and HUVECs | Pro-angiogenesis | [123] |
Family With Sequence Similarity 225 Member A lncRNA | By disappointing its receptors NETO2 and FOXP1 as a result of miR-206 mooching, the PI3K/Akt/NF-B/Snail axis is activated | HUVECs | Pro-angiogenesis | [124] |
High Mobility Group Box 3 | In vivo and in vitro, nEXOs that included HMGB3 sped up vasculature | HUVECs | Pro-angiogenesis | [125] |
Influence of interleukin-8 | Regulation via MAPK | HUVECs | Pro-angiogenesis | [126] |
Intercellular Adhesion Molecule 1, CD44v5 | p38 MAPK, RhoA/ROCK, ERK1/2 kinase, Src kinase, and eNOS | HUVECs | Pro-angiogenesis | [127] |
lncRNA UCA1 | The mechanism for AMOTL2/ERK1/2 Trafficking | HUVECs | Pro-angiogenesis | [128] |
IL-6, VEGF, and MMP-2 | Route for WNT5A signal | Endothelial cells | Pro-angiogenesis | [129] |
IL-8, PDGF | PI3K/AKT Trafficking | Endothelial cells | Pro-angiogenesis | [130] |
GM-CSF, HIF1α, HIF-2α | Increased VEGF transcription | ECs and M1/M2 macrophages | Pro-angiogenesis | [131] |
miR-148a-3p | Constraining ERRFI1 to activate the EGFR/MAPK transcription factors | HUVECs | Pro-angiogenesis | [132] |
miR-373 | β-catenin/ Wnt Trafficking | Endothelial cells | Pro-angiogenesis | [133] |
miR-155 | VEGF-A expression is increased through the VHL/HIF-1 route | ARPE-19 | Pro-angiogenesis | [134] |
miR-182-5p | concentrating on Elements 2 and 4 as Kruppel | HUVECs | Pro-angiogenesis | [135] |
miR-9 | JAK-STAT mechanism | Endothelial cells | Pro-angiogenesis | [136] |
miR-497 | VEGF and HIF-1 production are both downregulated | HUVECs | Anti-angiogenesis | [137] |
miR-135b | Elimination of FIH-1 | Endothelial cells | Pro-angiogenesis | [138] |
miR-141 | miR-141/KLF12 passageway in Exos | HUVECs | Pro-angiogenesis | [139] |
miR-10b | reduction in the amount of HOXD10 and KLF4 proteins | HUVECs | Promotes cell invasion | [140] |
miR-145 | STIM1 stimulates vasculature by inhibiting the IRS1-targeting exosomal miR-145 | HUVECs | Pro-angiogenesis | [141] |
miR-21 | VEGF overexpression | HUVECs | Pro-angiogenesis | [142] |
miR-27a | MiR-27a-loaded Exos from RCCC promote tumorigenesis and suppress SFRP1 transcription | HUVECs | Pro-angiogenesis | [143] |
miR-92a-3p | KLF2 is the target of exosomal-released miR-92a-3p, which controls morphogenesis | HUVECs | Pro-angiogenesis | [144] |
miR-122 | a reduction in PKM | Normal cells in the pre-metastatic niche | Promotes metastasis, before angiogenesis | [145] |
miR-210 | VEGF overexpression | Endothelial cells | Pro-angiogenesis | [146] |
miR-1290 | SMEK1 is targeted by miR-1290 to produce an angiogenesis phenotype | HUVECs | Pro-angiogenesis | [147] |
miR-549a | Exosomal miR-549a inhibits HIF1 in HUVECs, which has an impact on the vasculature and endothelial mobility | HUVECs | Pro-angiogenesis | [148] |
miR-21 | enhancing M2 polarity signal transcription in TAMs | CD14 + human monocytes | Pro-angiogenesis | [31] |
M-phase-related transcripts | Stimulation of cellular proliferation and modification of the M-phase of the cell growth | Endothelial cells | Initiate angiogenesis | [36] |
miR-23a | By attacking prolyl, exosomal miR-23a promoted vasculature and dilation of blood vessels. adhesion molecules protein ZO-1 and hydroxylase | HUVECs | Pro-angiogenesis | [149] |
miR-181a | Exos released by the hypoxic PTC carried miR-181a, which inhibits DACT2 by decreasing the expression MLL3 and causes YAP-VEGF-mediated vasculature | HUVECs | Pro-angiogenesis | [150] |
miR-221-3p | Exos produced from CC cells that contained miR-221-3p increased MVEC vasculature in CC via lowering MAPK10 | MVECs | Pro-angiogenesis | [31] |
miR-210 | Diminishment of EFNA3 | Endothelial cells | Pro-angiogenesis | [151] |
miR-130a | reduction of c-MYB | HUVECs | Pro-angiogenesis | [36] |
miR-21 | Rho decreased the expression | HUVECs | Anti-angiogenesis | [152] |
miR-141-3p | NF-B and JAK/STAT3 communication mechanisms activation | HUVECs | Pro-angiogenesis | [153] |
Neuraminidase | Overexpression of MMP-9 and CXCR4 | 786–0 | Enhance migration and invasion | [154] |
Neuraminidase | Src route | HUVECs | Pro-angiogenesis | [155] |
Neuraminidase | VEGF production is upregulated, whereas hepaCAM transcription is downregulated | HUVECs | Pro-angiogenesis | [31] |
PTCH 1, SMO, SHH, Ihh | Exos from CC cells stimulate pro-angiogenic responses in endothelium by upregulating Hh-GLI signaling and modifying target genes for angiogenesis upstream side | HUVECs | Pro-angiogenesis | [156] |
Profilin 2 | In H446 and ECs, t PFN2 stimulated Smad2/3 and pERK | HUVECs | Pro-angiogenesis | [31] |
PFKFB-3 | The development of lactose and Fru-2,6-P2 is rising | HUVECs | Pro-angiogenesis | [157] |
RAMP2-AS1 lncRNA | By depressing miR-2355-target 5p's VEGFR2 by miR-2355-5p syphoning, angiogenesis cell membrane receptors are increased | HUVECs | Pro-angiogenesis | [31] |
TIE2 | Exo-mediated induction of TIE2-expressing macrophages by TIE2-high cancer cells occurs | HUVECs | Pro-angiogenesis | [158] |
TGF-β | Transmission reliant on SMAD | Fibroblasts | Pro-angiogenesis and pro-tumorigenesis | [159] |
Tetraspanin Tspan8 (D6.1A) | MMP, VEGF, and VEGFR transcription is increased | Endothelial cells | Pro-angiogenesis | [160] |
VEGF | uses its tyrosine kinase domains to effect action | HUVECs | Pro-angiogenesis | [31] |
VEGF-A | The increased angiogenic capacity of brain ECs | Brain microvascular Endothelial cells | Pro-angiogenesis | [22] |
Vasorin | encourage cell migration and expansion | HUVECs | Pro-angiogenesis | [161] |
Wnt4 | β-catenin/ Wnt circuit | Endothelial cells | Pro-angiogenesis | [22] |