Table 1.
MSCs | Priming Treatments | MSC Product | Functional Factors Detected | Biological Effects | Reference |
---|---|---|---|---|---|
AMSCs | IFN-γ | EXOs | miR-23a, miR-26b, miR-125b, miR-130b, miR-140, miR-203a, miR-223, miR-224, miR-320a | Regulation of T cell activation/anergy and induction of M2-like polarized phenotype in monocytes | [20] |
AMSCs | 3D cultures/spheroids | CM EXOs | HGF, PDGF, TGF-β, VEGF, FGF1, GROα, SDF-1, EGF, IL-6, PGE2, LIF | Increased angiogenesis and inhibition of PBMC proliferation | [35] |
BM-MSCs | IL-1α/β; TNF-α; IFN-γ | CM | G-CSF | Reduction in the secretion of inflammatory mediators in LPS-activated microglial cells | [36] |
AdMSCs | Hypoxia | CM | IL-6, TNF-α, HGF, VEGF | Induced liver regeneration | [56] |
BM-MSCs | Hypoxia | CM | VEGF | Induced liver regeneration | [57] |
BM-MSCs | Hypoxia | CM | Wnt4 | Improvement of vascular and skeletal muscle fiber regeneration | [58] |
BM-MSCs | Hypoxia | CM | - | Induced cardiomyocytes proliferation | [59] |
MSCs | Hypoxia | EXOs | miR-26 | Improvement of cardiomyocyte survival | [60] |
BM-MSCs | Hypoxia | CM | HGF, VEGF | Improvement of neuronal cells proliferation | [61] |
UC-MSCs | Hypoxia | CM | HGF, BDNF, VEGF | Improvement of axonal survival | [62] |
AdMSCs | TNF-α | CM | BMP2 | Improvement of bone regeneration | [63] |
AdMSCs | TNF-α | EXOs | Wnt3a | Promoted the proliferation and osteogenic differentiation of primary osteoblastic cells | [64] |
DP-MSCs | bFGF; Hypoxia | CM | - | Improvement of bone formation | [65] |
BM-MSCs | cAMP, bFGF, PDGF, Heregulin β1 | CM | GDNF, BDNF | Induction of striatal dopaminergic nerve terminals regeneration | [67] |
BM-MSCs | cAMP, bFGF, PDGF, Heregulin β1 | CM | GDNF, BDNF | Reduction of striatal volume changes associated with quinolinic acid lesions | [68] |
BM-MSCs | Lithium, VPA | CM | - | Improvement of motor and behavior performance, and reduction of neuronal death and huntingtin aggregates in the striatum | [70] |
DP-MSCs | bFGF; Hypoxia | CM | VEGF | Improvement of vascularization | [97] |
DP-MSCs | Hypoxia | CM | VEGF | Improvement of vascularization | [98] |
AdMSCs | Hypoxia | EXOs | - | Increase of migration and tube formation by HUVEC | [99] |
AdMSCs | Hypoxia | CM | VEGF, HGF, bFGF | Increase of MSC angiogenic potential | [101] |
WJ-MSCs | Hypoxia | CM | Angiogenin and VEGF | Increase of migration and tube formation angiogenesis | [102] |
AdMSCs | Hypoxia | CM | EGF, VEGF, FGF, HGF | Improvement of functional recovery and neovascularization of the ischemic tissue | [103] |
MSCs | Hypoxia | CM | VEGF | - | [108] |
BM-MSCs | Hypoxia | EXOs | miR-125 | Improvement of cardiac function | [110] |
BM-MSCs | IL-17 | CM | IL-6 | Suppression of T cell proliferation; inhibition of both T cell activation and Th1 cytokines | [119] |
AdMSCs BM-MSCs CB-MSCs | IFN-γ | CM | IDO | Suppression of human lymphocyte proliferation | [120] |
BM-MSCs | IL-17 | CM | IL-6 | T cell immunosuppression | [122] |
BM-MSCs | IFN-γ; TNF-α | CM | PGE2, IDO | Inhibition of allogeneic MLR | [123] |
BM-MSCs | IFN-γ; LPS; TNF-α | CM | PGE2 | Induction of monocytes polarization toward an anti-inflammatory M2 phenotype | [124] |
BM-MSCs | IL-1β; IFN-γ | CM | IL-6 | Induction of monocytes polarization toward an anti-inflammatory M2 phenotype | [125] |
MSCs | IL-1β | EXOs | miR-21 | Induced macrophage M2 polarization and ameliorates sepsis | [126] |
UC-MSCs | IL-1β | EXOs | miR-146a | Amelioration of murine sepsis and induction of monocytes polarization toward an anti-inflammatory M2 phenotype | [127] |
BM-MSCs | IFN-γ; Spheroids | CM | IDO | Suppression of T-cell activation and proliferation in vitro | [128] |
BM-MSCs | Hypoxia | CM | PGE2, miR-210 | Induced macrophage M2 polarization and ameliorates fibrosis | [137] |
MSCs: mesenchymal stem cells; BM-MSCs: bone marrow-derived MSCs; AMSCs: amnion-derived MSCs; UC-MSCs: umbilical cord-derived MSCs; AdMSCs: adipose-derived MSCs; CB-MSCs: cord blood-derived MSCs; GMSCs: gingival-derived MSCs; WJ-MSCs: Wharton’s Jelly-derived MSCs; DP-MSCs: dental pulp-derived MSCs.