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. 2021 Jan 14;22(2):763. doi: 10.3390/ijms22020763

Table 1.

Priming treatments of MSCs and production of therapeutic factors.

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.