Table 1 MT is an effective agent to alleviate the apoptotic factors for protecting MSCs from injury, while it also acts as an inhibitory agent or a promotive agent according to MSC differentiation fate
Concentration | Time point | MSC resource | Effect | Mechanism | Ref |
|---|---|---|---|---|---|
10 nM, 1 μM, 100 μM | Cotreatment | Bone marrow | No effect on the proliferation of MSCs, inhibits adipogenic differentiation of MSCs, enhances MSC osteogenic differentiation | PPARc expression↓, Runx2 expression↑ | [49] |
50 nM | Cotreatment | Adipose | Increases the ALP expression | MT2 receptor↑, MEK/ERK (1/2) ↑ | [50] |
10 nM, 1 μM, 100 μM | Cotreatment | Synovium | Improves the proliferation of MSCs, protects cell viability in the presence of IL-1β, promotes MSC osteogenic differentiation when exposed to IL-1β | SOD↑ | [52] |
1 μM, 10 μM, 100 μM | Cotreatment | Adipose | Reduces the senescent progress and abnormal activation of autophagy | AKT↑, ROS↓ | [53] |
50 μM, 100 μM | Post-treatment | Bone marrow | Reduces cell death of MSCs | AMPK↑, acetyl-CoA carboxylase↑ | [54] |
1 μM | Pretreatment | Adipose | Enhances MSC proliferation and self-renewal and diminishes the extent of MSC apoptosis | PrPC-dependent pathway↑ | [55] |
10–300 nM | Pretreatment | Bone marrow | Protects against hypoxia/serum deprivation-induced injury | ERK1/2↑ | [56] |
5 μM | Pretreatment | Bone marrow | Prevents MSC apoptosis | Mitogenic factors↑ | [57] |
10 nM, 1 μM, 100 μM | Post-treatment | Bone marrow | Reverses H2O2-induced senescence | P38MAPK↓, p16INK4α↓, SIRT1↑ | [59] |
10 nM, 1 μM, 100 μM | Post-treatment | Bone marrow | Restores the impaired differentiation ability of MSCs induced by H2O2 | SIRT1↑ | [59] |
10 nM, 1 μM, 100 μM | Pretreatment | Bone marrow | Maintains the morphology, viability, and osteogenic differentiation ability of MSCs | ROS↓, p53/ERK/p38↓ | [61] |
50 nM | Cotreatment | Bone marrow | Inhibits adipogenic differentiation of MSCs at the early stage of adipogenic differentiation | ROS↓, phosphorylating ERK/GSK-3β↓ | [62] |
50 nM | Cotreatment | Bone marrow | Promotes chondrogenic differentiation of MSCs | MT receptor-dependent pathway↑ | [63] |
50 nM | Cotreatment | Bone marrow | Restores the pellet size and matrix accumulation, upregulates chondrogenic differentiation of MSCs, reduces cell apoptosis during the whole chondrogenesis | IL-1β-induced activation of NF-κB signaling↓ | [64] |
1 μM | Cotreatment | Synovium | Rescues the IL-1β and TNF-α impaired chondrogenesis of MSCs | ROS↓, SOD↑, MMPs↓ | [65] |
10 μM, 50 μM, 100 μM, 200 μM | Pretreatment | Adipose | Rescues MSCs from cell death induced by oxidative stress; 100 μM of MT confers greater cytoprotection on MSCs than 200 μM | ROS↓, P38MAPK↓, harmful inflammatory cytokines↓ |  |