Table 1.
Property | Study | Mechanism | Outcome | Reference |
---|---|---|---|---|
Enhance angiogenesis | Mouse ADSCs to mouse hind limb | Production of Cytokines (SDF-1, VEGF) | At 3 weeks, ADSC group had greater perfusion index and a higher capillary density compared to controls. | 30 |
Mouse SVF to mouse hind limb | EC and SMC differentiation | SVFs significantly increased vascular collateral development and capillary density of ischemic muscle. | 31 | |
Mouse ADSC to mouse hind limb | Production of Cytokines (VEGF, HGF) | At 4 weeks after transplantation of ADSCs into the ischemic mouse hindlimb, the angiogenic scores were improved in the ADSC-treated group. | 32 | |
Human SVF to mouse hind limb | EC differentiation | Cultured human SVF cells differentiate into endothelial cells, incorporate into vessels, and promote both post-ischemic neovascularisation in nude mice. | 33 | |
ADSCS to hindlimb of nude mice with FGF-2 | Production of Cytokine (FGF-2, VEGF and HGF) | ADSCs stimulated tube formation in an in vitro tube formation assay. | 34 | |
Enhance wound healing | Rat diabetic skin graft model | Increase of capillary density, collagen intensity, VEGF, and TGF-β3 expression | The gross and histological results showed increased survival, angiogenesis, and epithelialisation in ADSCs seeded full thickness skin grafts. | 35 |
Rat cutaneous skin wound | Production of cytokines (epidermal growth factor and vascular endothelial growth factor) | ADSCs enhanced the cell proliferation and neovascularisation of the regenerated skin. | 36 | |
Rat ulcer model | Promote new blood vessel formation | The wound size after ADSCs treatment for 3 weeks was significantly smaller compared to control (p < 0.01). | 37 | |
Murine full thickness wound defect | Down-modulate TNF-α-dependent inflammation, increase anti-inflammatory macrophage numbers, and induce TGF-β1-dependent angiogenesis, myofibroblast differentiation and granulation tissue formation | ADSCs delivered to murine wounds accelerated wound healing. | 38 | |
Full thickness rat wound defect | Enhanced total vessel formation after 3 weeks. | The ADSCs group showed smaller injury areas at all time points except day 21 and enhanced wound healing compared to the single layer ADSCs sheet at day 7, 10 and 14. | 39 | |
Anti-inflammatory actions | Mouse with SLE | Increasing levels of anti-inflammatory cytokines | ADSCs group showed higher survival rate with improvement of histologic and serologic abnormalities, immunologic function and decreased incidence of proteinuria. | 40 |
Murine model of arthritis | Decreased inflammatory cytokines and autoimmune TH1 cells | Thickening of the synovial lining, formation of enthesophytes associated with medial collateral ligaments and cruciate ligaments were significantly inhibited on day 42 after ADSC treatment, by 31 %, 89 %, and 44 %, respectively. | 41 | |
Suppression of alloreactive T cells | Co-culture of canine ADSCs with leukocyte | Paracrine cytokine production of TGF- β, HGF, prostaglandin E2 (PGE2), and indoleamine-2, 3-dioxygenase (IDO) | Leukocyte proliferation induced by mitogens was suppressed when co-cultured with irradiated ADSCs. | 42 |
Co-culture of human ADSCs and dendritic and T lymphocytes | Paracrine secretion of PGE2 | ADSCs inhibited the maturation of myeloid dentritic cells and plasmocytoid-dentritic cells. | 43 | |
Mouse ADSCs prevented graft versus host disease in mice transplanted with haploid identical hematopoietic grafts | 1. Inhibit the production of inflammatory cytokines (TNF-α, IFN- γ, and IL-12) of T cells so not to induce proliferation of allogeneic T cells | Infusion of ADSCs in mice transplanted with haploidentical haematopoietic grafts controlled the lethal GVHD that occurred in control recipient mice. | 44 | |
2. Suppress the proliferation of T cells induced either by mitogens or allogeneic cells |
Keys: EC endothelial cell; ADSCs adipose derived stem cell, SMC smooth muscle cell, SDF-1 stromal derived factor-1, HGF hepatocyte growth factor, FGF-2 fibroblast growth factor-2, TGF- β1 transforming growth factor-B1, IL-12 Interleukin 12, VEGF vascular endothelilal growth factor, TNF-α transforming growth factor-α, IFN- γ interferon- γ, SLE systemic lupus erythematosus