Table 3.
Therapeutic uses of ADSC-Exo
| Ref. | Author | Research in vitro | Research in vivo | Results |
|---|---|---|---|---|
| [47] | Zhi Liu | Exosomes labeled with PKH26 were incubated with the MCM cells |
1. The PKH26-labeled exosomes were taken up by MCM cells 2. Anti-apoptotic effects of ADSC-exosomes on MCM cells under oxidative stress |
|
| [48] | Xiaojun Cui | Rats myocardial I/R and H/R model |
1. ADSCs-ex protect against I/R-induced myocardial injury and suppress H/R-induced cell injury in H9c2 cells in vitro 2. ADSCs-ex activate Wnt/b-catenin signaling to protect against myocardial I/R injury |
|
| [49] | Huiyu Xu | Male SD rats myocardial infarction model |
1. The LVEF and LVFS of rats in the MI + BM-Exo, MI + AD-Exo, and MI + UC-Exo groups were significantly higher than the maternal stem cells 2. The apoptosis of cardiomyocytes and infarction area were significantly reduced in the MI + ADMSC and MI + AD-Exo groups |
|
| [50] | Shengqiong Deng | Mice myocardial infarction model |
1. ADSC-Exo exert a protective effect on myocardial injury by reversing MI-induced myocardial fibrosis and apoptosis and attenuate MI-induced inflammation by promoting macrophage M2 polarization 2. S1P/SK1/S1PR1 signaling pathway participated in the cardioprotective effects ADSC-Exo |
|
| [20] | Junjie Pan | H9c2 cells were transfected with the miR-146a overexpression vector or the EGR1 overexpression vector alone or both in combination | Male Sprague-Dawley (SD) rats myocardial infarction model |
1. MiR-146a abundant exosomes are more protective against suppressed AMI-induced myocardial damage 2. The expression of miR-146a in H9c2 inhibited hypoxic-induced myocardial cell injury by suppressing EGR1 |
| [22] | Vesna Bucan | The DRG neurons were cultured with and without exosomes | Adult rats sciatic nerve injury model | 1. ADSC-Exo can increase the axon length of dorsal root ganglion (DRG) neurons and regenerate damaged nerve |
| [51] | Jing Chen | SCs were cultured in the serum-free SCM added with PBS or ASC-Exos | Male Sprague Dawley (SD) rats sciatic nerve injury model |
1. ADSC-Exo could be easily internalized by Schwann cells (SCs) and significantly promoted their proliferation and migration 2. ASC-Exos increase neurotrophic factor expression and neurite outgrowth 3. The implantation of ASC-Exos improve sciatic nerve regeneration in vivo |
| [52] | Nianhua Feng | DiI-labeled ADSC-Exo were cocultured with BV2 cells |
1. ADSC-Exo suppressed the activation and decreased the toxicity of LPS-stimulated BV2 cells 2. ADSC-Exo inhibited neuroinflammation by suppressing NF-kB and MAPK signal pathway |
|
| [21] | Yujia Yang | BMECs were subjected to OGD for 4 h and then cultured with ADSC-Exo | 1. ADSC-Exo contribute to angiogenesis of BMECs following OGD in vitro through microRNA-181b/TRPM7 axis. | |
| [53] | Mijung Lee | Mice in vitro HD model | 1. ADSC-Exo treatment can reduce Huntington protein aggregation, improve mitochondrial dysfunction, and reduce the rate of apoptosis | |
| [54] | Mijung Lee | NSCs from G93A ALS mice model used in vitro ALS model |
1. ADSC-exo reduces mutant SOD1 aggregation in G93A neuronal cells 2. ADSC-exo reduce abnormally expressed mitochondrial functional proteins, and restore the normal cell phenotype of amyotrophic lateral sclerosis |
|
| [55] | Takeshi Katsuda | PKH67-labeled exosomes were incubated with N2a cells | 1. ADSC-exo- contain enzymatically active NEP and can be transferred to the neuroblastoma cell line N2a to reduce its intracellular Aβ level and reduce the accumulation of Aβ in the brain | |
| [56] | Li Hu | Skin fibroblasts were co-cultured with ASCs-Exos | Mice skin wound model |
1. Internalization of exosomes by fibroblasts and ASCs-Exos promoted fibroblasts migration, proliferation, collagen synthesis in vitro. 2. ASCs-Exos promoted collagen expression and cutanenous wound healing in vivo than local injection group |
| [57] | Wei Zhang | The HDFs were cocultured with different concentrations of ADSC-Exos | 20 male Balb/c mice full-thickness square wound |
1. ADSC-Exos activate intracellular collagen secretion in HDFs via the PI3K/Akt signaling pathway and induce the expression of growth factors in vitro 2. ADSC-Exos promote cutaneous wound healing in mice |
| [58] | Tao Ma | HaCaT cells were cultured with ADSC-Exo |
1. ADSC-Exo promote cell proliferation, migration, and inhibit cell apoptosis of HaCaT cells impaired by H2O2 2. ADSC-Exo activates Wnt/β-catenin signaling to prompt wound healing |
|
| [59] | Chen Yang | The HaCaT cells with or without pretreated with miR-21 plasmid were treated with the ADSCs with or without GW4869 pretreated、AD-exos | Full layer skin wound BALb/c mice model |
1. AD-exos and miR-21 could improve the migration and proliferation of the HaCaT cells 2. ADSC-Exos could improve the healing velocity in the full layer wound model of BALb/c mouse and higher miR-21 expression were detected in the experiment groups 3.The excess TGF-βI had negative feedback influence on the miR-21 expression 4. MiR-21 could enhance the MMP-9 and TIMP-2 protein expression but not MMP-2 and TIMP-1 protein via the PI3K/AKT pathway |
| [60] | K. LIU | Female nude mice acute cutaneous wound healing model |
1. The most prominent wound closure was observed in the ASC-Exo + HA group. 2. ASC-Exo + HA could markedly promote fibroblast activities, re-epithelialization and vascularization in wound healing |
|
| [61] | Xue Li | The Dil-labeled or denatured exosomes were incubated with EPCs | Adult female Sprague Dawley rats diabetic skin wound model |
1. ADSC-Exo reduce glucose-induced EPC senescence 2. Exosomes derived from Nrf2 overexpressing ADSCs inhibit ROS and inflammatory cytokine expression and promote cutaneous wound healing |
| [62] | Byong Seung Cho | Biostir®-AD cream-induced NC/Nga mice atopic dermatitis model |
1. ASC-Exo reduced the serum IgE levels, the number of inflammatory cells such as CD86 + and CD206 + and the symptoms of atopic dermatitis 2. ADSC-Exo can down-regulate the levels of IL-4, IL-23, IL-31, and TNF-α mRNA in a dose-dependent manner. |