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. 2021 Sep 23;9:741183. doi: 10.3389/fcell.2021.741183

FIGURE 2.

FIGURE 2

BMSC-Exos transorgan regulation. (A) Effects of BMSC-Exos on intervertebral disc. MiR-21 in BMC-Exos inhibits NPC apoptosis by targeting PTEN through PI3K/AKT signaling pathway. BMC-Exos can provide NPC with mitochondrial proteins, and repair damaged mitochondria by supplementing exosomes. BMC-Exos can increase the expression level of TIMP-1 and inhibit the aging of nucleus pulposus cells. BMSC-Exos can reduce the expression levels of MMP-1 and MMP-3 in nucleus pulposus cells and alleviate the aging of nucleus pulposus cells, play an anti-inflammatory role in NP cells by inhibiting the activation of NLRP3 inflammatory bodies and in AFC by inhibiting autophagy mediated by PI3K/AKT signaling pathway. BMSC-Exos inhibited IL-1β induced inflammation and apoptosis, and promoted AFC proliferation. (B) Effects of BMSC-Exos on heart and blood vessel. BMSC-Exos miR-126 up-regulated the expression of VEGF and Ang-1 and promoted angiogenesis; activated the PI3K/Akt signaling pathway by targeting PIK3R2, and significantly increased the number of new capillaries on the wound. BMSC-Exos can promote angiogenesis by activating HMGB1/AKT signal pathway. High expression of MIF-BMSC-Exos can better enhance cardiac function; miR-125b carried by BMSC-Exos has a therapeutic effect on myocardial ischemia reperfusion injury. Under hypoxia/reoxygenation conditions, cells can inhibit excessive autophagy through the PTEN/AKT/mTOR signal pathway, and change the expression level ofmiR-29c, so as to reduce myocardial ischemia reperfusion injury. (C) Effects of BMSC-Exos on brain and nerve. BMSCs can reduce the apoptosis of OGD neurons and cells by regulating the expression of PTEN and activating the AKT signaling pathway. The combined treatment of BMSC-Exos and Rosuvastatin was more effective in inhibiting arterial occlusion. BMSC-Exos enhanced the expression of NeuN, increased the level of microRNA-146a and decreased the level of NF-κB in astrocytes, thereby increasing the expression of microRNa-146aAD in hippocampus and improving cognitive dysfunction. BMSC-Exos can increase the level of microRNA-146a and decrease the level of NF-κB in astrocytes, thereby increasing the expression of microRNa-146aAD in hippocampus and improving cognitive dysfunction. By activating the SphK/S1P signal pathway, BMSC-Exos enhance the expression of SphK1 and S1P1, and reduce the deposition of Aβ. BMSC-Exos rich in miR-146a-5p can directly down-regulate the expression of IRAK1 and NFAT5, inhibit the polarization of microglia M1, and improve neurological function. BMSC-Exos can exert the anti-inflammatory and anti-apoptotic effects of miR129-5p by inhibiting the activity of HMGB1-TLR4 pathway. (D) Effects of BMSC-Exos on lung, liver and kidney. BMSC-Exos can down-regulate the expression of Sema 3A through the delivery of miR-199a-3p to renal cells, thus activating the AKT and ERK signal pathways, protecting the kidney and alleviating kidney damage. BMSC-Exos can reduce the TLR4 and NF- κB by reducing apoptosis and inflammation, inhibit the TLR4/NF-κB, and alleviate acute lung injury caused by ischemia-reperfusion; up-regulate the expression of LC3 and Beclin-1, reduce the apoptosis of hepatocytes after acute liver failure. (E) Effects of BMSC-Exos on tendon. BMSC-Exos can enhance the expression of Mohawk, Tenomodulin and type I collagen, as well as the mechanical properties of the new tendon, and promote the proliferation of local TSPC in vivo. (F) Effects of BMSC-Exos on skin. BMSC-Exos can effectively promote the proliferation of human keratinocytes and dermal fibroblasts and accelerate the healing of skin wounds. BMSC-Exos can also up-regulate the expression of TGF-β3 and Smad7 in the TGF-β/Smad signal pathway, down-regulate the expression of TGF-β1, Smad2, Smad3, and Smad4, and promote skin wound healing.