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Fig. 2 | Stem Cell Research & Therapy

Fig. 2

From: The potential use of mesenchymal stem cells and their exosomes in Parkinson’s disease treatment

Fig. 2

(1) Secretion of α-syn can occur via secretory lysosomes (exocytosis), microvesicle shedding, or multivesicular bodies, with the second and third methods including the release of α-syn into exosomes. α-Syn can be eliminated from the extracellular space by proteolysis. One of the tiny molecules implicated in the proteolytic degradation of aggregated α-syn would be MMP2, a factor generated from MSCs. MMP-2 produced from MSCs breaks freshly formed amyloid fibrils, resulting in a considerable decrease in the quantities of insoluble and oligomeric α-syn. (2) Furthermore, tiny compounds generated from MSCs alter PI3K/Akt signaling, which ultimately regulates multiple downstream targets to increase autophagy. Upregulation of PI3K/AKT promotes autophagy via regulating the expression of autophagy-related genes such as BECN1, ATG, and GABARAPL1. As a result, autophagic flux upregulation by MSC derived small molecules increases the clearance of harmful α-syn aggregates and so plays a vital role in maintaining α-syn homeostasis in the PD-related milieu. (3) MSC interactions with immune system cells, with primary signaling pathways revealed. (4) MSCs secrete neurotrophic factors like as BDNF, NGF, and FGF-2, which interact with injured axons and cause axonal regrowth. 5) When activated by pro-inflammatory mediators, MSCs release paracrine factors such as TSG-6 and IL-4. Paracrine factors stimulate M2 macrophage polarization, resulting in an elevated Th2 response

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