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Yen N. Diep,Hee Jung Park,Joon‑Ho Kwon,Minh Tran,Hae Young Ko,조한희,Jisu Kim,Jee‑In Chung,김태영,Dongwoo Kim,Jong Hee Chang,You Jung Kang,C. Justin Lee,윤미진,Hansang Cho 한국생체재료학회 2023 생체재료학회지 Vol.27 No.00
Background Glial scar formation is a reactive glial response confining injured regions in a central nervous system. However, it remains challenging to identify key factors formulating glial scar in response to glioblastoma (GBM) due to complex glia-GBM crosstalk. Methods Here, we constructed an astrocytic scar enclosing GBM in a human assembloid and a mouse xenograft model. GBM spheroids were preformed and then co-cultured with microglia and astrocytes in 3D Matrigel. For the xenograft model, U87-MG cells were subcutaneously injected to the Balb/C nude female mice. Results Additional glutamate was released from GBM-microglia assembloid by 3.2-folds compared to GBM alone. The glutamate upregulated astrocytic monoamine oxidase-B (MAO-B) activity and chondroitin sulfate proteoglycans (CSPGs) deposition, forming the astrocytic scar and restricting GBM growth. Attenuating scar formation by the glutamate– MAO-B inhibition increased drug penetration into GBM assembloid, while reducing GBM confinement. Conclusions Taken together, our study suggests that astrocytic scar could be a critical modulator in GBM therapeutics.