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Induced neural progenitor cell-derived extracellular vesicles promote neural progenitor cell survival via extracellular signal-regulated kinase pathway.

ABSTRACT: Proposed model for the anti-apoptotic effects of induced neural stem/progenitor cell (iNPC)-derived extracellular vesicles (EVs). iNPC release EVs that are abundantly loaded with growth factor-related proteins. These growth factor-enriched EVs enhance the phosphorylation of extracellular signal-regulated kinase (ERK), but not AKt. The EV-induced activation of ERK pathway then inhibit the apoptosis of NPCs in various pathological conditions including oxidative stress and starvation.

SUBMITTER: Ma Y

PROVIDER: S-EPMC8611769 | biostudies-literature | 2021 Dec

REPOSITORIES: biostudies-literature

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Induced neural progenitor cell-derived extracellular vesicles promote neural progenitor cell survival via extracellular signal-regulated kinase pathway.

Ma Yizhao Y Xu Xiaonan X Li Chunhong C Wang Yi Y Zhu Jie J Xia Xiaohuan X Zheng Jialin C JC

CNS neuroscience & therapeutics 20211013 12

Proposed model for the anti-apoptotic effects of induced neural stem/progenitor cell (iNPC)-derived extracellular vesicles (EVs). iNPC release EVs that are abundantly loaded with growth factor-related proteins. These growth factor-enriched EVs enhance the phosphorylation of extracellular signal-regulated kinase (ERK), but not AKt. The EV-induced activation of ERK pathway then inhibit the apoptosis of NPCs in various pathological conditions including oxidative stress and starvation. ...[more]

PMID: 34643059

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Project description:BackgroundGlioblastomas are lethal brain tumors under the current combinatorial therapeutic strategy that includes surgery, chemo- and radio-therapies. Extensive changes in the tumor microenvironment is a key reason for resistance to chemo- or radio-therapy and frequent tumor recurrences. Understanding the tumor-nontumor cell interaction in TME is critical for developing new therapy. Glioblastomas are known to recruit normal cells in their environs to sustain growth and encroachment into other regions. Neural progenitor cells (NPCs) have been noted to migrate towards the site of glioblastomas, however, the detailed mechanisms underlying glioblastoma-mediated NPCs' alteration remain unkown.MethodsWe collected EVs in the culture medium of three classic glioblastoma cell lines, U87 and A172 (male cell lines), and LN229 (female cell line). U87, A172, and LN229 were co-cultured with their corresponding EVs, respectively. Mouse NPCs (mNPCs) were co-cultured with glioblastoma-derived EVs. The proliferation and migration of tumor cells and mNPCs after EVs treatment were examined. Proteomic analysis and western blotting were utilized to identify the underlying mechanisms of glioblastoma-derived EVs-induced alterations in mNPCs.ResultsWe first show that glioblastoma cell lines U87-, A172-, and LN229-derived EVs were essential for glioblastoma cell prolifeartion and migration. We then demonstrated that glioblastoma-derived EVs dramatically promoted NPC proliferation and migration. Mechanistic studies identify that glioblastoma-derived EVs achieve their functions via activating PI3K-Akt-mTOR pathway in mNPCs. Inhibiting PI3K-Akt pathway reversed the elevated prolfieration and migration of glioblastoma-derived EVs-treated mNPCs.ConclusionOur findings demonstrate that EVs play a key role in intercellular communication in tumor microenvironment. Inhibition of the tumorgenic EVs-mediated PI3K-Akt-mTOR pathway activation might be a novel strategy to shed light on glioblastoma therapy. Video Abstract.

Dataset Information

Induced neural progenitor cell-derived extracellular vesicles promote neural progenitor cell survival via extracellular signal-regulated kinase pathway.

Publications

Induced neural progenitor cell-derived extracellular vesicles promote neural progenitor cell survival via extracellular signal-regulated kinase pathway.

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