Dataset Information

Microglia polarization and anti-glioma effects fostered by dual cell membrane-coated doxorubicin-loaded hexagonal boron nitride nanoplatelets

ABSTRACT: Glioblastoma multiforme (GBM) is a highly malignant brain cancer, and microglial cells play a critical role in its progression. Activation of microglia can either promote or inhibit GBM growth depending on the stage of tumour development and on the microenvironment. As current treatments for GBM have limited efficacy, there is an urgent need to develop novel strategies based on nanoplatforms for drug delivery and efficient targeting. This study investigated the microglial response and the therapeutic efficacy of dual cell membrane-coated and doxorubicin-loaded hexagonal boron nitride nanoplatelets, tested on human microglia and GBM cells. The results showed promising therapeutic effects on glioma cells and an M2 microglia polarization, highlighted through proteomic analysis.

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Brain, Cell Culture

SUBMITTER: Martina Bartolucci

LAB HEAD: Andrea Petretto

PROVIDER: PXD043557 | Pride | 2024-01-26

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	20220809_120612_Ozlem.sne	Other
	Ciofani_Ozlem_0822_C1_41.raw	Raw
	Ciofani_Ozlem_0822_C2_42.raw	Raw
	Ciofani_Ozlem_0822_C3_43.raw	Raw
	Ciofani_Ozlem_0822_Ch1_49.raw	Raw

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Publications

Microglia Polarization and Antiglioma Effects Fostered by Dual Cell Membrane-Coated Doxorubicin-Loaded Hexagonal Boron Nitride Nanoflakes.

Şen Özlem Ö Emanet Melis M Mazzuferi Martina M Bartolucci Martina M Catalano Federico F Prato Mirko M Moscato Stefania S Marino Attilio A De Pasquale Daniele D Pugliese Giammarino G Bonaccorso Francesco F Pellegrini Vittorio V Castillo Antonio Esau Del Rio AEDR Petretto Andrea A Ciofani Gianni G

ACS applied materials & interfaces 20231205 50

Microglial cells play a critical role in glioblastoma multiforme (GBM) progression, which is considered a highly malignant brain cancer. The activation of microglia can either promote or inhibit GBM growth depending on the stage of the tumor development and on the microenvironment conditions. The current treatments for GBM have limited efficacy; therefore, there is an urgent need to develop novel and efficient strategies for drug delivery and targeting: in this context, a promising strategy cons ...[more]

PMID: 38051559

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Project description:Microglia colonize the brain parenchyma at early stages of development and accumulate in specific regions where they actively participate in cell death, angiogenesis, neurogenesis and synapse elimination. A recurring feature of embryonic microglial distribution is their association with developing axon tracts which, together with in vitro data, supports the idea of a physiological role for microglia in neurite development. Yet the demonstration of this role of microglia is still lacking. Here, we have studied the consequences of microglial dysfunction on the formation of the corpus callosum, the largest connective structure in the mammalian brain, which shows consistent microglial accumulation during development. We studied two models of microglial dysfunction: the loss-of-function of DAP12, a key microglial-specific signaling molecule, and a model of maternal inflammation by peritoneal injection of LPS at E15.5. We performed transcriptional profiling of maternally inflamed and Dap12-mutant microglia at E17.5. We found that both treatments principally down-regulated genes involved in nervous system development and function, particularly in neurite formation. We then analyzed the functional consequences of these microglial dysfunctions on the formation of the corpus callosum. We also took advantage of the Pu.1-/- mouse line, which is devoid of microglia. We now show that all three models of altered microglial activity resulted in the same defasciculation phenotype. Our study demonstrates that microglia are actively involved in the fasciculation of corpus callosum axons. To investigate possible roles for microglial during brain development, we challenged microglial function by two complementary approaches. First, we induced maternal inflammation by peritoneal injection of LPS into pregnant dams. Next, we analyzed the consequences of a loss of function of DAP12, a signaling molecule specifically expressed in microglia that is crucial for several aspects of microglia biology (references in Wakselman et al., 2008). We compared the gene expression profiles of microglia from control, maternally-inflamed by LPS (MI), and Dap12-mutated embryos. We isolated RNA from FACS sorted maternally inflamed (by LPS) and Dap12-mutant microglia at E17.5 pooled per pregnant dam; as a control we included PBS treated and untreated (UT) microglia. We compared gene expression between maternally inflamed microlgia (PBSvsLPS) and DAP12-mutant microglia (UTvsDAP12KO).