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Harvesting Murine Alveolar Macrophages and Evaluating Cellular Activation Induced by Polyanhydride Nanoparticles
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Combining antimiR-25 and cGAMP Nanocomplexes Enhances Immune Responses via M2 Macrophage Reprogramming.

Marija Petrovic1, Oliwia B Majchrzak1, Rihana Amreen Mohamed Hachime Marecar1

  • 1Institute of Pharmaceutical Sciences of Western Switzerland (ISPSO), Faculty of Science, University of Geneva, 1206 Geneva, Switzerland.

International Journal of Molecular Sciences
|December 17, 2024
PubMed
Summary

Researchers developed antimiR-25/cGAMP nanocomplexes to reprogram immunosuppressive tumor-associated macrophages (TAMs) in glioblastoma. This approach aims to enhance anti-tumor immune responses by shifting TAMs towards a pro-inflammatory M1 phenotype.

Keywords:
EVsPAMAMSTING pathwayantagomir-25antimiR-25cGAMPcancer immunotherapyextracellular vesiclesnanomedicinepolymeric nanoparticles

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Area of Science:

  • Immunology
  • Nanotechnology
  • Oncology

Background:

  • Glioblastoma (GBM) exhibits a highly immunosuppressive tumor microenvironment (TME) characterized by tumor-associated macrophages (TAMs) with an M2 phenotype.
  • GBM-derived extracellular vesicles (EVs) containing microRNA-25 inhibit the cGAS-STING pathway, preventing TAMs from becoming pro-inflammatory M1 macrophages.
  • Targeting TAMs represents a promising strategy to overcome GBM's immune evasion.

Purpose of the Study:

  • To characterize antimiR-25/cGAMP nanocomplexes (NCs) for potential therapeutic applications in glioblastoma.
  • To evaluate the ability of these NCs to modulate TAM phenotype and enhance anti-tumor immunity.

Main Methods:

  • Synthesis and characterization of antimiR-25/cGAMP NCs, including particle size analysis and stability testing across various pH and temperature conditions.
  • Assessment of NC interaction with transferrin (Tf) to evaluate potential for blood-brain barrier (BBB) penetration.
  • Biological assays to determine the effect of NCs on macrophage phenotype, including cGAS-STING pathway activation, type I interferon (IFN-β) production, and M1 polarization markers.

Main Results:

  • Complexation with antimiR-25 resulted in smaller, more stable nanoparticles.
  • AntimiR-25 NCs showed strong interaction with transferrin, indicating potential BBB passage.
  • cGAMP NCs activated the cGAS-STING pathway in macrophages, increasing IFN-β production and promoting M1 polarization; combined antimiR-25/cGAMP NCs further enhanced M1 markers.

Conclusions:

  • AntimiR-25/cGAMP NCs are stable and possess characteristics suitable for glioblastoma therapy.
  • These NCs effectively reprogram TAMs from an immunosuppressive M2 phenotype to a pro-inflammatory M1 phenotype by activating the cGAS-STING pathway.
  • The findings provide a foundation for optimizing antimiR-25/cGAMP NCs to enhance anti-tumor immune responses in glioblastoma.