Literature DB >> 35020000

MicroRNA-181c-5p modulates phagocytosis efficiency in bone marrow-derived macrophages.

Sarojini Singh1, John Henderson1, Mallikarjun Patil1, Praveen K Dubey1, Shubham Dubey1, Ramaswamy Kannappan1, Jianyi Zhang1, Prasanna Krishnamurthy2.   

Abstract

OBJECTIVE AND
DESIGN: Phagocytosis and clearance of apoptotic cells are essential for inflammation resolution, efficient wound healing, and tissue homeostasis. MicroRNAs are critical modulators of macrophage polarization and function. The current study aimed to investigate the role of miR-181c-5p in macrophage phagocytosis.
MATERIALS AND METHODS: miR-181c-5p was identified as a potential candidate in microRNA screening of RAW264.7 macrophages fed with apoptotic cells. To investigate the role of miR-181c-5p in phagocytosis, the expression of miR-181c-5p was assessed in phagocyting bone marrow-derived macrophages. Phagocytosis efficiency was measured by fluorescence microscopy. Gain- and loss-of-function studies were performed using miR-181c-5p-specific mimic and inhibitor. The expression of the phagocytosis-associated genes and proteins of interest was evaluated by RT2 profiler PCR array and western blotting, respectively.
RESULTS: miR-181c-5p expression was significantly upregulated in the phagocyting macrophages. Furthermore, mimic-induced overexpression of miR-181c-5p resulted in the increased phagocytic ability of macrophages. Moreover, overexpression of miR-181c-5p resulted in upregulation of WAVE-2 in phagocyting macrophages, suggesting that miR-181c-5p may regulate cytoskeletal arrangement during macrophage phagocytosis.
CONCLUSION: Altogether, our data provide a novel function of miR-181c-5p in macrophage biology and suggest that targeting macrophage miR-181c-5p in injured tissues might improve clearance of dead cells and lead to efficient inflammation resolution.
© 2022. The Author(s), under exclusive licence to Springer Nature Switzerland AG.

Entities:  

Keywords:  Macrophage; Phagocytosis; miR-181c-5p; miRNAs

Mesh:

Substances:

Year:  2022        PMID: 35020000      PMCID: PMC8919373          DOI: 10.1007/s00011-022-01539-5

Source DB:  PubMed          Journal:  Inflamm Res        ISSN: 1023-3830            Impact factor:   4.575


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