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Cell Mol Neurobiol. 2020 Jan 16. doi: 10.1007/s10571-020-00790-w. [Epub ahead of print]

Silencing the Cytoskeleton Protein Iba1 (Ionized Calcium Binding Adapter Protein 1) Interferes with BV2 Microglia Functioning.

Author information

1
Department of Anatomy, Animal Physiology and Biophysics, Faculty of Biology, University of Bucharest, Splaiul Independentei 91-95, Sector 5, 050095, Bucharest, Romania.
2
Institute of Cellular Biology and Pathology 'Nicolae Simionescu' of the Romanian Academy, Bucharest, Romania.
3
Department of Molecular Cell Biology, Institute of Biochemistry, Romanian Academy, Splaiul Independentei 296, 06003, Bucharest, Romania.
4
Pharma Serv International, Sabinelor 52, 050853, Bucharest, Romania.
5
Department of Anatomy, Animal Physiology and Biophysics, Faculty of Biology, University of Bucharest, Splaiul Independentei 91-95, Sector 5, 050095, Bucharest, Romania. v_ristoiu@yahoo.com.

Abstract

Iba1 (ionized calcium binding adapter protein 1) is a cytoskeleton protein specific only for microglia and macrophages, where it acts as an actin-cross linking protein. Although frequently regarded as a marker of activation, its involvement in cell migration, membrane ruffling, phagocytosis or in microglia remodeling during immunological surveillance of the brain suggest that Iba1 is not a simple cytoskeleton protein, but a signaling molecule involved in specific signaling pathways. In this study we investigated if Iba1 could also represent a drug target, and tested the hypothesis that its specific silencing with customized Iba1-siRNA can modulate microglia functioning. The results showed that Iba1-silenced BV2 microglia migrate less due to reduced proliferation and cell adhesion, while their phagocytic activity and P2x7 functioning was significantly increased. Our data are the proof of concept that Iba1 protein is a new microglia target, which opens a new therapeutic avenue for modulating microglia behavior.

KEYWORDS:

BV2 microglia; Iba1 protein; Migration; Phagocytosis; Proliferation; siRNA

PMID:
31950314
DOI:
10.1007/s10571-020-00790-w

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