Galectin-3 (MAC-2) Controls Microglia Phenotype Whether Amoeboid and Phagocytic or Branched and Non-phagocytic by Regulating the Cytoskeleton.

ABSTRACT: Myelin surrounding central nervous system (CNS) axons breaks down in multiple sclerosis (MS) and following traumatic axonal injury. Myelin-debris so produced is harmful to repair since it impedes remyelination in MS and the regeneration of traumatized axons. These devastating outcomes are largely due to inefficient removal by phagocytosis of myelin-debris by microglia. Therefore, revealing mechanisms that control phagocytosis is vital. We previously showed that in phagocytosis, filopodia and lamellipodia extend/engulf and then retract/internalize myelin-debris. Moreover, cofilin activates phagocytosis by advancing the remodeling of actin filaments (i.e., existing filaments disassemble and new filaments assemble in a new configuration), causing filopodia/lamellipodia to protrude, and furthe

SUBMITTER: Reichert F 

PROVIDER: S-EPMC6427835 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature