Integrin-Kindlin3 requirements for microglial motility in vivo are distinct from those for macrophages.

ABSTRACT: Microglia play a critical role in the development and homeostasis of the CNS. While mobilization of microglia is critical for a number of pathologies, understanding of the mechanisms of their migration in vivo is limited and often based on similarities to macrophages. Kindlin3 deficiency as well as Kindlin3 mutations of integrin-binding sites abolish both integrin inside-out and outside-in signaling in microglia, thereby resulting in severe deficiencies in cell adhesion, polarization, and migration in vitro, which are similar to the defects observed in macrophages. In contrast, while Kindlin3 mutations impaired macrophage mobilization in vivo, they had no effect either on the population of microglia in the CNS during development or on mobilization of microglia and subsequent microgliosis i

SUBMITTER: Meller J 

PROVIDER: S-EPMC5453700 | biostudies-literature | 2017 Jun

REPOSITORIES: biostudies-literature