Endothelial cells and macrophages as allies in the healthy and diseased brain

Adam Denes, Cathrin E. Hansen, Uemit Oezorhan, Sara Figuerola, Helga E. de Vries, Lydia Sorokin, Anna M. Planas, Britta Engelhardt, Markus Schwaninger

Research output: Contribution to journalReview articleAcademicpeer-review

3 Citations (Scopus)

Abstract

Diseases of the central nervous system (CNS) are often associated with vascular disturbances or inflammation and frequently both. Consequently, endothelial cells and macrophages are key cellular players that mediate pathology in many CNS diseases. Macrophages in the brain consist of the CNS-associated macrophages (CAMs) [also referred to as border-associated macrophages (BAMs)] and microglia, both of which are close neighbours or even form direct contacts with endothelial cells in microvessels. Recent progress has revealed that different macrophage populations in the CNS and a subset of brain endothelial cells are derived from the same erythromyeloid progenitor cells. Macrophages and endothelial cells share several common features in their life cycle—from invasion into the CNS early during embryonic development and proliferation in the CNS, to their demise. In adults, microglia and CAMs have been implicated in regulating the patency and diameter of vessels, blood flow, the tightness of the blood–brain barrier, the removal of vascular calcification, and the life-time of brain endothelial cells. Conversely, CNS endothelial cells may affect the polarization and activation state of myeloid populations. The molecular mechanisms governing the pas de deux of brain macrophages and endothelial cells are beginning to be deciphered and will be reviewed here.
Original languageEnglish
Article number38
Pages (from-to)38
JournalActa Neuropathologica
Volume147
Issue number1
DOIs
Publication statusPublished - 1 Jun 2024

Keywords

  • Alzheimer’s disease
  • Angiogenesis
  • Antigen presentation
  • Endothelial cells
  • Microglia
  • Multiple sclerosis
  • Neuroinflammation
  • Perivascular macrophage
  • Stroke
  • Vascular remodelling

Cite this