Potential role of exosome in post-stroke reorganization and/or neurodegeneration

Abstract

Currently, stroke is a common and devastating condition, which is sometimes associated with permanent cerebral damages. Although in early time after stroke, the related treatments are mainly focused on the restoration of cerebral blood flow (CBF), at the same time, some changes are commencing that continue for a long time and need to be specially noticed. Previous studies have proposed several molecular mechanisms in these post-stroke events. Exosomes are a type of vesicle, which are formed and secreted by most cells as a mean to transfer cellular constituents such as proteins, DNA and/or RNA to distant cells. Therefore, they are considered as a novel mechanism of cellular communication. Herein, we reviewed the current knowledge on cascades, which are activated after stroke and consequently lead to the reorganization and/or continuance of tissue damage and development of other disorders such as Neurodegenerative diseases (ND). Thereafter, we summarized the latest proofs about the possible participation of exosomes in transferring some components such as proteins and micro-RNAs (miRs), from the affected areas to other parts of the brain and eventually cause the above-mentioned post-stroke events.

Keywords: exosome; miR124; miR9; neurodegenerative diseases; stroke.

Figure 1. Two events may occur after a stroke, Reorganization or Neurodegeneration. The green arrow indicates the organization and the factors involved. Two coupled processes, angiogenesis and neurogenesis and growth factors play a key role in a functional reorganization after stroke. The red arrow indicates the factors which may lead to post-stroke Neurodegeneration.

Figure 2. This schematic representation illustrates cell-to-cell communication through exosomes. (A) Exosomes attach to the cell surface and bind to receptors (Yellow icon) to activate intracellular signaling pathways. (B) Exosomes fusion with the target cell membrane. (C) Exosomes enter target cells by endocytic mechanisms (phagocytosis, macropinocytosis, or receptor-mediated endocytosis).

Figure 3. This schematic representation illustrates the release of exosomes from injured neural cells. These exosomes contain numerous types of signaling or pathological molecules which can be transferred from cell to cell. See text for complete details.