Journal
PROGRESS IN NEUROBIOLOGY
Volume 152, Issue -, Pages 181-199Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pneurobio.2016.04.004
Keywords
Non-cell autonomous; Help-me signal; CX3CL1/CX3CR1; IL-34; FGF2; Lipocalin-2; TNF; CCL2; VEGF; Transcriptome; Secretome
Categories
Funding
- NINDS NIH HHS [P01 NS055104, R01 NS093415, R37 NS037074] Funding Source: Medline
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Self-preservation is required for life. At the cellular level, this fundamental principle is expressed in the form of molecular mechanisms for preconditioning and tolerance. When the cell is threatened, internal cascades of survival signaling become triggered to protect against cell death and defend against future insults. Recently, however, emerging findings suggest that this principle of self-preservation may involve not only intracellular signals; the release of extracellular signals may provide a way to recruit adjacent cells into an amplified protective program. In the central nervous system where multiple cell types coexist, this mechanism would allow threatened neurons to ask for help from glial and vascular compartments. In this review, we describe this new concept of help-me signaling, wherein damaged or diseased neurons release signals that may shift glial and vascular cells into potentially beneficial phenotypes, and help remodel the neurovascular unit. Understanding and dissecting these non-cell autonomous mechanisms of self-preservation in the CNS may lead to novel opportunities for neuroprotection and neurorecovery. (C) 2016 Elsevier Ltd. All rights reserved.
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