中国神经再生研究(英文版) ›› 2023, Vol. 18 ›› Issue (5): 1031-1032.doi: 10.4103/1673-5374.355758

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中枢神经系统胶质细胞的机械转导机制

  


  • 出版日期:2023-05-15 发布日期:2022-11-01

Mechanotransduction mechanisms in central nervous system glia

Brenan Cullimore, Jackson Baumann, Christopher N. Rudzitis, Andrew O. Jo, Denisa Kirdajova, David Križaj*#br#   

  1. Department of Ophthalmology and Visual Sciences, University of Utah School of Medicine, Salt Lake City, UT, USA (Cullimore B, Baumann J, Rudzitis CN, Jo AO, Križaj D)
    Department of Cellular Neurophysiology, Institute of Experimental Medicine, Czech Academy of Sciences, Prague, Czech Republic (Baumann J, Kirdajova D)
    Department of Bioengineering, University of Utah, Salt Lake City, UT, USA (Križaj D)
    Department of Neurobiology, University of Utah, Salt Lake City, UT, USA (Križaj D)
  • Online:2023-05-15 Published:2022-11-01
  • Contact: David Križaj, PhD, david.krizaj@hsc.utah.edu.
  • Supported by:
    This work was supported by the National Institutes of Health (R01EY027920: Cellular and Molecular Mechanisms that Contribute to Pressure-Induced Retinal Inflammation to DK), EY027920, Molecular mechanisms of mechanotransduction in the aqueous outflow pathway (to DK); T32EY024234, Vision Research Training award (to JMB and CNR); P30EY014800, Vision Core Grant at the University of Utah (to DK), Stauss-Rankin Foundation (to DK), and an Unrestricted Grant from Research to Prevent Blindness to the Department of Ophthalmology at the University of Utah. 

摘要: https://orcid.org/0000-0003-4468-3029 (David Križaj)

Abstract: Mechanical forces shape the development, function, and survival of every cell within the central nervous system (CNS) but are particularly important for astroglia, a subtype of glial cell that mediates communication between neurons and blood vessels. Astrocytes utilize changes in intracellular concentration of the 2nd messenger calcium [Ca2+]i to integrate local electrical, chemical, and mechanical microenvironments, with Ca2+-dependent release of gliotransmitters and cytokines implicated in the regulation of neurovascular coupling, short- and long-term synaptic plasticity, and neuronal excitability. These functions may be perturbed by age, tissue swelling (edema), ischemia, physical trauma, and chronic elevations in intraocular or intracranial pressure, to produce a reactive response that manifests as increases in hypertrophy, cell proliferation, and proinflammatory signaling. Astroglial activation by acute and chronic mechanical trauma compromises the integrity of blood-CNS barriers and neuronal function yet information about molecular sensors that transduce mechanical forces into astroglial [Ca2+]i is surprisingly sparse. We know that large tissue deformations that activate astroglia and injure CNS induce [Ca2+]i 
elevations (Rzigalinski et al., 1998; Lindqvist et al., 2010) but it is not known whether the cells are capable of responding to physiological deformations of the extracellular matrix (< 5% strain) and what such force transducers might be.