Actin-myosin network influences morphological response of neuronal cells to altered osmolarity.

Autor: Bober BG; Department of Bioengineering, University of California, San Diego, La Jolla, California., Love JM; Fischell Department of Bioengineering, University of Maryland, College Park, Maryland., Horton SM; Department of Orthopaedic Surgery, University of California, San Diego, La Jolla, California., Sitnova M; Fischell Department of Bioengineering, University of Maryland, College Park, Maryland., Shahamatdar S; Fischell Department of Bioengineering, University of Maryland, College Park, Maryland., Kannan A; Fischell Department of Bioengineering, University of Maryland, College Park, Maryland., Shah SB; Department of Bioengineering, University of California, San Diego, La Jolla, California.; Fischell Department of Bioengineering, University of Maryland, College Park, Maryland.; Department of Orthopaedic Surgery, University of California, San Diego, La Jolla, California.
Jazyk: angličtina
Zdroj: Cytoskeleton (Hoboken, N.J.) [Cytoskeleton (Hoboken)] 2015 Apr; Vol. 72 (4), pp. 193-206. Date of Electronic Publication: 2015 May 25.
DOI: 10.1002/cm.21219
Abstrakt: Acute osmotic fluctuations in the brain occur during a number of clinical conditions and can result in a variety of adverse neurological symptoms. Osmotic perturbation can cause changes in the volumes of intra- and extracellular fluid and, due to the rigidity of the skull, can alter intracranial pressure thus making it difficult to analyze purely osmotic effects in vivo. The present study aims to determine the effects of changes in osmolarity on SH-SY5Y human neuroblastoma cells in vitro, and the role of the actin-myosin network in regulating this response. Cells were exposed to hyper- or hypoosmotic media and morphological and cytoskeletal responses were recorded. Hyperosmotic shock resulted in a drop in cell body volume and planar area, a persisting shape deformation, and increases in cellular translocation. Hypoosmotic shock did not significantly alter planar area, but caused a transient increase in cell body volume and an increase in cellular translocation via the development of small protrusions rich in actin. Disruption of the actin-myosin network with latrunculin and blebbistatin resulted in changes to volume and shape regulation, and a decrease in cellular translocation. In both osmotic perturbations, no apparent disruptions to cytoskeletal integrity were observed by light microscopy. Overall, because osmotically induced changes persisted even after volume regulation occurred, it is possible that osmotic stress may play a larger role in neurological dysfunction than currently believed.
(© 2015 Wiley Periodicals, Inc.)
Databáze: MEDLINE
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