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 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The migration of Schwann cells is critical for development of peripheral nervous system and is essential for regeneration and remyelination after nerve injury. Although several factors have been identified to regulate Schwann cell migration, intrinsic migratory properties of Schwann cells remain elusive. In this study, based on time-lapse imaging of single isolated Schwann cells, we examined the intrinsic migratory properties of Schwann cells and the molecular cytoskeletal machinery of soma translocation during migration. We found that cultured Schwann cells displayed three motile phenotypes, which could transform into each other spontaneously during their migration. Local disruption of F-actin polymerization at leading front by a Cytochalasin D or Latrunculin A gradient induced collapse of leading front, and then inhibited soma translocation. Moreover, in migrating Schwann cells, myosin II activity displayed a polarized distribution, with the leading process exhibiting higher expression than the soma and trailing process. Decreasing this front-to-rear difference of myosin II activity by frontal application of a ML-7 or BDM (myosin II inhibitors) gradient induced the collapse of leading front and reversed soma translocation, whereas, increasing this front-to-rear difference of myosin II activity by rear application of a ML-7 or BDM gradient or frontal application of a Caly (myosin II activator) gradient accelerated soma translocation. Taken together, these results suggest that during migration, Schwann cells display malleable motile phenotypes and the extension of leading front dependent on F-actin polymerization pulls soma forward translocation mediated by myosin II activity.
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PMID:Intrinsic migratory properties of cultured Schwann cells based on single-cell migration assay. 2325 34

Surface plasmon resonance (SPR) has developed into a powerful approach for label-free monitoring of cellular behavior. Most cellular responses, however, involve a complex cascade of molecular events which makes identifying the specific components of cellular behavior dynamics contributing to the aggregate SPR signal problematic. Recently, a number of groups have used surface plasmon-enhanced fluorescence (SPEF) microscopy on living cells. In this work, we show that SPEF microscopy can be used to identify the molecular mechanisms responsible for SPR detection of cellular processes. By specifically labeling the actin cytoskeleton in human epithelial kidney cells (HEK 293) and rat vascular smooth muscle cells (A7r5), we correlate cell reorganization observed in SPEF with SPR signal variations reflecting aggregate cellular changes. HEK 293 cells stimulated with angiotensin-II exhibited transient contraction, appearing as an SPR signal decrease with a subsequent increase above the initial baseline. SPEF micrographs showed a decrease in cellular area followed by actin densification and cell spreading. A7r5 stimulated with Latrunculin A showed actin cytoskeleton depolymerization, generating a steady SPR signal decrease, with SPEF micrographs showing extensive collapse of cell actin structures. We observed that SPR monitoring of cellular response is strongly dependent on minute variations in cellular footprint on the substrate as well as changes in the molecular density in the basal portions of the cells. Therefore, combining SPR with imaging of selective fluorescent markers by SPEF allows a more comprehensive deconvolution of the cellular signal in relation to molecular events within the cells.
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PMID:Identification of the molecular mechanisms in cellular processes that elicit a surface plasmon resonance (SPR) response using simultaneous surface plasmon-enhanced fluorescence (SPEF) microscopy. 2384 90