Nitric Oxide Modulates Postnatal Bone Marrow-Derived Mesenchymal Stem Cell Migration

• Published in: Frontiers in cell and developmental biology 2016-11, Vol.4, p.133-133
• Main Authors: Fuseler, John W, Valarmathi, Mani T
• Format: Article
• Language: English
• Subjects: Actin; Bone marrow stromal cells; Cell and Developmental Biology; Cytoskeleton; fractal analysis; Mesenchymal Stem Cells; Nitric Oxide
• ISSN: 2296-634X; 2296-634X
• DOI: 10.3389/fcell.2016.00133

Nitric oxide (NO) is a small free-radical gas molecule, which is highly diffusible and can activate a wide range of downstream effectors, with rapid and widespread cellular effects. NO is a versatile signaling mediator with a plethora of cellular functions. For example, NO has been shown to regulate actin, the microfilament, dependent cellular functions, and also acts as a putative stem cell differentiation-inducing agent. In this study, using a wound-healing model of cellular migration, we have explored the effect of exogenous NO on the kinetics of movement and morphological changes in postnatal bone marrow-derived mesenchymal stem cells (MSCs). Cellular migration kinetics and morphological changes of the migrating MSCs were measured in the presence of an NO donor (S-Nitroso-N-Acetyl-D,L-Penicillamine, SNAP), especially, to track the dynamics of single-cell responses. Two experimental conditions were assessed, in which SNAP (200 μM) was applied to the MSCs. In the first experimental group (SN-1), SNAP was applied immediately following wound formation, and migration kinetics were determined for 24 h. In the second experimental group (SN-2), MSCs were pretreated for 7 days with SNAP prior to wound formation and the determination of migration kinetics. The generated displacement curves were further analyzed by non-linear regression analysis. The migration displacement of the controls and NO treated MSCs (SN-1 and SN-2) was best described by a two parameter exponential functions expressing difference constant coefficients. Additionally, changes in the fractal dimension ( ) of migrating MSCs were correlated with their displacement kinetics for all the three groups. Overall, these data suggest that NO may evidently function as a stop migration signal by disordering the cytoskeletal elements required for cell movement and proliferation of MSCs.