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Real-Time Imaging of CCL5-Induced Migration of Periosteal Skeletal Stem Cells in Mice

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

John W Fuseler¹, Mani T Valarmathi²

¹Department of Pathology, Microbiology and Immunology, School of Medicine, University of South Carolina Columbia, SC, USA.

Frontiers in Cell and Developmental Biology

|December 10, 2016

Summary

This summary is machine-generated.

Nitric oxide (NO) acts as a stop signal for mesenchymal stem cells (MSCs) migration. This study shows NO disrupts cytoskeletal elements, hindering MSC movement and proliferation in wound healing models.

Keywords:

actin adult stem cell migration adult stem cell proliferation bone marrow stromal cells cytoskeleton fractal analysis mesenchymal stem cells nitric oxide

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Area of Science:

Cell Biology
Stem Cell Biology
Biochemistry

Background:

Nitric oxide (NO) is a signaling molecule with diverse cellular functions, including regulation of cytoskeletal dynamics.
Mesenchymal stem cells (MSCs) are crucial for tissue repair and their migration is a key process in wound healing.
Understanding NO's role in MSC migration is vital for regenerative medicine applications.

Purpose of the Study:

To investigate the effect of exogenous nitric oxide (NO) on the migration kinetics and morphology of bone marrow-derived mesenchymal stem cells (MSCs).
To analyze the impact of NO on single-cell responses during wound healing.
To determine if NO acts as a pro-migratory or anti-migratory signal in MSCs.

Main Methods:

Utilized a wound-healing model with postnatal bone marrow-derived MSCs.
Applied an NO donor, S-Nitroso-N-Acetyl-D,L-Penicillamine (SNAP), in two conditions: immediate application post-wounding (SN-1) and 7-day pretreatment (SN-2).
Measured migration kinetics and morphological changes, including fractal dimension (D), analyzed via non-linear regression.

Main Results:

NO significantly affected MSC migration displacement, with kinetics best described by two-parameter exponential functions.
Changes in the fractal dimension (D) of migrating MSCs correlated with their displacement kinetics across all groups.
Data suggest NO acts as a stop signal, disordering cytoskeletal elements essential for MSC movement and proliferation.

Conclusions:

Exogenous nitric oxide (NO) functions as an inhibitory signal for mesenchymal stem cell (MSC) migration.
NO's mechanism involves the disruption of cytoskeletal organization, thereby impeding cell movement and proliferation.
These findings highlight NO's complex role in cellular processes and have implications for therapeutic strategies involving MSCs.