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Maximal homing of iv-infused MSC may be critical for cell therapies. Molecular responses from the primarily mechanical effects of pulsed focused ultrasound (pFUS) (i.e., mechanotransduction) in healthy or diseased murine kidneys generate a “molecular zip-code” consisting of local increases in chemoattractants (cytokines, chemokines, cell adhesion molecules) to enhance MSC homing. These findings have substantial potential to improve cell therapies for regenerative medicine. Since molecular signaling post-pFUS drives enhanced MSC homing, other drugs also aiming to treat disease could potentially interfere with molecular responses and subsequent cell migration to targeted tissue thus undermining cell therapy approaches. This study characterized temporal molecular changes post-pFUS to identify critical signals that drive larger changes observed in the chemoattractants and investigates whether inhibition of the early signals could suppress MSC homing to kidneys.

Mesenchymal stem cell (MSC) homing to kidneys is suppressed by inhibiting interleukin 1-α, tumor necrosis factor-α, or cyclooxygenase-2 signaling