Background and Objectives Photobiomodulation (PBM) describes the influence of light irradiation on biological tissues. Laser light in the near‐infrared (NIR) spectrum has been shown to mitigate pain, reduce inflammation, and promote wound healing. The cellular mechanism that mediates PBM's effects is generally accepted to be at the site of the mitochondria, leading to an increased flux through the electron transport chain and adenosine triphosphate (ATP) production. Moreover, PBM has been demonstrated to reduce oxidative stress through an increased production of reactive oxygen species (ROS)‐sequestering enzymes. The aim of the study is to determine whether these PBM‐induced effects expedite or interfere with the intended stem cell differentiation to the adipogenic lineage. Study Design/Materials and Methods To determine the effects of 1064 nm laser irradiation (fluence of 8.8–26.4 J/cm2) on human mesenchymal stem cells (hMSCs) undergoing adipogenic differentiation, the ATP and ROS levels, and adipogenic markers were quantitatively measured. Results At a low fluence (8.8 J/cm2) the ATP increase was essentially negligible, whereas a higher fluence induced a significant increase. In the laser‐stimulated cells, PBM over time decreased the ROS level compared with the non‐treated control group and significantly reduced the extent of adipogenesis. A reduction in the ROS level was correlated with a diminished lipid accumulation, reduced production of adipose‐specific genetic markers, and delayed the chemically intended adipogenesis. Conclusion We characterized the use of NIR light exposure to modulate adipogenesis. Both the ATP and ROS levels in hMSCs responded to different energy densities. The current study is expected to contribute significantly to the growing field of PBM as well as stem cell tissue engineering by demonstrating the wavelength‐dependent responses of hMSC differentiation. Lasers Surg. Med. © 2020 Wiley Periodicals LLC.

Blast-induced traumatic brain injury (bTBI) can result in cell/tissue damage and lead to clinical and neuropsychiatric symptoms. Shock waves from a blast propagate through the brain and initiate cascades of mechanical and physiological events that can adversely affect the brain function. Although studies using animal models and brain slices have shown macroscale changes in the brain tissue in response to blast, systematic elucidation of coupling mechanisms is currently lacking. One mechanism that has been postulated and demonstrated repeatedly is the blastinduced generation and subsequent collapse of micron-size bubbles (i.e., microcavitation). Using a custom-designed exposure system, we have previously reported that upon collapsing of microbubbles, astrocytes exhibited changes in the cell viability, cellular biomechanics, production of reactive oxygen species, and activation of apoptotic signaling pathways. In this paper, we have applied microfabrication techniques and seeded astrocytes in a spatially controlled manner to determine the extent of cell damage from the site of the collapse of microbubbles. Such a novel experimental design is proven to facilitate our effort to examine the altered cell viability and functionality by monitoring the transient calcium spiking activity in real-time. We now report that the effect of microcavitation depends on the distance from which cells are seeded, and the cell functionality assessed by calcium dynamics is significantly diminished in the cells located within ∼800 μm of the collapsing microbubbles. Both calcium influx across the cell membrane via N-type calcium channels and intracellular calcium store are altered in response to microcavitation. Finally, the FDA-approved poloxamer 188 (P188) was used to reconstitute the compromised cell membrane and restore the cell's reparative capability. This finding may lead to a feasible treatment for partially mitigating the tissue damage associated with bTBI.

Significant efforts have been committed to better understand and regulate insulin secretion as it has direct implications on diabetes. The first phase of biphasic insulin secretion in response to glucose lasts about 10 minutes, followed by a more sustained release persisting several hours. Attenuated insulin release in the first phase is typically associated with abnormal β‐cells. While near‐infrared photobiomodulation (PBM) demonstrates potential for multiple therapeutic applications, photostimulatory effects on α‐ and β‐cells remain to be further elucidated. Herein, we demonstrate that 810 nm PBM exposure at fluence of 9 J/cm2 can elevate the intracellular reactive oxygen species within 15 minutes following photostimulation. In addition, calcium spiking showed an approximately 3‐fold increase in both ATC1 (α‐cells) and BTC6 (β‐cells) and correlates with hormone secretion in response to PBM stimulation. Our findings could lay a foundation for the development of non‐biologic therapeutics that can augment islet transplantation.

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