Siddaraju V. Boregowda

TL;DR: It is shown that MSCs manage intracellular oxidative stress by targeting depolarized mitochondria to the plasma membrane via arrestin domain-containing protein 1-mediated microvesicles and simultaneously shed micro RNA-containing exosomes that inhibit macrophage activation by suppressing Toll-like receptor signalling.

TL;DR: It is demonstrated that exposure to atmospheric oxygen rapidly induced p53, TOP2A, and BCL2‐associated X protein (BAX) expression and mitochondrial reactive oxygen species (ROS) generation in primary mouse MSCs resulting in oxidative stress, reduced cell viability, and inhibition of cell proliferation.

TL;DR: The structural mechanism by which SR1664 actively antagonizes PPARγ is identified, and findings are extended to develop the inverse agonist SR2595, which promotes induction of osteogenic differentiation and suggests a therapeutic approach to promote bone formation.

TL;DR: By mechanistically linking stem/progenitor and effector functions, the studies provide a unifying framework in the form of an MSC hierarchy that models the functional complexity of populations that predicts how donor-to-donor heterogeneity and culture conditions impact the therapeutic efficacy of MSC populations for different disease indications.

TL;DR: It is shown that basal p53 levels are necessary to maintain MSC bi-potency, and oxygen-induced increases in p53 expression modulate cell fate and survival decisions, and that treatment of cells with FGF2 mitigates these effects by inducing TWIST2.