Recent studies suggest important roles for long non-coding RNAs as essential regulators of myogenic differentiation. Here, we report that lncRNA Irm is upregulated during myogenesis. Functional analyses show that the overexpression of Irm enhances myogenic differentiation, whereas the inhibition of Irm has completely opposite effects in vitro. Notably, the inhibition of Irm blocks damage-induced muscle regeneration in vivo. Mechanistically, Irm regulates the expression of myogenic genes by directly binding to MEF2D, which in turn promotes the assembly of MyoD/MEF2D on the regulatory elements of target genes. Collectively, we have identified a novel lncRNA that interacts with MEF2D to regulate myogenesis.

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Objectives: Inflammation and apoptosis play a critical role in the pathological progress of traumatic brain injury (TBI). Isoliquiritigenin is a bioactive component extracted from licorice roots, which possesses anti-inflammatory and anti-apoptotic properties. This study aims to investigate the potential effects of isoliquiritigenin on neuroinflammation in a rat model of TBI. Methods: The SH-SY5Y cells were subjected to cell injury induced by shear stress and the effect of isoliquiritigenin on cell apoptosis was measured. Male rats received a controlled cortical impact to induce TBI and were then treated with isoliquiritigenin (20 mg/kg). Brain edema and contusion volume were measured to assess brain damage. Morris water maze, the beam-balance test, and the beam-walk test were performed to evaluate the cognitive and motor functions. Results: Levels of proinflammatory cytokines and apoptotic regulators were measured. Results showed that isoliquiritigenin reduced shear stress-induced cell apoptosis in vitro. In young rats subjected to TBI, treatment of isoliquiritigenin reduced brain damage and attenuated motor and cognitive impairments. Isoliquiritigenin also reduced the level of proinflammatory cytokines and Bax and increased Bcl-2 and Bcl-xL in TBI rats. Conclusions: These findings suggest that isoliquiritigenin possesses beneficial effects in TBI by inhibiting inflammation and apoptosis.

Tissues and organs undergo structural deterioration and functional decline during aging. DNA damage is considered a major cause of stem cell senescence. Although stem cells develop sophisticated DNA repair systems, when the intrinsic and extrinsic insults exceed the DNA repair capacity, cellular senescence, and age-related diseases inevitably occur. Therefore, the prevention and alleviation of DNA damage is an alternative to DNA repair in attenuating stem cell senescence and preventing age-related diseases. Pre-B-cell leukaemia homeobox 1 (PBX1) participates in maintaining the pluripotency of human embryonic and haematopoietic stem cells. Our recent studies showed that PBX1 promotes hair follicle-derived mesenchymal stem cell (HF-MSC) proliferation, decreases cellular senescence and apoptosis, and enhances induced pluripotent stem cell generation. Whether PBX1 attenuates HF-MSC senescence and apoptosis by alleviating DNA damage or by enhancing DNA repair remains unknown. In this study, we aimed to determine the effects of PBX1 on the intrinsic ROS or extrinsic H2O2-induced cellular senescence of HF-MSCs. To this end, we generated HF-MSCs overexpressing either PBX1, or poly (ADP-ribose) polymerase 1, or both. Our results showed that PBX1 overexpression attenuates HF-MSC senescence and apoptosis by alleviating reactive oxygen species (ROS)-mediated DNA damage instead of enhancing DNA repair. This is the first study to report that PBX1 attenuates stem cell senescence and apoptosis by alleviating DNA damage. It provides new insight into the mechanism of stem cell senescence and lays the foundation for the development of strategies for age-related disease prevention and treatment, and in particular, hair follicle repair and regeneration.