Jiali Tan

Teeth are formed through sequential and reciprocal interactions between epithelial and mesenchymal tissues and they are essential to physical and psychological health. In-depth knowledge of tooth development, from histology to the underlying mechanisms, is necessary for the regeneration of lost teeth. Therefore, the review firstly introduced tooth development, and summarized the use of tooth-derived stem cells. To date, epigenetic regulation has been shown to have roles in numerous activities, including odontogenesis. DNA methylation, histone modification and non-coding RNAs contribute to regulatory mechanisms in several dental stem cells.The statements also include the underlying epigenetic mechanisms of stem cells, and what’s more, the potential use of stem cells for tooth regeneration.

Background: Dual loading drug delivery system with tumor targeting efficacy and sequential release function provides a promising platform for anticancer drug delivery. Herein, we established a novel AuCOOH@FACS nanogel system for co-delivery miR-218 mimics (as bio-drug) and Temozolomide(as chemo-drug). Methods: DLS and TEM were employed to determine the characteristics of particles and nanogels. The cell viability was calculated for study synergistic effect of both drugs coadministration and in nanogel forms. The amounts of Au uptake were measured by ICP-MS in cell and tumors to quantify the targeting drug delivery efficacy. Tumor weight and mice weight were investigated to study the targeting antitumor efficacy of nanogel system. Results: The results revealed that using AuCOOH@FACS nanogel as delivery vehicles, drugs could be targeting delivery to tumor site, the intracellular uptake is enhanced to a greater extent, and significant antitumor efficacy is fold increase compared with free drug administration group, without noticeable system cytotoxicity. Conclusions: This system offers an efficient approach to cancer therapy and holds significant potential to improve the treatment of cancer in the future.

Mesenchymal stem cells (MSCs) are ideal candidates for different cellular therapies due to their simple isolation, extensive expansion potential, and low immunogenicity. For various therapeutic approaches, such as bone and cartilage repair, MSCs are expected to replace the damaged tissues by direct differentiation. However, age-related changes in MSCs lead to the loss of differentiation potential, loss of proliferation potential and increase in senescent cell numbers, which involve a steady loss of bone mass and frequently result in osteoporosis. In this review, we will introduce the characteristic and age-related changes of MSCs. In addition, we will also summarize the potential rescue mechanisms of age-related bone loss involved in differentiation regulation and proliferation regulation, including transcription factors, signal pathways, epigenetic regulation, and oxidative stress regulation.

Age related defect of the osteogenic differentiation of mesenchymal stem cells (MSCs) plays a key role in osteoporosis. Mechanical loading is one of the most important physical stimuli for osteoblast differentiation. Here, we compared the osteogenic potential of MSCs from young and adult rats under three rounds of 2 h of cyclic stretch of 2.5% elongation at 1 Hz on 3 consecutive days. Cyclic stretch induced a significant osteogenic differentiation of MSCs from young rats, while a compromised osteogenesis in MSCs from the adult rats. Accordingly, there were much more reactive oxygen species (ROS) production in adult MSCs under cyclic stretch compared to young MSCs. Moreover, ROS scavenger N-acetylcysteine rescued the osteogenic differentiation of adult MSCs under cyclic stretch. Gene expression analysis revealed that superoxide dismutase 1 (SOD1) was significantly downregulated in those MSCs from adult rats. In summary, our data suggest that reduced SOD1 may result in excessive ROS production in adult MSCs under cyclic stretch, and thus manipulation of the MSCs from the adult donors with antioxidant would improve their osteogenic ability.