MicroRNAs in Small Extracellular Vesicles from Amniotic Fluid and Maternal Plasma Associated with Fetal Palate Development in Mice.

Cleft palate (CP) is a common congenital birth defect. Cellular and morphological processes change dynamically during palatogenesis, and any disturbance in this process could result in CP. However, the molecular mechanisms steering this fundamental phase remain unclear.

Inhibition of Disrupts Mouse Embryonic Palatal Mesenchymal Cell Migration and Induces Cleft Palate Occurrence.

Many processes take place during embryogenesis, and the development of the palate mainly involves proliferation, migration, osteogenesis, and epithelial-mesenchymal transition. Abnormalities in any of these processes can be the cause of cleft palate (CP). There have been few reports on whether C-X-C motif chemokine receptor 4 (CXCR4), which is involved in embryonic development, participates in these processes.

Osteogenic microenvironment affects palatal development through glycolysis.

Palate development involves various events, including proliferation, osteogenic differentiation, and epithelial-mesenchymal transition. Disruption of these processes can result in the cleft palate (CP). Mouse embryonic palatal mesenchyme (MEPM) cells are commonly used to explore the mechanism of palatal development and CP.

Comparative analysis of mouse embryonic palatal mesenchymal cells isolated by two primary culture methods.

Cell culture plays a vital role in mechanism research, as a supplement to experiments in vivo. At present, there are two main methods to obtain mouse embryonic palatal mesenchymal (MEPM) cells, while no systematic investigation about characteristics of cells using these two methods to get a clear application. In this study, using the traditional two-step primary culture method as the control group, we found that the MEPM cells of the simplified one-step method and the control group were both consistent with the surface markers of mesenchymal stem cells.

The production, detection, and origin of irisin and its effect on bone cells.

Irisin is a muscle factor discovered in 2012 that plays an important role in many tissues, including bone. Eight years since its discovery, there are still many controversies regarding its molecular biology, detection, and effects on bone. This article summarizes the points raised to date, and discusses the mechanisms by which irisin regulates bone cells.

Cartilage Extracellular Matrix Scaffold With Kartogenin-Encapsulated PLGA Microspheres for Cartilage Regeneration.

Repair of articular cartilage defects is a challenging aspect of clinical treatment. Kartogenin (KGN), a small molecular compound, can induce the differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) into chondrocytes. Here, we constructed a scaffold based on chondrocyte extracellular matrix (CECM) and poly(lactic-co-glycolic acid) (PLGA) microspheres (MP), which can slowly release KGN, thus enhancing its efficiency.

Immunomodulation of MSCs and MSC-Derived Extracellular Vesicles in Osteoarthritis.

Osteoarthritis (OA) has become recognized as a low-grade inflammatory state. Inflammatory infiltration of the synovium by macrophages, T cells, B cells, and other immune cells is often observed in OA patients and plays a key role in the pathogenesis of OA. Hence, orchestrating the local inflammatory microenvironment and tissue regeneration microenvironment is important for the treatment of OA.

An Ultrashort Peptide-Based Supramolecular Hydrogel Mimicking IGF-1 to Alleviate Glucocorticoid-Induced Sarcopenia.

Sarcopenia is a common disease in older people due to aging, and it can also occur in midlife because of diseases including cancer. Sarcopenia, characterized by rapid loss of muscle mass and accelerated loss of function, can lead to adverse outcomes such as frailty, falls, and even mortality. The development of pharmacological and therapeutic approaches to treat sarcopenia remains challenging.

Exosomes derived from Wharton's jelly of human umbilical cord mesenchymal stem cells reduce osteocyte apoptosis in glucocorticoid-induced osteonecrosis of the femoral head in rats via the miR-21-PTEN-AKT signalling pathway.

: Glucocorticoid-induced osteonecrosis of the femoral head (GIONFH) is a common disease after long-term or high-dose glucocorticoid use. The pathogenesis of GIONFH is still controversial, and abnormal bone metabolism caused by glucocorticoids may be one of the important factors. Exosomes, owing to their positive effect on bone repair, show promising therapeutic effects on bone-related diseases.