Numerous studies have demonstrated that interferon-γ (IFN-γ) is an important inflammatory cytokine, which may activate the immunomodulatory abilities of mesenchymal stem cells (MSCs), and may influence certain other functions of these cells. MicroRNAs are small non-coding RNAs that regulate the majority of the biological functions of cells and are important in a variety of biological processes. However, few studies have been performed to investigate whether IFN-γ affects the microRNA profile of MSCs. The aim of the present study was to analyze the microRNA profile of MSCs derived from the umbilical cord (UC-MSCs) cultured in the presence or absence of IFN-γ (IFN-UC-MSCs). An array that detects 754 microRNAs was used to determine the expression profiles. Statistical analysis of the array data revealed that 8 microRNAs were significantly differentially expressed in UC-MSCs and IFN-UC-MSCs. Reverse transcription-quantitative polymerase chain reaction validated the differential expression of the 8 identified microRNAs. The target genes of the 8 microRNAs were predicted through two online databases, TargetScan and miRanda, and the predicted results were screened by bioinformatics analysis. The majority of the target genes were involved in the regulation of transcription, signal transduction, proliferation, differentiation and migration. These results may provide insight into the mechanism underlying the regulation of the biological functions of MSCs by IFN-γ, in particular the immunomodulatory activity.

The pro-survival transcription factor myocyte enhancer factor 2D (MEF2D) is identified to exhibit pro-tumor effects based on clinical and experimental studies. However, the detailed mechanisms underlying IGF-1-MEF2D pathway-induced tumor biology in cardiac myxoma (CM) was not clear. Here, we investigated the role of MEF2D in CM tissues and cells using RT-PCR, western blot, gene silencing, et al. Our findings revealed MEF2D was significantly increased in CM tissues compared with adjacent normal tissues and closely related to tumor size. In vitro assay demonstrated that IGF-1 enhanced CM cell proliferation in a time-dependent fashion. However, knockdown of MEF2D reversed the IGF-1-induced proliferative effects on CM cells in a time-dependent fashion and further resulted in cell cycle arrest. Based on the molecular level, IGF-1 enhanced the expression of epidermal growth factor receptor (EGFR) and matrix metalloprotein 9 (MMP9) in CM cells, whereas knockdown of MEF2D was able to reduce the expression of EGFR and MMP9 compared with vector control. Furthermore, we found knockdown of MEF2D directly affected G1/S transition in cultured CM cells. In conclusion, MEF2D regulates IGF-1-induced proliferation and apoptosis in CM development, indicating IGF-1-MEF2D pathway may be a useful target for treatment.

Lidocaine (Lido) is an amide local anesthetic that has both excitatory and inhibitory effects on the central nervous system, and is one of a group of commonly used local nerve block drugs that are used in the clinic. However, traditional Lido does not meet the transdermal performance requirements of surface anesthetic agents for treating pain in patients. Optimizing the preparation of a Lido transdermal preparation and improving the control of anesthetic depth and efficiency has become a challenge in the field of topical anesthesia. In this study, a new type of Lido nano-transdermal preparation, carboxymethyl chitosan-modified lidocaine liposomes (Lido-CMCSNLP), were constructed based on nano-liposomes. Carboxymethyl chitosan can enhance the permeability of hydrophilic macromolecular pathways by interacting with negatively charged membrane glycoproteins, which is beneficial for the transdermal absorption of Lido. Therefore, Lido-CMCS-NLP provides a new approach for research in clinical topical anesthesia and perioperative topical analgesics.