There are many types of intercellular communication, and extracellular vesicles are one of the important forms of this. They are released by a variety of cell types, are heterogeneous, and can roughly be divided into microvesicles and exosomes according to their occurrence and function. Of course, exosomes do not just play a role in cell-to-cell communication. In the nervous system, exosomes can participate in intercellular communication, maintain the myelin sheath, and eliminate waste. Similarly, exosomes in the brain can play a role in central nervous system diseases, such as stroke, Alzheimer’s disease (AD), Parkinson’s disease (PD), prion disease, and traumatic encephalopathy (CTE), with both positive and negative effects (such as the transfer of misfolded proteins). Exosomes contain a variety of key bioactive substances and can therefore be considered as a snapshot of the intracellular environment. Studies have shown that exosomes from the central nervous system can be found in cerebrospinal fluid and peripheral body fluids, and that their contents will change with disease occurrence. Because exosomes can penetrate the blood brain barrier (BBB) and are highly stable in peripheral circulation, they can protect disease-related molecules well and therefore, using exosomes as a biomarker of central nervous system diseases is an attractive prospect as they can be used to monitor disease development and enable early diagnosis and treatment optimization. In this review, we discuss the current state of knowledge of exosomes, and introduce their pathophysiological roles in different diseases of the central nervous system as well as their roles and applications as a viable pathological biomarker.

An increasing number of research studies over recent years have focused on the function of microRNA (miRNA) molecules which have unique characteristics in terms of structure and function. They represent a class of endogenous noncoding single-strand small molecules. An abundance of miRNA clusters has been found in the genomes of various organisms often located in a polycistron. The miR-17-92 family is among the most famous miRNAs and has been identified as an oncogene. The functions of this cluster, together with the seven individual molecules that it comprises, are most related to cancers, so it would not be surprising that they are considered to have involvement in the development of tumors. The miR-17-92 cluster is therefore expected not only to be a tumor marker, but also to perform an important role in the early diagnosis of those diseases and possibly also be a target for tumor biotherapy. The miR-17-92 cluster affects the development of disease by regulating many related cellular processes and multiple target genes. Interestingly, it also has important roles that cannot be ignored in disease of the nervous system and circulation and modulates the growth and development of bone. Therefore, it provides new opportunities for disease prevention, clinical diagnosis, prognosis, and targeted therapy. Here we review the role of the miR-17-92 cluster that has received little attention in relation to neurological diseases, cardiac diseases, and the development of bone and tumors.

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Injured articular cartilage has a poor capacity for spontaneous healing. So far, satisfactory solution to this subsistent problem has not been found, but transgenic therapy may be a promising way. This study aims to evaluate the effectiveness of a tissue-engineered cartilage that was transfected with morphogenetic protein 7 (BMP 7) in repairing the cartilaginous defects of rabbit knee joints. Chondrocytes were transfected with BMP-7 gene (5 x 10(6) cells/ml), inoculated into the collagen-fibrin gel scaffolds, and cultured for 14 days. Then, the scaffolds were implanted onto the created defects (5.0 mm in diameter) in rabbits' knee joints. After 12 weeks, the rabbits were sacrificed and histological sections were evaluated using modified O'Driscoll cartilage scores; In situ hybridization and immunohistochemistry were performed to detect the expression of BMP-7 mRNA and BMP-7 at the implanted site while the content of DNA and GAG was determined as well. A better quality of repairs was observed at the 12th week after implantation when compared to the control group using histological analyses. The content of DNA and specific secretion of GAG in the treatment group is statistically significant different compared with the control group. Gene therapy may be a promising treatment method, but the novel therapy approach needs further studies with respect to a longer follow-up period.

Injured articular cartilage has a poor capacity for spontaneous healing. So far, a satisfactory solution to repair the injured cartilage has not been found, but transgenic therapy might be a promising treatment. This study aims to evaluate the potential of transfecting bone morphogenetic protein-7 (BMP-7), a secretory protein, into bone marrow-derived mesenchymal stem cells (BMSCs), in inducing the differentiation of bone marrow stromal cells into chondrocytes in vitro. The phenotypes of the cells were observed by alcian blue staining and H&E staining with an inverted microscope. The glycosaminoglycan (GAG) content of BMSCs transfected with pcDNA3.1-BMP7 or induced by inducing medium was examined after 7, 14, or 21 days of incubation. A standard curve as reference for BMSCs' GAG content was plotted using galacturonic acid. The content of type II collagen in culture medium was detected by ELISA. Our results demonstrated that BMP7-transfected BMSCs or BMSCs incubated with inducing medium possess the ability to differentiate into chondrocytes. BMP7-induced BMSCs secrete type II collagen and GAG. There was no significant difference between BMP7-induced BMSCs in their secreted protein content when compared with the positive control group (TGF-β1 and dexamethasone) (P > 0.05), but there was significant difference in the secreted protein profile when compared with the negative control group (P < 0.05).