Exosomes are a type of extracellular vesicles, produced within multivesicular bodies, that are then released into the extracellular space through a merging of the multivesicular body with the plasma membrane. These vesicles are secreted by almost all cell types to aid in a vast array of cellular functions, including intercellular communication, cell differentiation and proliferation, angiogenesis, stress response, and immune signaling. This ability to contribute to several distinct processes is due to the complexity of exosomes, as they carry a multitude of signaling moieties, including proteins, lipids, cell surface receptors, enzymes, cytokines, transcription factors, and nucleic acids. The favorable biological properties of exosomes including biocompatibility, stability, low toxicity, and proficient exchange of molecular cargos make exosomes prime candidates for tissue engineering and regenerative medicine. Exploring the functions and molecular payloads of exosomes can facilitate tissue regeneration therapies and provide mechanistic insight into paracrine modulation of cellular activities. In this review, we summarize the current knowledge of exosome biogenesis, composition, and isolation methods. We also discuss emerging healing properties of exosomes and exosomal cargos, such as microRNAs, in brain injuries, cardiovascular disease, and COVID-19 amongst others. Overall, this review highlights the burgeoning roles and potential applications of exosomes in regenerative medicine.

https://www.mdpi.com/2073-4409/10/8/1959/pdf

Mesenchymal Stem Cell-Derived Exosomes: Applications in Regenerative Medicine.

The classic understanding of molecular disease-mechanisms is largely based on protein-centric models. During the past decade however, genetic studies have identified numerous disease-loci in the human genome that do not encode proteins. Such non-coding DNA variants increasingly gain attention in diagnostics and personalized medicine. Of particular interest are long non-coding RNA (lncRNA) genes, which generate transcripts longer than 200 nucleotides that are not translated into proteins. While most of the estimated ~20,000 lncRNAs currently remain of unknown function, a growing number of genetic studies link lncRNA gene aberrations with the development of human diseases, including diabetes, AIDS, inflammatory bowel disease, or cancer. This suggests that the protein-centric view of human diseases does not capture the full complexity of molecular patho-mechanisms, with important consequences for molecular diagnostics and therapy. This review illustrates well-documented lncRNA gene aberrations causatively linked to human diseases and discusses potential lessons for molecular disease models, diagnostics, and therapy.

/pdf/disease-causing-mutations-and-rearrangements-in-long-non-3s7xkg1rtb.pdf

Disease-Causing Mutations and Rearrangements in Long Non-coding RNA Gene Loci.

Long non-coding RNA ASMTL-AS1 inhibits tumor growth and glycolysis by regulating the miR-93-3p/miR-660/FOXO1 axis in papillary thyroid carcinoma.

Long non-coding RNAs (lncRNAs) and microRNAs are involved in numerous physio-pathological conditions included cancer. To better understand the molecular mechanism of the oral antitumor multikinase inhibitor sorafenib, we profiled the expression of a panel of lncRNAs and miRNAs by qPCR array in a sorafenib-treated hepatocellular carcinoma (HCC) cell line. Among the most affected ncRNAs, we found that sorafenib mediated the dysregulation of the lncRNAs GAS5, HOTTIP and HOXA-AS2 and the miR-126-3p, in a panel of human cancer cell lines (HCC, renal and breast carcinomas). By luciferase gene reporter assay, we discovered that GAS5 may act as a sponge for miR-126-3p in HCC cells. The expression level of GAS5 and miR-126-3p was verified in human liquid and/or solid biopsies from HCC patients. miR-126-3p expression in HCC tissues was decreased respect to their correspondent peritumoral tissues. The levels of plasmatic circulating miR-126-3p and GAS5 were significantly higher and lower in HCC patients compared to healthy subjects, respectively. This study highlighted the capability of sorafenib to modulate the expression of a wide range of ncRNAs and specifically, GAS5 and miR-126-3p were involved in the response to sorafenib of different cancer cell types.

/pdf/differential-expression-profiling-of-long-non-coding-rna-a115j209e9.pdf

Differential expression profiling of long non-coding RNA GAS5 and miR-126-3p in human cancer cells in response to sorafenib.

LINC00612 functions as a ceRNA for miR-214-5p to promote the proliferation and invasion of osteosarcoma in vitro and in vivo.

FAL1: A critical oncogenic long non-coding RNA in human cancers

OBJECTIVE
Recombinant humanized type III collagen (rhCol III) is a highly adhesive biomaterial composed of 16 adhesion-related tandem repeats refined from human type III collagen. Here, we aimed to investigate the effect of rhCol III on oral ulcers and reveal the underlying mechanism.


METHODS
Acid-induced oral ulcers were induced on the murine tongue, and rhCol III or saline drops were administered. The effect of rhCol III on oral ulcers was assessed using gross and histological analyses. The effects on the proliferation, migration, and adhesion of human oral keratinocytes were investigated in vitro. The underlying mechanism was explored using RNA-sequencing.


RESULTS
Administration of rhCol III accelerated the lesion closure of oral ulcers, reduced the release of inflammatory factors, and alleviated pain. rhCol III promoted the proliferation, migration, and adhesion of human oral keratinocytes in vitro. Mechanistically, the enrichment of genes associated with the Notch signaling pathway was upregulated after rhCol III treatment.


CONCLUSION
rhCol III promoted the healing of oral ulcers, showing promising therapeutic potential in oral clinics.

Recombination Humanized Type III Collagen Promotes Oral Ulcer Healing.

Aim: To discover the potential roles of plasma exosomal miRNAs in Hirschsprung's disease (HSCR) and identify potential noninvasive biomarkers for early diagnosis of HSCR. Materials & methods: Plasma samples were collected from HSCR patients and matched controls. Exosomes were isolated before high-throughput Illumina sequencing was utilized to gain a profile of dysregulated exosomal miRNAs, followed with further verification in two separate cohorts. Bioinformatics analyses were also adopted to explore the molecular functions of dysregulated miRNAs in Hirschsprung's disease. Results & conclusion: 31 dysregulated miRNAs were identified with five considered as promising HSCR signatures. Gene enrichment analysis disclosed that the upregulated miRNAs were most likely to participate in 'extracellular matrix-receptor interaction' and contribute to HSCR through interfering in cell junctions.

Molecular function predictions and diagnostic value analysis of plasma exosomal miRNAs in Hirschsprung's disease.

m6A demethylase ALKBH5 suppresses proliferation and migration of enteric neural crest cells by regulating TAGLN in Hirschsprung's disease

Alpha-ketoglutarate (αKG) is an essential metabolite that plays a crucial role in skeletal homeostasis. Here we aim to investigate the effect of αKG on alveolar socket healing and reveal the underlying mechanism in the view of macrophage polarization.In a murine model pretreated with or without αKG, mandibular first molars were extracted. Mandibular tissues were harvested for microCT and histological analyses. Immunofluorescence was used to evaluate macrophage polarization during healing process. Macrophages with αKG/vehicle supplementation in vitro were proceeded to quantitative real-time PCR and flow cytometry to further elucidate the mechanism.MicroCT and histological analyses showed accelerated healing and enhanced bone regeneration of extraction sockets in experimental group. αKG increased new bone volume in alveolar sockets and promoted the activity of both osteoblastogenesis and osteoclastogenesis. αKG administration reduced M1 pro-inflammatory macrophages in an early phase and promoted anti-inflammatory M2 macrophage polarization in a later phase. Consistently, the expressions of M2 marker genes were augmented in αKG group, while M1 marker genes were downregulated. Flow cytometry revealed the increased ratio of M2/M1 macrophages in cells treated with αKG.αKG accelerates the healing process of extraction sockets via orchestrating macrophage activation, with promising therapeutic potential in oral clinics. 

Alpha-ketoglutarate promotes alveolar bone regeneration by modulating M2 macrophage polarization.

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