Background: Glioma is a common malignant tumor worldwide. Sevoflurane (Sev) has been reported to inhibit the metastasis of glioma cells, but the underlying molecular mechanism needs further exploration. Methods: Cell Counting Kit-8 (CCK8) assay was used to check cell viability. Flow cytometry assay was hired to check cell apoptosis. The protein levels of B-cell lymphoma-2 (Bcl-2), BCL2-Associated X (Bax), hexokinase 2 (HK2) and magnesium transporter 1 (MAGT1) in samples were measured by Western blot. The abilities of cell migration and invasion were estimated by transwell assay. Glucose colorimetric assay kit and lactate colorimetric assay kit were used to check glucose consumption and lactate production, respectively. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the levels of circular RNA (circRNA) circ_0002755 (also known as the circRNA1656) and microRNA (miR)-628-5p in samples. The interaction between miR-628-5p and circ_0002755 or MAGT1 was predicated by starBase, which was verified by the dual-luciferase reporter assay. Xenograft tumor model was established to explore the biological role of circ_0002755 in vivo. Results: Sev inhibited cell viability, migration, invasion and promoted cell apoptosis, and also reduced glucose consumption and lactate production. Circ_0002755 was significantly upregulated in glioma tissues and cells, while its level was notably declined under Sev treatment. Besides, overexpression of circ_0002755 overturned Sev-mediated inhibitory effect on glioma progression. Further research indicated that circ_0002755 targeted miR-628-5p, and miR-628-5p targeted MAGT1, and Sev modulated glioma progression via circ_0002755/miR-628-5p/MAGT1 axis. Moreover, Sev hindered tumor growth in vivo. Conclusion: Sev mediated glioma progression via circ_0002755/miR-628-5p/MAGT1 axis.

Mesenchymal stem cells (MSCs) and regulatory T cells (Tregs) both have been shown to modulate the alloimmune response and promote transplant survival. Mounting evidence suggests that MSCs augment Treg function, but the mechanisms underlying this phenomenon have not been fully deciphered. Here, we identified that MSCs express substantial levels of CD80 and evaluated its immunoregulatory function using in vivo and in vitro experiments. Our in vitro culture assays demonstrated that MSCs induce expression of FoxP3 in Tregs in a contact‐dependent manner, and the blockade of CD80 abrogates this FoxP3 induction and Treg‐mediated suppression of T cell proliferation. Moreover, supplementation of soluble CD80 significantly upregulated FoxP3 expression. Using a well‐characterized murine model of corneal transplantation, we show that silencing CD80 in MSCs diminishes the capacity of MSCs to promote selective graft infiltration of Tregs, promote FoxP3 expression and upregulate suppressive function of Tregs. Consequently, MSCs, following CD80 knockdown, failed to promote corneal allograft survival.

Dry eye disease (DED), a multifactorial ocular surface disease, is estimated to affect up to 34% of individuals over 50 years old. Although numerous animal models, including rodents and rabbits, have been developed to mimic the pathophysiologic mechanisms involved in dry eye, there is a lack of non-human primate (NHP) models, critical for translational drug studies. Here, we developed a novel desiccating stress-induced dry eye disease model using Rhesus macaque monkeys. The monkeys were housed in a controlled environment room for 21 to 36 days under humidity, temperature, and airflow regulation. Following desiccating stress, NHPs demonstrated clinical symptoms similar to those of humans, as shown by increased corneal fluorescein staining (CFS) and decreased tear-film breakup time (TFBUT). Moreover, corticosteroid treatment significantly reduced CFS scoring, restored TFBUT, and prevented upregulation of tear proinflammatory cytokines as observed in dry eye patients following steroid treatment. The close resemblance of clinical symptoms and treatment responses to those of human DED patients provides great translational value to the NHP model, which could serve as a clinically relevant animal model to study the efficacy of new potential treatments for DED.